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Annals Vol 22 (2014)

Published by RACDS, 2020-10-24 02:13:28

Description: Annals Vol 22 (2014)

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49 ensuring accurate muscular reconstruction is essential for the 1a) 1b) development of speech. A significant percentage of patients with cleft palate have middle ear disease due to eustachian 1c) dysfunction and require ventilation tubes. With the eruption of the primary dentition, paediatric dental assessment begins 1d) and a speech assessment undertaken as soon as possible to detect any degree of velopharyngeal incompetence. 1e) Fig 1. 17 year old male, pre-treatment with right unilateral cleft As in our Centre, the majority of international cleft Units lip/palate: a), b) - Frontal and profile views; c), d), e) - maxillary delay grafting of the alveolar maxillary cleft until 8 – 12 years, and lateral occlusal views to minimize the restriction of maxillary growth. In unilateral cases, the lesser segment on the cleft side collapses palatally whereas in bilateral alveolar clefts, both buccal segments may rotate palatally. Orthodontic expansion of the displaced segments is required prior to alveolar grafting and a variety of expansion devices are available such as the standard hyrax appliance. This is banded to the first molars and has extension arms that extend to the primary canines. “Fan-screw” expansion devices may also be used for greater differential expansion of the anterior portion of the displaced segments. Cancellous bone from the iliac crest remains the most popular donor graft material. Labial and palatal flaps are raised, intervening tissue is cleared from the cleft and the flaps rotated to close the nasal communication and 1-2cc of graft inserted to unite the alveolar segments followed by passive mucosal closure. Ideally alveolar bone grafting is undertaken when the canine route is half to two-thirds formed5 to enable eruption of the canines through the graft into a healthy periodontium.6 On the eruption of the permanent dentition, a high proportion of cleft patients have a hypoplastic maxilla, often in all dimensions. There is an intrinsic lack of mid-facial development as has been noted6,7 but the secondary cleft deformities also relate to the effects of primary surgery and subsequent procedures that introduce scarring. Assuming a mandible of normal dimensions, this restriction of growth in the cleft maxilla can thus alter the overall pattern from a Class I skeletal malocclusion to a Class III skeletal relationship. An inherited Class III skeletal malocclusion becomes even more severe. In patients with a degree of mandibular hypoplasia, the maxillary deficiency may then result in a Class I dental relationship but with poor facial aesthetics and cannot be regarded as a good outcome in contemporary management. The indication for maxillary advancement to correct the dento-facial disproportion varies between Centres but has been reported as between 5- 60%. Factors that may account for this range relate to the technique of the primary repair, the treatment goals of particular centres and patient expectations. Varying access to an appropriate multidisciplinary team as well as the economic constrains of different health services also influence treatment decisions. However, it is generally agreed that for a large group of patients, a combination of orthognathic surgery and orthodontic treatment is required. This is often followed by a lip revision and a septorhinoplasty to achieve patent nasal airways and better nasal symmetry and aesthetics (Figs 1, 2). For severe skeletal Class III patterns in the cleft population, a two-stage advancement procedure may be required. Distraction osteogenesis has been advocated as a preliminary step also but there is yet to be a consensus on the role of this technique. Outcome measures for the cleft lip and patient at the completion of growth have yet to be established but the expectation of good facial symmetry, a balanced profile, and a functional occlusion with patent nasal airways should be minimum criteria.

50 2. CRANIOFACIAL MICROSOMIA 2a) This interesting disorder of facial growth has an incidence of between 1:5000-1:6000 and involves abnormalities of the structures of the first and second branchial arch. There have been many names for the varied phenotypical expressions of this anomaly including Goldenhar syndrome and Oculo-auriculo-vertebral syndrome. There is no known cause but rupture of the stapedial artery in mouse embryos was initiated in a study using a teratogenic drug and similar abnormalities were demonstrated.7 However, this does not account for bilateral involvement and the many extra- craniofacial manifestations. There have been many genetic investigations of affected patients and families but there is no 2b) consistent pattern of chromosomal abnormalities. However, deletions on chromosome 22 have been described in a number of cases.8 Craniofacial microsomia exhibits abnormalities of the ears, ranging from absence of the auricle and middle ear structures to bizarre pinna morphology and skin tags. Facial nerve dysfunction is variable from weakness to full facial palsies. Abnormal mandibular development of the condyle/ ramus unit(s) is a prominent feature that has major functional significance. Patients may also demonstrate hypoplasia of the orbito-zygomatic complex, a deficiency in the soft tissues of the face and macrostomia. Epibulbar dermoids and colobomas may be noted in bilateral cases. Fusion of cervical spine segments, cardiac and renal abnormalities have 2c) also been recorded. With such a diverse range of features, the condition is now best described as an “oculo-auriculo- vertebral spectrum”. With respect to facial growth, affected sides develop disproportionately less and as the maxillo- mandibular complex matures, there is a more marked occlusal cant. The mandibular deformities have been classified for practical management into unilateral hypoplasia (Type I), hypoplasia with an abnormal ramus/condyle (Type IIA), severe hypoplasia and medial displacement of the complex (Type IIB) to absence of the ramus and condyle (Type III).9 At the Royal Children’s Hospital Melbourne, an analysis of a cohort of patients revealed the incidence of Types I/ IIA and Types IIB/III to be 57% and 43% respectively.10 For patients in the less affected group, orthodontic treatment 2d) and orthognathic surgery is undertaken in the mid- to late teenage years to correct the facial asymmetry and occlusion. Those more severely affected require TMJ reconstruction and undergo grafting procedures, most commonly, a costo- chondral segment from the sixth or seventh rib to create a new joint and to lengthen the mandible on the affected side. An orthodontic occlusal appliance is placed to bridge the created gap and progressively adjusted to enable descent of the maxillary dentition on the affected side. In the following years, the graft thickens under functional loading to form a strong “neo-TMJ” that enables corrective jaw surgery at the completion of growth (Figs 3, 4). Any residual deficiency of facial contour can then be addressed by onlay alloplastic materials and/or autogenous fat transfer that is proving to give a more natural appearance. 2e) Fig 2. Post-treatment surgically-assisted expansion, maxilla- mandibular repositioning and septorhinoplasty: a), b) - Frontal and profile views; c), d), e) - maxillary and lateral occlusal views

51 Fig 3. 11 year old female, right hemifacial microsomia, Type IIB; a) Frontal facial view; b) Occlusion; c) C- OPG of right ramus/ condyle Type IIB deformity; d) Intraoperative costo-chondral graft for reconstruction; e) Right buccal open bite post-graft; f) 3D CT scan of reconstructed condyle/ramus Fig 4. Post-treatment: a) Frontal facial view; b) Profile facial view; c) Occlusion 3. CRANIOSYNOSTOSIS head shape and a low “bullet-shaped” occiput with frontal bossing. Trigonocephaly is due to metopic synostosis giving The craniosynostoses are uncommon disorders that are a triangular shape to the forehead. The incidence of this caused by premature closure of cranial sutures and involve a condition appears to be increasing worldwide for unknown large proportion of treatment time within craniofacial centres. reasons. Frontal plagiocephaly is a flattening of the forehead Brain growth in the infant is rapid in the first 24 months of on the affected side where the coronal suture prematurely life and early suture closure causes a restriction of growth fuses and this must be distinguished from deformational at right angles to the suture. This results in recognizable plagiocephaly that is a result of constant pressure, usually on skull deformities as the pressure of brain growth distorts one side of the occiput, resulting in a parallelogram deformity the calvarium where it is unrestricted. Scaphocephaly, is in the absence of synostosis. The genetic background to the commonest deformity of the single suture group and single-suture synostoses remains uncertain. results from sagittal suture synostosis giving a long narrow

52 The syndromic cranial synostoses have a much more profound intracranial volume. The growing brain pushes into the inner table effect on facial growth as multiple sutures are fused and of the calvarian and can produce a “copper beaten” appearance extend to the base of the skull. Anomalies in this group of the skull on imaging. Hence, a fronto-orbital advancement is with recognizable phenotypes include Crouzon, Apert and undertaken within the first 18 months to increase intracranial Pfeiffer syndromes. Common characteristics include a lack volume and to make use of the high regenerative capacity of of frontal development resulting in retrusion of the forehead, bone in this age group to heal any residual defects over the marked mid-facial hypoplasia resulting in prominence of the duramater. However, the mid-facial retrusion persists as there ocular globes as the infraorbital and supraorbital margins is an inherent lack of antero-posterior and vertical growth. As are well behind the most anterior part of the cornea. These the child develops, the mid-facial deformity relatively worsens patients usually have a significant Class III malocclusions with normal mandibular growth. For those with symptoms and, in the case of Apert syndrome, a markedly constricted of obstructive sleep apnea, early mid-facial advancement maxilla with an upwardly tilted occlusal plane resulting in a is undertaken. Otherwise, advancement is performed prior large anterior open bite. However, mandibular growth and to puberty between 8 and 12 years. Traditionally, the mid- development is relatively normal. For these syndromes, the face was repositioned with a Le Fort III advancement in one genetic abnormalities are mutations in fibroblastic growth procedure with internal fixation and bone grafting, but there is factor receptors (FGFR). These receptors are transmembrane a limitation in the amount of advancement possible due to soft polypeptides with an immunoglobulin-like extracellular domain tissue restriction. In our Unit, distraction of the mid-face is now and the intracellular portion interacts with tyrosine kinase undertaken by performing a Le Fort III and then either applying that triggers a cascade of intracellular events. Amino acid internal devices to push forward the segment12 or “pulling”, substitution in these receptors results in a “gain of function” using a halo frame anchored to the calvarian and traction wires mutation where activity is up-regulated and leads to greater attached to the pyriform apertures of the nose and other sites osteoblastic activity and premature closure of sutures.11 such as the infraorbital region or lateral orbital regions. This latter approach appears to be less invasive and effective for With multiple fused sutures, these patients are at a significant producing sufficient advancement with over correction (Fig 5).13 risk of raised intracranial pressure due to the restriction of Fig 5. Five year old female with Crouzon syndrome and obstructive sleep apnoea. a) Lateral facial view; b) Lateral cephalogram; c) External device at completion of distraction, d) Follow-up 12 months Despite this advancement, the mid-face does not continue to grow into the teenage years and in many patients, a Class III skeletal pattern returns and further stages of mid-facial correction, orthodontic treatment and orthognathic surgery are required to complete treatment to as close to normal facial proportions as possible (Fig 6).

53 Fig 6. Six year old male proportion of these patients required surgical procedures with Crouzon syndrome. such as a tongue-lip adhesion or a tracheostomy to maintain a), b) - Frontal and profile the airway. However, over the past decade, distraction facial views; c), d) - Frontal osteogenesis techniques have been introduced to lengthen and profile view post mid- the mandible thus moving the tongue base anteriorly and facial advancement age 6; opening the pharyngeal space. Originally, a retromolar e), f) - Frontal and profile osteotomy of the mandible was undertaken followed by the views post orthognathic insertion of extraoral transcutaneous pins attached to a surgery / septorhinoplasty; distraction device to enable slow elongation of the mandibular g) Occlusion; h) Lateral body. In our Maxillofacial Unit, the use of paediatric internal cephalogram distractors devices was pioneered by insertion via a submandibular access incision bilaterally with the activation 4. MICROGNATHIA arm now protruding transcutaneously, just below the ears.16 Distraction is undertaken at 1.5 mm per day for 10 days and Marked hypoplasia of the mandible occurs in a number patients are usually extubated on the 5th postoperative day of infant syndromes and may be associated with upper with complete resolution of airway obstruction. Feeding has airway obstruction, gastroesophageal reflux and feeding also noted to improve and with normal nocturnal oxygen difficulties. Pierre Robin Syndrome was first described saturation, more normal development has been noted at 12 with features of micrognathia and a posteriorly positioned months follow-up. This technique has proved to be highly tongue (glossoptosis).14 Usually these infants also have a wide successful over the past 12 years and is now a highly reliable “U-shaped” cleft palate. The genetics of Robin sequence technique for managing patients with the Robin sequence yet to be understood despite some familial inheritance with and upper airway obstruction. A number of patients who evidence of abnormalities on chromosome 17.15 The restricted were tracheostomy-dependent have also been decannulated pharyngeal space a may result in mild to severe upper airway using this distraction technique. In other syndromic patients obstruction requiring in-patient care in a neonatal intensive with upper airway obstruction and micrognathia, such care unit. as severe Craniofacial Microsomia and Treacher-Collins syndrome, relapse may occur due to their unusual mandibular Management has varied from prone positioning to prevent morphology and further distraction has been required. the tongue from falling posteriorly, to the placement of a nasopharyngeal tube to bypass the obstructed anatomical Even rare micrognathic conditions, which were previously site and occasionally these patients are incubated with phenotypically classified as syngnathia and dysgnathia, positive pressure oxygen therapy. In previous decades, a small have presented with severe hypoplastic and malformed symmetrical mandibles, the absence of normal tongue formation and unusual auricle formation. These patients are now more accurately described as Auriculo-condylar syndrome and genetic insights have been proposed as to the cause of the abnormal mandible.17 5. MISCELLANEOUS DISORDERS Congenital macroglossia secondary to enlargement of the musculature of the tongue is a prominent feature in Beckwith Wiedemann syndrome. This is a rare, congenital overgrowth disorder with an instance of 1:15000 births. Most cases are sporadic but 15% are thought to be inheritable with complex genetics. There is an operational imprinted growth regulatory gene on chromosome 11 and epigenetic factors are also thought to be involved.18 These infants have a high birth weight, may have anterior abdominal wall defects and demonstrate ear creases or pits. They require regular ultrasonography to screen for embryonal tumours that occur in approximately 5% of patients. The pressure of the tongue enlargement can distort the mandibular alveolus and result in spacing of primary teeth. Drooling, speech impairment and importantly for the parents, an incorrect perception of intellectual disability to the public give a pressing indication for tongue reduction surgery. This is undertaken between 12 and 24 months the volume removed is performed according to the degree of macroglossia and is usually a permanent correction of this major feature of the condition (Fig 5). The presence of multiple keratocystic odontogenic tumours in a young patient raises the possibility of Gorlin syndrome

54 (Multiple Basal Cell Naevus syndrome). Affected patients REFERENCES may have frontal bossing, a degree of hypertelorism and imaging demonstrates calcification of the falx cerebri. In later 1. Dawkins R. The Selfish Gene. Oxford University Press Inc; Great years, multiple skin lesions (basal cell naevi and carcinomas) Clarendon Street, Oxford OX2 6DP; 1976. develop and require dermatological surveillance and removal is required.19 2. Betters E, Liu Y, Kjaeldgaard A, Sundström E, García-Castro MI. Analysis of early human neural crest development. Dev Biol 2010;344:578-592. The propensity to develop to jaw cysts appears to reduce following the completion of growth. Mutations on chromosomes 3. Richards AJ, Laidlaw M, Whittaker J, Breacy B, Rai H, Bearcroft P, 1, 9 and 10 have been recorded. Close followup is required to Baguley DM, Poulson A, Ang A, Scott JD, Snead MP. High efficiency intercept extensive cyst formation during growth. of mutation detection in type 1 Stickler syndrome using a two-stage approach:vitreoretinal assessment coupled with exon sequencing for SUMMARY screening COL2A1. Hum Mutat 2006;27:696-704. Many of the common cleft and craniofacial anomalies 4. Lam FS, Bendeus M, Wong RW. A multidisciplinary ream approach on appear to have a complex genetic background with many cleft lip and palate management. Hong Kong Dent J 2007;4:38-45. factors involved and it is likely to take many years for a clear understanding. 5. Bergland O, Semb G, Abyholm FE. Elimination of the residual alveolar cleft by secondary bone grafting and subsequent orthodontic treatment. The classification of cleft and craniofacial anomalies is a Cleft Palate J 1986;23:175–205. dynamic process due to the constantly updates and insights that are gained by genetic investigation of both patients 6. Hogan L, Shand JM, Heggie AA, Kilpatrick K Canine eruption into grafted and their families. While phenotypical description has been alveolar clefts:A retrospective study. Aust Dent J 2003;48:119-124. the best method of attempting to understand the spectrum of disorders, a transition to classifications based on genetic 7. Poswillo D, Hemorrhage in the development of the face. Birth Defects characterization will take place and provide families and Orig Artic Ser 1975;11:61-81. clinicians a better understanding of the aetiology, the behaviour and long-term expectations of each disorder. 8. Derbent M, Yilmaz Z, Baltaci V, Saygili A, Varan B, Tokel K. Chromosome 22q11.2 deletion and phenotypic features in 30 patients with conotruncal The management of craniofacial anomalies is best undertaken heart defects. Am J Med Genet 2003;116A:129-135. in a multi-disciplinary unit with a team approach where each speciality clinician can provide timely intervention. A 9. Mulliken JB, Kaban LB. Analysis and treatment of hemifacial microsomia protocol-driven approach to treatment planning through to in childhood. Clin Plast Surg 1987;14:91-100. maturity is seen to provide superior final outcomes and many should be better benchmarked for the future. 10. Poon C-H, Meara JG, Heggie AA. Hemifacial Microsomia:use of the OMENS Plus classification at the Royal Children’s Hospital of Melbourne. ACKNOWLEDGEMENTS Plast Reconstr Surg 2003;111:1011-1018. The assistance of Clinical Professor Anthony Holmes in 11. Levi B1, Wan DC, Wong VW, Nelson E, Hyun J, Longaker MT. Cranial suture the management of the patient in Figure 6 is gratefully biology: from pathways to patient care. J Craniofac Surg 2012;23:13-9. acknowledged. 12. Holmes AD, Wright GM, Meara J, Heggie AA, Probert T Le Fort III internal distraction in syndromic craniosynostosis. J Craniofac Surg 2002;13:262-272. 13. The role of distraction osteogenesis in the management of craniofacial syndromes. Heggie AA, Kumar R, Shand JM. Ann Maxillofac Surg 2013;3:4-10. 14. Robin P. Glossoptosis due to atresia and hypotrophy of the mandible. Am J Dis Child 1934;48:541-547. 15. Benko S1, Fantes JA, Amiel J, Kleinjan DJ, Thomas S, et al. Highly conserved non-coding elements on either side of SOX9 associated with Pierre Robin sequence. Nat Genet 2009; 41:359-364. 16. Chigurupati R, Massie J, Dargaville P, Heggie AA. Internal mandibular distraction to relieve airway obstruction in infants and young children with micrognathia. Pediatr Pulmonol 2004;37:230-235. 17. Rieder MJ, Green GE, Park SS, Stamper BD, Gordon CT et al. A human homeotic transformation resulting from mutations in PLCB4 and GNA13 causes auriculocondylar syndrome. Am J Hum Genet 2012;91:907-914 18. Heggie AA, Vujcich NJ, Portnof JE, Morgan AT Tongue reduction for macroglossia in Beckwith Wiedemann syndrome: review and application of new technique. Int J Oral Maxillofac Surg 2013;42:185-191. 19. Cysts of the jaws and advances in the diagnosis and management of naevoid basal cell carcinoma syndrome. Shand JM, Heggie AA Oral Maxillofac Surg Clin North Am 2005;17:403-414. Fig 7. Robin sequence infant. a) Lateral facial view showing micrognathia; b) Schematic diagram of distraction technique.

55 Fig 8. Beckwith Weidemann Syndrome, 12-mo-old male. a) Macroglossia with tongue protruding; b) Pattern of tongue reduction; c) Final tongue repair with tip behind anterior teeth. Address for correspondence [email protected] Permission has been granted by patients/ parents to publish identifiable photographs

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 56-59 APPLICATION OF SWEPT-SOURCE OPTICAL COHERENT TOMOGRAPHY TO CARIES DIAGNOSIS Professor Junji Tagami, D.D.S., Ph.D. Dr. Tagami is Dean of the Faculty of Dentistry and Dean of Graduate School at Tokyo Medical and Dental University. ABSTRACT Swept-source optical coherence tomography(SS-OCT) is a new imaging technology using optical light with the wavelengths around 1300nm. The SS-OCT provides us the 3 dimensional image with much higher resolution than dental X-ray. The extent of caries lesion is very clearly observed in the obtained image. The purposes of this article is to introduce the recent research on the SS-OCT imaging of tooth and to discuss the possibility of clinical application of the SS-OCT for diagnosing occlusal caries, inter-proximal caries, recurrent caries, root caries, cracks, and monitoring the early caries lesion. INTRODUCTION OCT.8 De- and remineralized lesions in bovine enamel and dentin blocks were sectioned into 300- to 400-µm-thick Optical coherence tomography (OCT) can construct images slices, and placed on a metal plate to capture images of through the wave interference that occurs when backscattered sound, de- and remineralized regions transversely by the SS- light from a sample is coupled with a reference light.1, 2 OCT OCT. Mean n at each depth level of the lesion (20- or 40-µm visualizes differences in the tissue’s optical properties, which steps for enamel or dentin) was measured by the optical path includes the effects of both optical absorption and scattering. length-matching method and used to plot n through lesion In particular, swept-source OCT (SS-OCT) can construct depth. The specimens were further polished and processed images by the ultra-highspeed scanning of the time-encoded for transverse microradiography for analysis of MC. wavelength of a near-infrared laser. It has been shown that this modality allows for the non-invasive construction of The n and MC ranged from 1.52 to 1.63 and 50 to 87 (vol.%) tomographic images of biological substrates in a short period in enamel, and from 1.43 to 1.57 and 11 to 48 (vol.%) in dentin, of time. The application of this technology in the practice of respectively, indicating strong positive linear correlations dentistry for imaging teeth will facilitate the clinical diagnosis between n and MC8,9). Experimental data were validated with a of caries.3–6 theoretical calculation of n from MC. De- and remineralization of enamel and dentin resulted in measurable changes of n, THE SS-OCT SYSTEM and, in turn, MC changes of the tissue could be estimated with good accuracy from this long-known optical property by the Fig. 1 shows a Dental OCT System (Santec, Japan) and its new analytical approach. Compositional changes of enamel specification. The SS-OCT system consists of a hand-held crystallites after remineralization affect n. probe, a light source, interferometer, and a computer. The schematic illustration in Fig. 1 is the fundamental components It is expected that the non-invasive evaluation of n using of the system. A high-speed frequency swept laser light with a the SS-OCT will be an indicator of mineral content in center wavelength of 1330 nm was projected to the specimen clinical situation. The effect of mineralization therapies for and scanned across the area in two dimensions using hand- incipient caries lesion is also monitored with this clinical held probe. Backscattered light from the object is coupled evaluation method. back to the system, digitized over a time scale, and analyzed in the Fourier domain to reveal the depth information of the DIAGNOSIS OF SMOOTH SURFACE CARIES object, thus creating two-dimensional images. The extent of dental caries and possible progress of the REFRACTIVE INDEX OF ENAMEL AND DENTIN lesion from enamel to dentin are very important factors for the decision making of invasive restorative treatment. The caries process is initiated by loss of minerals due to a Unfortunately, reliable imaging technology for caries shift in the dynamic balance between demineralization and diagnosis is not available in the clinic. remineralization. Understanding of the changes induced by this process such as mineral content, hardness, discoloration The cross-sectional image obtained by SS-OCT clearly and so on is a basic element of dental research. demonstrated enamel and dentin caries outlined by visible boundary.4 Though the depth of analysis is limited, the extent The refractive index ( n ) is an important parameter in light of caries lesion was clearly shown to be beyond dentin enamel propagation through biological tissues including teeth. The n of junction (Fig.s 2, 3). The dentinal caries at smooth surface the tissue can serve as an indicator of its scattering properties, was detected with the SS-OCT imaging showing the higher as scattering itself is the end result of local n variation.7 sensitivity(0.96) and Az value(0.96) than those(0.49 and 0.73 respectively) with visual inspection. However, clinical The relationship between the local n and mineral content experience and SS-OCT image interpretation skills were (MC) of enamel and dentin was investigated using the SS- required to improve the diagnostic ability.

57 DIAGNOSIS OF OCCLUSAL CARIES specificity in all diagnostic thresholds, no significant difference was found between SS-OCT and radiography SS-OCT was evaluated as a diagnostic methodology for (Student’s t-test, p > 0.05). occlusal caries in the laboratory comparing with the visual inspections.3 The caries lesion were diagnosed under the Considering the obtained area under the ROC curve, SS-OCT confocal laser scanning microscope after sectioning as the also presented higher values. The detection rate of enamel gold standard. The sensitivity for visual inspection was 0.80 demineralization, cavitated enamel caries and dentin caries for caries lesion and 0.36 for dentine caries. The sensitivity for SS-OCT was significantly higher than that of radiography values for the SS-OCT were over those of the visual inspection; (Student’s t-test, p < 0.05). 0.98 for caries lesion and 0.60 for dentine caries. Specificity for visual inspection was 0.69 for caries lesion and 1.00 for Though the range of the imaging depth of SS-OCT is limited dentine caries, whereas those for the SS-OCT were 0.75 and in dentin, SS-OCT is considered to be a reliable and accurate 0.98, respectively. method for the detection and estimation of the depth of proximal lesions in clinical situations. Since it can be used at Regarding to the enamel caries at pit and fissure can be clearly chair side and the real time observation is available, it is much discriminated as a highlighted area due to scattering of lights. more convenient and safer than X-ray radiography. The highlighted area matched the location of demineralized area at the base of fissure, which was confirmed under the EVALUATION OF RESTORATIONS confocal laser scanning microscope as the gold standard. SS-OCT is considered to be able to evaluate the defects such DIAGNOSIS OF PROXIMAL CARIES as gap and voids in and around composite resin restorations, since composite resins depending on their composition, have Caries at contacting proximal surfaces of posterior teeth is refractive indices near to those of dental hard tissues (nC one of the most difficult diagnosis due to the restricted access = 1.4–1.6).12 In the case of the resin composite restorations, for examination. Diagnosis of proximal caries with visual and prevention of gap formation is one of the most important tactile examination is not thought to be so reliable as dental issue for the clinical success. The gap is considered to be radiograph. The bitewing radiography is well accepted among propagated by the contraction stress of the composite resin the clinicians for detection of proximal caries as well as the during polymerization. The post operative tooth sensitivity non-cavitated proximal lesion. In general, caries diagnosis is explained to be caused by debonding of the restoration, with dental radiography provides low sensitivity, but rather which results in the gap formation between dentin and high specificity, while the true extent of caries lesions seems restoration. The gap height is variable, and it may be less to be underestimated.10,11 than 10 µm at minimum. The current trend in caries management is to move away from The axial resolution of OCT is 11 µm, which may not be enough the surgical model towards preventive and non-operative for detecting the gap less than 10 µm. However, because of therapeutic approach. The aims of the therapeutic approach the so called Fresnel phenomenon, which is the reflection are to control the initiation and prevent progression of caries, of a fraction of light at an interface between two media and heal the existing lesions. However, the detection of early with different refractive indices, gaps that were only a few caries lesion is not possible with the conventional and present micrometres in height can be detected.13 The gap is filled with methodologies. air or another medium such as water, their refractive index(n) is 1.0 and 1.33 respectively, which is different from those of The diagnostic accuracy of SS-OCT equipped with an intra- teeth and composite resin (n=1.5-16)14). When the interfacial oral scanning probe for proximal caries of posterior teeth was gap is large enough in height, e.g. 100 µm, it appears as an evaluated in a real clinical situation, comparing with those optically dark non-scattering area with sharp and bright top of bitewing radiographs.6 The clinical cases were diagnosed and bottom outlines.15 The height of such dark area between after the invasive restorative procedure according to the two distinct lines indicates the gap height on the image. well accepted criteria, ICDAS. The clinical cases in which the accurate observation was difficult and consensus to intervene When 132 composite restorations in 52 patients were was not reached among the examiners were excluded from examined using the SS-OCT image, marginal adaptation, the examination. large porosity and gap formation were 65.2 percent, 27.3 percent, and 15.2 percent, respectively. Only 18.9 percent of The sensitivity of radiography for detecting enamel the restorations had no defects.16 demineralization was 0.88 (cut-off 0 vs. 1–4), whereas the sensitivities for detecting cavitated enamel lesions and In the future, relationship between clinical symptoms and dentin caries were 0.65 (cut-off 0–1 vs. 2–4) and 0.35 (cut-off the defects of composite resin restoration is expected to be 0–2 vs. 3–4), respectively. The sensitivity values of SS-OCT clarified. were greater than those of the radiography: 0.92 for enamel demineralization, 0.84 for cavitated enamel lesions, and 0.56 FUTURE OF SS-OCT IMAGING for dentin caries. SS-OCT showed a higher sensitivity than radiography for the detection of cavitated enamel lesions As mentioned above, compared to the conventional diagnosing and dentin caries (Student’s t-test, p < 0.05). Specificity for methods including dental radiography, more accurate radiography was 0.47 for enamel demineralization, 0.73 diagnosis of caries lesion in various situation is provided with for cavitated enamel caries, and 0.91 for dentin caries, SS-OCT. The crack is also very accurately observed in the SS- whereas the values for the SS-OCT were 0.58, 0.82, and OCT images, showing the precise information of crack extent 0.94, respectively. Although SS-OCT showed higher nominal even in dentin.17,18 The possibility of SS-OCT for diagnosing root caries and recurrent caries is also reported.5,16

58 The SS-OCT is expected to be applied in the dental clinic as the modality for diagnosis of disease and defects of dental hard tissues. SS-OCT is available as a convenient, easy-to-use chair-side device for inspection of teeth and restorations. It also provides visual feedback from clinician to patients, thus helping them understand the status and problems of their teeth (Fig.s 4,5). This new noninvasive approach will help improve the diagnosis, monitor caries and restorations, select the most appropriate treatment, and assure a favourable clinical outcome. Future advances in OCT imaging techniques will allow more definite evaluation and further contribute to the diagnosis and treatment. REFERENCES Fig 1. Dental OCT System (Santec Inc., Japan), and its schematic illustration of the fundamental components of 1. Huang D, Swanson EA, Lin CP, Schuman JS, StinsonWG, Chang W, Hee the system. A high-speed frequency swept laser light with a MR, Flotte T, Gregory K, Puliafito CA, Fujimoto JG. Optical Coherence center wavelength of 1330 nm was projected to the specimen Tomography. Science 1991;254:1178–1181. and scanned across the area in two dimensions using hand- held probe. Backscattered light from the object is coupled 2. Fujimoto JG. Drexler W . Introduction to optical coherence tomography. back to the system, digitized over a time scale, and analyzed In:Drexler W, Fujimoto JG. eds. Optical Coherence Tomography, Springer, in the Fourier domain to reveal the depth information of the 2008;1–45. object, thus creating two-dimensional images. 3. Shimada Y, Sadr A, Burrow MF, Tagami J. Validation of swept-source Fig 2. SS-OCT image of a smooth surface carious lesion. optical coherence tomography (SS-OCT) for the diagnosis of occlusal Despite the minimal enamel surface damage in this case, the caries. J Dent 2010;38:655-665. bright area boundary (finger pointer) appeared to be beyond DEJ (green arrows) in OCT cross-sectional image. The blue 4. Nakagawa H, Sadr A, Shimada Y, Tagami J, Sumi Y. Validation of swept arrows indicate the crack in enamel. source optical coherent tomography (SS-OCT) for the diagnosis of smooth surface caries in vitro. J Dent 2013;41:80-89. Fig 3. Photograph of the same specimen of Fig. 2, but after sectioning. The lesion extended in dentin can be observed. 5. Natsume Y, Nakashima S, Sadr A, Shimada Y, Tagami J, Sumi Y. Estimation of lesion process in artificial root caries by swept source optical coherence tomography in comparison to transverse microradiography. J Biomed Opt 2011;16:071408. 6. Shimada Y, Nakagawa H, Sadr A, Wada I, Nakajima M, Nikaido T, Otsuki M, Tagami J, Sumi Y. Noninvasive cross-sectional imaging of proximal caries using swept-source optical coherence tomography (SS-OCT) in vivo. J Biophotonics 2013;1-8. 7. Knuttel A, Bonev S, Knaak W:New method for evaluation of in vivo scattering and refractive index properties obtained with optical coherence tomography. J Biomed Opt 2004;9:265–273. 8. Hariri I, Sadr A, Nakashima S, Shimada Y, Tagami J, Sumi Y. Estimation of enamel and dentin mineral content from refractive index. Caries Res 2013;47:18-26. 9. Hariri I, Sadr A, Shimada Y, Tagami J, Sumi Y. Effects of structural orientation of enamel and dentin on light attenuation and local refractive index:an optical coherence tomography study. J Dent 2012;40:3873- 3896. 10. Soviero VM, Leal SC, Silva RC, Azevedo RB, Validity of MicroCT for in vitro detection of proximal carious lesions in primary molars. J Dent 2012;40:35-40. 11. Mitropoulos P, Rahiotis C, Stamatakis H, and Kakaboura A, Diagnostic performance of the visual caries classification system ICDAS II versus radiography and micro-computed tomography for proximal caries detection:an in vitro study. J Dent 2010;38:859-867. 12. Meng Z, Yao XS, Yao H, Liang Y, Liu T, Li Y, et al. Measurement of the refractive index of human teeth by optical coherence tomography. J Biomed Opt 2009;14:034010. 13. Bakhsh TA, Sadr A, Shimada Y, Tagami J, Sumi Y. Non-invasive quantification of resin-dentin interfacial gaps using optical coherence tomography:validation against conforcal microscopy. Dent Mater 2011;27:915-925. 14. Hubbezoglu I, Akaoglu B, Dogan A, Keskin S, Bolayir G, Ozcelik S, et al. Effect of bleaching on color change and refractive index of dental composite resins. Dental Materials Journal 2008;27:105–116. 15. Sadr A, Shimada Y, Mayoral JR, Hariri I, Bakhsh TA, Sumi Y, et al. Swept source optical coherence tomography for quantitative and qualitative assessment of dental composite restorations. Proc SPIE 2011;7884:78840C. 16. Ishibashi K, Ozawa N, Tagami J, Sumi Y. Swept-source optical coherence tomography as a new tool to evaluate defects of resin-based composite restorations. J Dent 2011;39:543–8. 17. Imai K, Shimada Y, Sadr A, Tagami J, Sumi Y. Noninvasive cross-sectional visualization of enamel cracks by optical coherence tomography. J Endod 2012;38:1269-1274. 18. Nakajima Y, Shimada Y, Miyashin M, Takagi Y, Tagami J, Sumi Y. Noninvasive cross-sectional imaging of incomplete crown fractures (cracks) using swept-source optical coherence tomography. Int Endod J 2012;45:933-941.

59 Fig 4. OCT image at the scanned line of a canine tooth indicating the proximal lesion extended into dentin. The scanned line is shown as a red line. The lesion is visually observed as a white spot (white arrow). Fig 5. SS-OCT image of a molar indicating a sub- gingival area. The scanned line is shown as a red line. The lesion cannot be observed visually (white arrow). Address for correspondence Professor and Chair, Cardiology and Operative Dentistry, Department of Restorative Sciences, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Japan [email protected]

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 60-63 ROOT CARIES – THE EMERGING CHALLENGE IN DENTAL CARIES MANAGEMENT Laurence J. Walsh BDSc, PhD, DDSc, GCEd, FFOP(RCPA) Professor Walsh is the Director of Continuing Professional Education (CPD), School of Dentistry and Program Coordinator, Bachelor of Oral Health. ABSTRACT The prevalence and severity of root surface caries is increasing as the risk factors for root exposure and cariogenic attack become stronger at the population level. Prevention for root caries can be thought of as a multifaceted approach involving (1) methods to protect roots from exposure, (2) protection of roots once they become exposed to the oral environment by using various coating materials, (3) and the application of fluorides, CPP-ACP and other materials to roots to make them more resistant to dental caries. With an increase in the number of vulnerable elderly in the population, specific efforts should be made to pro- actively screen older adults for root surface lesions, so that the least invasive methods of care are needed and teeth are not lost because of pulpal involvement. When restorations are indicated, glass ionomer cements are preferred over other materials. Root surface caries presents a significant challenge for the dental profession in the 21st century. The lesions can be difficult to identify in clinical and radiographic examinations, both of which when used alone underscore the true number of root surface caries lesions by approximately 50%.1 Taking this into account, the severity of root surface caries lesions may well be much higher than has been reported in large surveys which did not use dental radiographs. EPIDEMIOLOGY – most likely with accompanying partial dentures. In fact, the wearing of partial dentures in this group is a significant Key drivers of the rise in prevalence and severity of root consideration since partial dentures leads to a six-fold surface caries over the past generation include factors increase in the prevalence of root surface caries. which increase the number of root surfaces at risk (reducing edentulism and greater retention of teeth into the later adult RISK FACTORS years), and the increasing average age of the adult population in Australia (with more patients on medicines which adversely Any condition which leads to exposure of the root surface will affect salivary flow). According to current data from the increase the risk of root surface caries, including attachment Australian Bureau of Statistics, over the 20 year period loss from recession, periodontitis, or periodontal surgery. leading up 2025, the proportion of the Australian population Given the fundamental aetiological role of dental plaque in aged 65 years and above will have doubled, while all other the pathogenesis of root surface caries, the well known risk age groups will have grown by only some 10%. This is largely factors for coronal root surface caries are also risk factors for the result of the so called “baby boomers” who were born root surface caries (Table 1).2,3 between 1946 and 1964. While any root surface which is exposed to the oral For those aged 75 years and above, the prevalence rates for environment could be at risk of root surface caries, both root surface caries and periodontitis are three times mandibular molar teeth are the most frequently involved greater than in the population at large. As the population teeth, particularly the buccal and proximal surfaces, becomes more “grey”, root surface caries will become a followed by the mandibular premolar teeth. The single substantial treatment burden for the dental profession most at risk surface is the furcation region of a mandibular because, on average, root surface caries increases the molar tooth. Conversely, the most resistant surfaces to treatment needs of the elderly affected dentate population by root surface caries attack are the lingual surfaces of the some 60%. The increase is even more dramatic in dependent mandibular incisors and canines. This clinical pattern is a residents in nursing homes, who are between two and seven clear reflection of the protective properties of unstimulated times more likely to develop root surface caries. One can then saliva.4 add into this discussion the impacts of the rising prevalence of dementia in the oldest members of the Australian community, The lifelong benefits of water fluoridation include a reduction which will increase demands for them to be institutionalized in root caries of between 30 and 75%. With the majority of in high care nursing homes. the Australian population exposed to fluoridated water, this factor will attenuate the prevalence of root surface caries Many baby boomers will enter their older years with natural in the lifespan of those who receive this benefit, although teeth (and indeed significant numbers of heavily restored it remains to be seen whether this benefit will be enough to teeth), and be at risk of both coronal caries and root surface counter the onslaught driven by the same dietary and lifestyle caries. The rates of complete edentulism in the baby boomer factors which have led to epidemic levels of obesity and type group are falling, so that when they reach advanced ages of 2 diabetes in this same cohort. 85 years and above, some natural teeth will still be retained

61 MINIMAL INTERVENTION DENTISTRY APPLIED TO that if a topical fluoride product is used, such as a neutral ROOT SURFACE CARIES sodium fluoride gel, the uptake of fluoride into the tooth surface can be increased up to three-fold by the application The approaches and techniques for prevention of root surface of intense light, including a conventional lamp used for curing caries are summarized in Tables 2 to 4. For primary prevention, resin composite materials.7 This effect, known as photonic the emphasis is on preventing the root surface becoming conversion, relies upon the tendency of apatite minerals exposed to the oral environment in the first instance, while to convert from carbonated apatites or hydroxylapatite to for secondary prevention, the goal is to identify and address fluorapatite,8 and has been proven successful in clinical risk factors and to stabilize early lesions which are still at the studies at both preventing root surface caries, and arresting leathery stage so that these do not go on to cavitate. Once lesions.9 the root surface is broken and the trigger for restorative care is present, tertiary prevention principles are followed so that The first evidence the topical application of casein both healthy tooth structure is preserved and the vitality of phosphopeptide-amorphous calcium phosphate (CPP-ACP) the dental pulp is maintained. could cause the rest of root surface caries lesions appeared in the literature in 2007.10 To date, most studies using CPP- Lesions of root surface caries typically have a broad front of ACP have focused on the arrest and prevention of enamel attack, which reflects the overlying deposits of mature dental caries, and this highlights the need for more work in how plaque, and the combined effects of acid demineralization CPP-ACP materials can be delivered with maximal benefit for and proteolysis of dentine. The lesions can remain leathery preventing and arresting root surface caries. Glass ionomer for prolonged periods of time before cavitation occurs, a cement materials with CPP-ACP have been developed,11 and desirable feature since this allows a considerable opportunity these appear promising both for application in thin layers for for caries arrest to occur in the lesions which are accessible to protecting at-risk tooth surfaces, as well as for lining a cavity oral hygiene and to saliva. Once cavitation has occurred, the or as the bulk restorative material for a cavity preparation on lesions are challenging to restore because of their tendency a root surface.12 to develop a “ringbarking” pattern at the cemento-enamel junction of the affected tooth. This unusual configuration A particular challenge in managing root surface lesions makes it difficult both to isolate and access the areas to over time and making appropriate clinical decisions around undertake restorative treatment. Adding to these technical interventions is the accurate assessment of both mineral loss issues is the risk posed by mechanical removal of caries and bacterial invasion of the dentine. While one can assess dentine from a tooth surface which is in close proximity to the hardness of the lesion by using a blunt periodontal probe, the dental pulp, increasing the likelihood of iatrogenic pulp care must be taken that this does not damage the surface exposure. and create microcavitations. Assessing the colour of a root surface lesion can be unreliable13 because the colour reflects Contemporary approaches to restoring cavitated root both the production of pigments by bacteria within the services include those which use hand instruments, ultra- infected dentine, and the trapping of exogenous pigments low speed rotary instruments, or chemo mechanical caries from the diet into the outer porous dentine. removal methods to carefully remove the infected outer dentine,5 after which a glass ionomer cement material is A range of methods based on fluorescence can be used placed to both provide a seal and encourage internal re- successfully including those employing ultraviolet, visible mineralization of the underlying affected dentine. blue or red light as the excitation source. These will elicit fluorescent light at a longer wavelength, giving patterns which EMERGING METHODS FOR THE PREVENTION AND allow interpretation of the amount of mineral present or the TREATMENT OF ROOT SURFACE CARIES extent of bacterial infection of the root surface. A caveat with using such fluorescence methods is that they are susceptible Prevention for root caries can be thought of as a multifaceted to interference from potent oxidants, which cause quenching approach involving (1) methods to protect roots from exposure of fluorescence emissions for several days. This could lead (Table 2), (2) protection of roots once they become exposed to a false belief that the bacterial load has dramatically to the oral environment (Table 3) by using various coating changed. A case in point is when ozone is applied to the materials, (3) and the application of fluorides, CPP-ACP and root surface, which will cause two major effects – oxidation other materials to roots to make them more resistant to of organic acids (such as lactic acid and pyruvic acid) and dental caries. other biomolecules, resulting in the root surface hardening over time, and a transient reduction in the load of organisms Because materials with high concentrations of fluoride can present in the most outer layers of the infected dentine.14,15 significantly reduce acid production by cariogenic bacteria, The latter change is prone to being misread. While there is there is considerable value in the use of high fluoride clinical evidence to support the use of ozone in arresting dentifrices and repeated applications of fluoride varnish both and hardening root surface caries lesions, the effects on in the prevention of root surface caries in at risk patients, and bacteria cannot reliably be monitored by assessing changes as therapies which aim to arrest the progression of lesions in fluorescence patterns immediately after the application of from a leathery stage to cavitation. There is evidence from ozone, because of this problem of quenching. clinical trials that the use of a dentifrice with 5,000 ppm fluoride is more effective than a similar “regular strength” The development of high fluoride release glass ionomer dentifrice with 1,000 or 1,100 ppm, in terms of the likelihood of cement materials, such as GC Fuji VII®, has opened up the arresting or reversing leathery lesions of root surface caries possibility of tooth surface protection, using these materials within a six month period.6 There is considerable evidence in a thin layer on the root surface in the same manner as a glass ionomer cement material or resin is used to seal the

62 pits and fissures on the occlusal surface. With high fluoride REFERENCES release materials there can be a considerable influence on the metabolism of dental plaque overlying or adjacent to the 1. Walsh LJ, Gan A. Proximal root surface caries in an Australian material, with reduced acid production. There is also evidence periodontal population. Periodontol 1991;12:33-6. . for a peripheral protection zone from such materials because of the release of ions which contribute to re-mineralization. 2. Walsh LJ, Brostek AM. Minimal intervention dentistry principles and objectives. Aust Dent J 2013; 58(1 Suppl):3-16. [12,16] 3. Walsh LJ. Lifestyle impacts on oral health. In: Mount GJ, Hume WR. Advice to patients at high risk of root surface caries should Preservation and restoration of teeth, 2nd edition. Brisbane, Knowledge include the following elements:17,18 (1) Dietary restriction Books and Software, 2005: 83-109. of sucrose, other fermentable simple sugars, and starches between meals, and the replacement of sucrose by 4. Walsh LJ. Clinical aspects of salivary biology for the dental clinician. alternative sweeteners such as stevia, Isomalt® or others. Internat Dent 2007;2:16-30. (2) Dietary restriction of highly acidic foods and drinks. (3) Use of sorbitol- or xylitol-containing chewing gums to boost 5. Mount GJ, Walsh LJ, Brostek A. Instruments used in cavity preparation. salivary flow. (4) Use of milk-based foods, such as low fat In: Mount GJ, Hume WR. Preservation and restoration of teeth, 2nd cheese, as snacks, rather than confectionery. (5) At-home edition. Brisbane, Knowledge Books and Software, 2005:119-43. topical application of GC Tooth Mousse Plus ® before bed. (6) Twice daily toothbrushing with a high fluoride (5000 ppm) 6. Baysan A, Lynch E, Ellwood R, Davies R, Petersson L, Borsboom P. dentifrice, to reduce the thickness of the dental plaque biofilm Reversal of primary root caries using dentifrices containing 5,000 and and its acid production. (7) Use of a neutral or alkaline saliva 1,100 ppm fluoride. Caries Res 2001;35:41-46. substitute if there are symptoms of xerostomia. Patients can also rinse with a home-made sodium bicarbonate solution. 7. Vlacic J, Meyers IA, Kim J, Walsh LJ. Laser-activated fluoride treatment of enamel against an artificial caries challenge: comparison of five In terms of in-office treatments for at risk patients, there wavelengths. Aust Dent J 2007;52:101-5. is good evidence for 38% silver diamine fluoride solutions professionally applied annually to at-risk surfaces, and for 8. Vlacic J, Meyers IA, Walsh LJ. Photonic conversion of hydroxyapapite to 22,500 ppm sodium fluoride varnish professionally applied fluorapatite: a possible mechanism for laser-activated fluoride therapy. every 3 months to softened surfaces.19 Such measures can be J Oral Laser Appl 2008;8:95-102. applied during regular maintenance visits. 9. Walsh LJ. Strategies for remineralization. In: Limeback H (ed) CONCLUSIONS Comprehensive Preventive Dentistry, Ames Iowa: Blackwell Publishing 2012:298-312. Practitioners should be cognizant of the risk of root surface caries in all patients and particularly in those with a strong 10. Vlacic J, Meyers IA, Walsh LJ. Combined CPP-ACP and photoactivated history of past coronal caries or salivary hypofunction. disinfection (PAD) therapy in arresting root surface caries: a case Particular attention should be also directed to patients with report. Br Dent J 2007;203:457-9. periodontitis, because of root surface exposure from multiple factors, which makes such patients prone to root surface 11. Mazzaoui SA, Burrow MF, Tyas MJ, Dashper SG, Eakins D, Reynolds EC. caries. Left untreated, root surface caries can compromise Incorporation of casein phosphopeptide-amorphous calcium phosphate the long-term success and survival of the entire dentition but into a glass-ionomer cement. Incorporation of casein phosphopeptide- most notably periodontally affected mandibular molars with amorphous calcium phosphate into a glass-ionomer cement. J Dent Res furcation involvement.20 With an increase in the number of 2003;82:914-8. vulnerable elderly in the population, specific efforts should be made to pro-actively screen older adults for root surface 12. Yap J,Walsh LJ,Naser-ud Din S, Ngo H, Manton DJ. Evaluation of a novel lesions, so that the least invasive methods of care are needed approach in the prevention of white spot lesions around orthodontic and teeth are not lost because of pulpal involvement. When brackets. Aust Dent J 2014; 59:1-11. restorations are indicated, glass ionomer cements are preferred over other materials.21 13. Lynch E, Beighton D. A comparison of primary root caries lesions classified according to colour. Caries Res 1994;28:233-9. 14. Baysan A, Lynch E. Clinical reversal of root caries using ozone: 6-month results. Am J Dent 2007;20:203-8. 15. Holmes J. Clinical reversal of root caries using ozone, double-blind, randomised, controlled 18-month trial. Gerodontol 2003;20:106-14. 16. Arbabzadeh-Zavareh F, Gibbs T, Meyers IA, Bouzari M, Mortazavi S, Walsh LJ. Recharge pattern of contemporary glass ionomer restoratives. Dent Res J 2012;9:139-45. 17. Walsh LJ. Preventive dentistry for the general dental practitioner. Aust Dent J 2000;45:76-82. 18. Walsh LJ. Dental plaque fermentation and its role in caries risk assessment. Internat Dent 2006;1:4-13. 19. Gluzman R1, Katz RV, Frey BJ, McGowan R. Prevention of root caries: a literature review of primary and secondary preventive agents. Spec Care Dentist 2013;33:133-40. 20. Bignozzi I1, Crea A, Capri D, Littarru C, Lajolo C, Tatakis DN. Root caries: a periodontal perspective. J Periodontal Res 2013. doi: 10.1111/jre.12094. 21. Amer RS1, Kolker JL. Restoration of root surface caries in vulnerable elderly patients: a review of the literature. Spec Care Dentist 2013;33:141-9.

63 Risk factors for root surface caries Secondary prevention of root surface caries Root surface exposure Attachment loss OBJECTIVE METHODS accumulating with age Periodontal surgery Identify at-risk patients Dentifrices to inhibit periodontitis (triclosan Salivary hypofunction Xerostomia-inducing copolymer) medicines Lifestyle factors affecting Periodontal screening and Topical CPP-ACP or CPP- fluid balance charting ACP crème Salivary gland injury or Saliva and plaque tests for disease caries risk Past coronal caries Frequency of exposure to Dietary and lifestyle substrate and acids analysis Updated medical history (xerostomia-inducing agents) Plaque levels and oral High fluoride dentifrices hygiene compliance Arrest softened roots Ozone therapy Table 3. Secondary prevention of root surface caries Table 1. Risk factors for root surface caries Primary prevention of root surface caries Tertiary prevention of root surface caries OBJECTIVE METHODS OBJECTIVE METHODS Prevent attachment loss Dentifrices to inhibit Conservative caries Chemomechanical caries periodontitis (triclosan removal removal (Carisolv®) copolymer) Protect exposed roots Vaccines to periodontitis Atraumatic restorative Fluorescence assisted (experimental) technique caries excavation • GIC coating materials (e.g. (DIAGNOdent®, SoproLife®) GC Fuji VII®) • GIC+CPP-ACP coating Prevent iatrogenic pulp Photoactivated disinfection materials (Fuji VII EP®) injury • High fluoride (5000 ppm) Table 4. Tertiary prevention of root surface caries dentifrices Address for correspondence • Fluoride varnishes The University of Queensland School of Dentistry, and Cooperative Research Centre for Oral Health Sciences • Enhanced fluoride uptake [email protected] through light exposure Community water fluoridation Table 2. Primary prevention of root surface caries

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 64-66 THE RESTORATIVE MANAGEMENT OF DEVELOPMENTAL ENAMEL DEFECTS Kathryn Harley BDS MSc FDSRCSEng FDSRCSEd FDSRCPSG FFGDP(UK) Kathryn Harley is a consultant in Paediatric Dentistry at the Edinburgh Dental Institute, and Dean of the Faculty of Dental Surgery, The Royal College of Surgeons of England. ABSTRACT Previously children with enamel defects tended to fall into two groups, those who had received extensive treatment or those who had received none at all. With an increase in the types of restorative interventions available, advances in dental materials and a greater understanding of the nature of enamel defects, treatment of young patients to improve aesthetics and function is not only extremely successful but also conservative. Ideally any technique used should be minimally invasive, not destructive of healthy enamel and should not leave the tooth structurally weaker as a consequence. Children with either hypomineralised or hypoplastic enamel often complain of sensitivity or the poor appearance of their teeth. Early diagnosis and prompt management of this age group to reduce symptoms and improve the aesthetics will greatly improve their quality of life. TYPES OF ENAMEL DEFECTS Fig 2. Hypomaturation Amelogenesis Imperfecta (Mild) Enamel defects may be classified simply into Hypoplastic or Hypomineralised defects which are either congenital or acquired. The aetiology may be the same for each e.g. there are hypomineralised and hypoplastic types of amelogenesis imperfecta (Figures 1 - 4) or linear defects (Figures 5, 6) and indeed both hypomineralised enamel and hypoplastic enamel may be observed within the same tooth.1 It is important for the restorative management of a tooth to distinguish between the two types of defect. In hypoplastic enamel the ameloblasts are disturbed during the secretory phase of amelogenesis but the enamel matrix which is laid down during tooth formation mineralises normally. Clinically these teeth range in appearance from having enamel which has a localised area of hypoplasia in the form of a pit to a widespread lack of enamel throughout the anatomical crown. It is described as a quantitative defect due to a reduction in the quantity or thickness of the enamel in an isolated area or throughout the crown. Key to understanding what restoration may be provided for a hypoplastic tooth is the fact that the enamel which is present is mineralised normally hence use of adhesive materials which rely on an acceptable bond strength between the etched enamel surface and the restoration are predictable. Their longevity will be no different to that achieved for unaffected/normal teeth. Fig 3. Hypomaturation Amelogenesis Imperfecta (Moderate) Fig 1. Hypoplastic Amelogenesis Imperfecta (Random Pitted)

65 Fig 4. Hypocalcified Amelogenesis Imperfecta (Severe) In Amelogenesis Imperfecta (AI) examples of hypoplastic and Where hypomineralised enamel is observed the ameloblasts hypomineralised teeth can be seen such that this condition is have been disturbed during the maturation phase of often classified according to which type of enamel is clinically amelogenesis resulting in a reduction of mineral within the dominant. The term dominant is used rather than present as enamel. The matrix is laid down in normal thickness but fails to histologically both hypoplastic and hypomineralised enamel mineralise fully either in an isolated area producing a blemish/ can be observed microscopically when examining the same opacity within the enamel or throughout the anatomical crown. tooth hence the clinical description of what is observed is This is described as a qualitative defect whereby the quality of considered to be a pragmatic classification on the basis of the enamel present is sub-optimal in the affected area. In these the clinical appearance. This is of great significance for those teeth where the enamel is hypomineralised, adhesion will be wishing to restore the teeth. Amelogenesis imperfecta is a compromised as hypomineralised enamel gives a poor etch term used to describe a group of hereditary conditions that profile and its removal is recommended to allow the margins of affect the structure and appearance of dental enamel, which any restoration to finish on sound enamel.2 may be in conjunction with changes in other tissues. It can exist in isolation or in association with other features in Fig 5. Linear Hypoplasia syndromes and is present in both the primary and permanent dentition. In hypoplastic forms of amelogenesis the clinical appearance is often used to further (subdivide) classify the type of hypoplastic AI e.g. random pitted hypoplastic amelogenesis imperfecta accurately sums up what is observed (Figure 1). In hypomineralised AI attempts to distinguish between the different types are less clear separating the teeth into hypomaturation AI (Figures 2, 3) or hypocalcified AI (Figure 4) on the basis of severity. Hypomaturation AI is the less severe of the two with the clinical appearance of the enamel displaying diffuse opaque areas which may be white or brown indicating a reduction in mineral content within the enamel thickness of teeth or generalised discolouration with a cream/brown appearance throughout. In contrast the teeth in hypocalcified AI have a dramatic reduction in mineralised enamel such that it is lost almost immediately the incisal edges or cusp tips appear in the mouth. These teeth are referred to as “moth-eaten” in appearance a term which is almost as bad as “cheese molars”! Hypomineralisation and hypoplasia similarly are both seen in Molar Incisor Hypomineralisation (MIH). Strictly speaking the “H” in MIH should refer to hypomineralistion alone however the difficulty here is how to explain the presence of hypoplasia, might two different mechanisms with distinct aetiologies act on the same tooth during formation? In practice the diagnosis may be more appropriately made whether the defects are hypoplastic or hypomineralised as most clinicians do not distinguish between the two and are merely recognising that the enamel present is “defective”. MIH is defined as hypomineralisation of one to four first permanent molars frequently associated with affected incisors.3 The first permanent molars and incisors start to mineralise around birth hence a disturbance of the ameloblasts during crown formation of these teeth will result in a failure of matrix to be laid down, a failure of maturation or reduced mineralisation. A number of causes of MIH have already been identified such as illness in the neonatal period or early childhood, hypoxia, medication, dioxins in breast milk.4 and environmental toxins however there is still no consensus as to why MIH appears to be on the rise. A number of these factors can act synergistically to increase the risk of MIH although continued work is necessary to explain the reported increase which is unlikely to be merely better recognition. Fig 6. Linear Hypomineralisation

66 Whatever the cause of the enamel defects, the principles for of a) removing sufficient enamel so that the margins of the restorative management are the same. restoration finish on sound, normally mineralised tooth tissue where possible, and b) removing sufficient material to achieve Anterior Teeth Hypoplasia the desired result i.e. remove the white opaque area on the tooth surface. If the depth of enamel removed is insufficient Where a defect is hypoplastic, restoration of aesthetics and the “white” blemish will be seen through the thin layer of function is directed at replacing the enamel which is missing. composite resin covering it. The treatment options are thus: POSTERIOR TEETH Direct: Composite resin - localised restorations or veneers Indirect: Porcelain - veneers or crowns With regard to posterior teeth the aim of restoration is often to manage sensitivity and replace the missing tooth HYPOMINERALISATION structure, protecting the tooth against further enamel loss and restoring adequate function. Children with affected teeth In contrast if the defect present is due to hypomineralisation often present with sensitivity as the over-riding symptom.3 treatment is primarily concerned with changing the The options available include the use of the following: appearance or/and structure of the enamel. The range of options thus includes all of the above plus bleaching and Direct: Glass-ionomer cement microabrasion allowing for a more conservative approach. Composite resin The treatment options are: Amalgam 1. Bleaching 2. Microabrasion Indirect: Stainless steel crowns 3. Composite resin Porcelain 4. Porcelain Nickel-chrome VITAL BLEACHING Gold Vital bleaching at home with low concentrations of carbamide However, for children with MIH the best option may be peroxide is particularly useful and its suitability for each extraction of the first permanent molar. Children with defective individual case should be considered first.5 enamel have been shown to undergo dental treatment nearly ten times as often as the children in a healthy control group It can act in two ways: by the age of nine years.6 The affected children had more fear 1. white blemishes - where white blemishes are present and anxiety as a consequence. It has also been demonstrated bleaching the anterior teeth will reduce the contrast that extraction of first permanent molars produced between the blemish and the surrounding more “cream/ acceptable results in 87% of children.7 Where the child has yellow” tooth structure such that the white blemish(es) a complete developing permanent dentition, including third is (are) no longer visible permanent molars and presentation is before 9 years of age 2. cream/yellow/brown blemishes - bleaching will lighten there should be a very good reason not to extract the affected the discoloured appearance such that they become teeth. One such is if the hypoplastic/hypomineralised first almost invisible. permanent molars are present in a child with AI where all the permanent teeth are similarly affected. In MIH removing However bleaching alone may not provide sufficient the affected teeth allows for their replacement, hopefully improvement in the aesthetics and not all teeth will with spontaneous alignment with teeth which have normal bleach satisfactorily, particularly in young patients with healthy enamel. In amelogenesis no such option exists hence hypomaturation amelogenesis imperfecta where the cream/ all molars should be maintained until a full assessment can be brown discolouration often changes hue to become more made of the erupted dentition. “yellow” and almost less acceptable after vital bleaching. Careful selection of cases, appropriate technique and The presence of caries or significant wear may influence any adequate consent with a clear explanation of the limitations treatment decision hence the procedures outlined above are is imperative. For some patients a combination of more than what should be considered in the absence of any dental disease. one procedure is ideal. Microabrasion may be carried out to remove widespread diffuse white/brown blemishes followed REFERENCES by bleaching to improve the overall colour. Bleaching followed by removal of a single or multiple white opacities may be 1. Darling AJ. Some observations an amelogenesis imperfecta and necessary where the aesthetics are compromised by a lack calcification of the dental enamel. Proc Roy Soc Med 1956;49:759. of translucency of the blemish rather than its colour. How much treatment is required will depend on the expectations 2. Jalevik B, Dietz W, Noren JG. Scanning electron micrograph analysis of of the patient: for many bleaching alone will be sufficient but hypomineralized enamel in permanent first molars. Int J Paediatr Dent for others an obvious area of white opaque enamel will be 2005;15:233-40. unacceptable. The responsibility of the dentist is to ensure that the patient fully understands the implications of any 3. Weerheijm KL, Jalevik B, Alaluusua S. Molar-incisor hypomineralisation. treatment being proposed. If the dentist is to use a handpiece Caries Res 2001;35:390-391. and remove tooth structure just because it is opaque the patient needs to appreciate that this restoration will require 4. Alaluusua S, Lukinmaa PL, Vartiainen T Etal. Polychloroinated bibenzo- life-long maintenance and is not a “quick fix”. All treatment p-dioxins and dibenzofurans via mother’s milk cause developmental should be undertaken with the aim of conserving as much tooth defects in child’s teeth. Environ Toxicol Pharmacol 1996; 1:193-197. structure as possible however removal of hypomineralised enamel in the form of an opacity will require consideration 5. Bannister R, Harley K. Vital bleaching for the management of hypomineralised enamel defects. Fac Den J 2012; 3:146-151. 6. Jalevik B and Klingberg GA. Dental treatment, dental fear and behaviour management problems in children with severe enamel hypomineralisation of their permanent first molars. Int J Paediatr Dent 2002; 12:24-31. 7. Mejare I, Bergman E, Grindefjord M. Hypomineralised molars and incisors of unknown origin: treatment outcome at 18 years. Int J Paediatr Dent 2005;15:20-28.

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 67-70 ELECTRONIC HEALTH RECORDS AND eHEALTH - THE PERSONALLY CONTROLLED ELECTRONIC HEALTH RECORD (PCEHR) Frederic Shane Fryer, BDS, MDSc, FRACDS. Shane Fryer is the Immediate Past Federal President of the Australian Dental Association (ADA) and the current Chairman of the ADA’s Special Purpose Committee on eHealth. ABSTRACT eHealth provides an important opportunity to improve the quality and safety of healthcare. Every year Australians have an average of 22 interactions with the health system. Most of the information from these visits is currently held in paper based records in separate locations. The PCEHR is designed to assist in information sharing with multiple sources of health information being summarised and accessed through a central point. There are many misconceptions regarding eHealth both from a health practitioner and patient perspective. It is important to realise what the eHealth system is and is not. Dental Practitioners should also be aware of secure messaging, e prescriptions and e pathology. Dental Practitioners to be ready for eHealth should consider among other things having broadband internet access, have computer terminals in the clinical rooms, have appropriate dental software and utilise electronic dental records. This presentation will attempt to clarify the current state of play of eHealth including the PCEHR with particular reference to dental practice. The World Health Organisation defines eHealth as ‘the These are all related to the Personally Controlled Electronic combined use of electronic communication and information Health Record, the PCEHR. The PCEHR is officially referred to technology in the health sector.’ Although this is the WHO as an “Electronic Health Record System” and its goal is the definition of eHealth in more practical terms eHealth, is sharing of important clinical information between healthcare the means of ensuring that the right health information is providers. provided to the right person at the right place and time in a secure, electronic form for the purpose of optimising the But before we delve further into eHealth I would like to quality and efficiency of health care delivery. take you back and just give you some history. It was back in early 2008 when the Australian Health Ministers, through eHealth manifests itself in many ways in our general work the Australian Health Minister’s Advisory Council (AHMAC) environment as a dental practitioner and implementation commissioned Deloitte to develop a strategic framework of eHealth technologies is currently ongoing globally with and plan to guide national coordination and collaboration in billions of dollars being spent. I can say that eHealth is not eHealth. As part of this process, Deloitte conducted a series of new to dentistry as many practices have digital dental records national consultations which included Commonwealth, State and have been using computers for receipts and accounts for and Territory Governments, general medical practitioners, many years. As a matter of fact, Australian Dental Association specialist medical practitioners, nursing and allied health, Practice Survey 2010 revealed that: pharmacy and academics to name just a few. The national eHealth strategy developed by Deloitte together with the key • Greater than 40% of members use computers for staff stakeholders adopted an incremental and staged approach to and patient education. developing eHealth capabilities to: • Greater than 60% of members use a computer at the • leverage what currently existed in the Australian chair side eHealth landscape • Greater than 86% of practices used computers for • to manage the underlying variation in capacity across patient accounts, practice accounts and patient the health sector, and payments. • to allow scope for change as lessons are learned and Just as a quick summary eHealth in dentistry may be broken technology is developed further (and this last point is down into a number of separate but not siloed categories particularly important) which are: From this Australian Health Minister’s Conference came the • e-Diagnostics, that is, radiographs etc. vision that eHealth will enable a safer, higher quality, more equitable and sustainable health system for all Australians by • e-Discharge transforming the way information is used to plan, manage and deliver health care services. Of course I do not have to tell you • e-Medication Management that there has been considerable debate on how this vision is going and when it will be achieved but again remember what I • e-prescriptions said before about scope for change as we learn. • e-referrals

68 Given the strong national consensus on the eHealth strategy NEHTA’s CT products aim to create a comprehensive and there was a need to move quickly to establish an appropriate non-ambiguous national vocabulary to support the eHealth long term eHealth governance regime. In 2008 an requirements of the Australian healthcare community. organisation called the National eHealth Transition authority (NEHTA) already existed but in a much simpler form to that NEHTA’s CT solutions include SNOMED CT-AU and Australian of today. This original NEHTA organisation was leveraged off Medicines Terminology (AMT). From our perspective we and built upon, with modifications to its constitution, board are interested in SNODENT which stands for systemized and operating model to create a vehicle for the progression Nomenclature for Dentistry. This was originally developed of the national eHealth agenda. by the American Dental Association and it is embedded within SNOMED. I can tell you that when the ADA started So we move to 2009 and a new player gets involved with communicating with NEHTA some years ago it was unclear eHealth. The National Health and Hospitals Reform Commission that SNODENT was inside SNOMED. Originally when we (NHHRC) which handed down a report recommending to the started thinking about SNODENT we had some concerns as government that they action the introduction of a system the American’s do not use exactly the same terminology in of individual electronic health records, that is, a personally Dentistry as we do in the ADA’s “The Australian Schedule of controlled electronic health record and that rather than this Dental Services and Glossary”. However, I was told by the be a gradual and incremental roll out, it needed to be done software vendors at the time that this would not be a problem quickly and be in place by 2012. as they would just provide an interface so that what is seen on the computer screen at the surgery front desk would look The government in April 2011 prepared and released a draft exactly as it does now, that is, with our item numbers etc. concept of operations document for public comment, known as Con Ops. A final version of this Con Ops was released in So back to the Personally Controlled Electronic Health September 2011 and the timeline for going live was July the Record. The PCEHR is an ‘opt in’ system for both patients and following year. The PCEHR was launched in July 2012 and it health care providers. With agreement between the patient was from this date that people could register to participate and the health care provider a shared health summary can be in the system. As an aside I would point out to you that this created by that nominated health care provider. The basics of was an extremely rapid build and launch process and thus the health summary would be a brief medical history, current was something that had not been done anywhere else in the medications, immunisations, allergies and adverse reactions. world. Examples of Clinical Documents that may be available on the The National eHealth Transition Authority (NEHTA) also PCEHR are: provided the needed foundations or infrastructure for the PCEHR to operate and this include four main points: • Shared Health Summaries 1. Healthcare identifiers both for individuals, healthcare • Event Summaries providers and health provider organisations. Thus we have: • Discharge Summaries • Healthcare Provider Identifier – Individual (HPI-I) • Medication Records • Healthcare Provider Identifier – Organisation (HPI-O) • eReferrals • Individual Healthcare Identifier (IHI) – for individuals receiving healthcare services. • Specialist Letters Please note that we all have an Individual Healthcare Identifier With the ‘opt in’ system patients can withdraw at any time. number and this was allocated to us by Medicare Australia. An They are also able to enter their own information into the important component of the Health Identifier service is the consumer area of the portal such as the current medications Healthcare Provider Directory (HPD) which is an opt-in listing they are taking. There are now over 1.43 million consumers, of healthcare providers both individuals and organisations that is, people with a PCEHR and 6500 healthcare that registered with the Health Identifier Service. Being listed organisations registered on the National eHealth System. It and linked in the Healthcare Provider Directory enables you is considered that the people that will benefit the most from to be selected to receive referrals and other forms of secure having an eHealth record are: electronic information. • People with chronic and complex conditions 2. Secure messaging which I will discuss in greater detail. • Older Australians 3. National security and access framework • Aboriginal and Torres Strait Islander peoples In order to safely share and manage access to information in the healthcare system it is essential to be able to authenticate • People with mental health conditions users, that is, organisations and people. In the eHealth system this is achieved through the use of digital certificates • People in regional, rural and remote communities and these are the National Authentication Service for Health (NASH) Public Key Infrastructure (PKI) Certificate which I will These are the very patients that we need to pay particular expand on a little later. attention to as their medical conditions may compromise dental treatment. 4. National clinical terminologies Patients cannot edit information created by others on the A clinical terminology (CT) is a structured vocabulary, or PCEHR but they can choose what information will be shared. language, used in clinical practice to accurately describe the Thus patients can hide information they do not want recorded care and treatment of patients. and choose which healthcare providers can access that information. This is an important point.

69 Fig. 1 I would now like to give you one of the take home messages The SMD specifications focus on the secure message from this presentation. The Australian PCEHR is only a delivery of messages containing clinical documents and/or health summary. Primary health care records should still be information, between healthcare organisations either directly maintained and stored locally. We as dental practitioners will or using one or more intermediaries (Fig 1). continue to maintain and use our own records as the primary data source for a patient’s medical history. The PCEHR is thus There are a number of message service providers that are just a collection of summary documents and data uploads not currently SMD specification compliant to send and receive from a variety of sources. As I have indicated we should all some types of clinical documents electronically. A limitation maintain primary health records within our dental practices, of the non SMD compliant services is that messages may only and with this comes the responsibility of having appropriate be exchanged between practice organisations and clinicians security measures in place to protect the information from who use the same messaging service provider. This means inappropriate use. that dentists A and B will have a particular program in their office software that will encrypt a message for sending and The Dental Board of Australia (DBA) has issued a Code of when it is received the same program at the other practice Conduct which has a section on Health Records. The DBA will decipher the message and allow it to be read. This states that good practice with respect to record keeping limitation can result in health practices having to use multiple involves,“ensuring that records are held securely and are not messaging services in order to send and/or receive messages subject to unauthorised access, regardless of whether they with a broad network of participating practitioners. are held electronically and/or in hard copy.” In addition to the DBA’s advice, The Office of the Australian Information By using SMD compliant Desktop Software products in Commissioner (OAIC) in April 2013 released a Guide to conjunction with SMD compliant secure messaging service Information Security called ‘Reasonable steps’ to protect providers the situation can be simplified. Dental practices personal information. This guide provides information on that implement SMD compliant products and services, the reasonable steps that entities are required to take under either directly or indirectly via an intermediary, will be able the Privacy Act to protect the personal information they to connect and exchange a broad range of message types, hold from misuse or loss and from unauthorised access, securely and reliably, with any other healthcare organisation use, modification or disclosure. The guide is a one page that also uses SMD compliant software. They will also be document but the part that is particularly relevant here is the able to communicate even where the sender and receiver Information and Communication Technology (ICT) Security use different intermediaries to route messages provided section. This refers to: that those intermediaries have established commercial interconnect agreements. • Regulating Access, that is, authorised participation There are a number of SMD compliant secure message • Up to date software security providers and they are able to register on the NEHTA website under the eHealth Product Register. I have recently checked • Network security measures, and this register and .several providers were listed (Table1). • Communication security measures which would include For secure messaging to be reliable and have the correct encryption of security there are a number of components that need to be correctly configured. This includes: • electronic communications 1. that the Health Identifier (HI) Service is set up correctly There are also other points, but where I am leading to here is Secure Message Delivery (SMD) or secure messaging. 2. that your practice uses an Endpoint Location Service (ELS). The ELS contains the necessary information such NEHTA is responsible for the development of eHealth as the electronic address and the associated Public standards which includes information security standards Key Infrastructure (PKI) certificate, for your Desktop and with this is secure message delivery. SMD is a set of Software (via a SMD compliant messaging service) to specifications developed by the eHealth community which transmit and receive messages for your practice. includes NEHTA, Standards Australia, Desktop Software vendors and secure messaging service providers. SMD has 3. that your practice has the National Authentication been designed for use by General practitioners, Specialists, Service for Health PKI certificate for Healthcare Provider Clinics, Hospitals, Dentists and Allied Health Providers. Organisations configured for use in your Desktop Software. Thus the security of information and the way The SMD specifications focus on the secure message we communicate with each other professionally over delivery of messages containing clinical documents and/or the internet is becoming or should I say has become an information, between healthcare organisations either directly important issue which we all need to be aware of. or using one or more intermediaries.

70 PRODUCT NAME LISTED If the pharmacy is not using ePrescriptions the medication is dispensed via the standard manual methods of manual ARGUS 17 Oct 2012 transcribing the prescription details. Therefore in summary, my messages for today are: HTR TELHEALTH 02 Nov 2012 1. eHealth has been developing for some time. PRACTIX 27 Nov 2012 2. Originally NEHTA did not have Dentistry on its radar as it HEALTHLINK MESSAGING 04 Dec 2012 had to focus on medicine first. SYSTEMS 3. The American Dental Association has already developed MEDICAL OBJECTS 11 Dec 2012 SNODENT a systemised computer terminology for CAPRICORN dentistry, so the IT language is here. REFERRALNET AGENT 16 Jan 2013 4. The PCEHR is a health summary and does not replace your own records as the primary data source for a patient MMEX 23 Jan 2013 medical history. AIITALK 31 Jan 2013 5. Emailing unencrypted patient medical data is a concern and secure message delivery should be enacted within MIYA PLATFORM 22 Feb 2013 the dental profession. REPORTNET 03 Mar 2014 6. We should all access the NEHTA website and register for eHealth. The days of emailing unencrypted x-rays and referral letters between, for example, dentists and specialist dentists should To conclude I can tell you that eHealth is here to stay. Its be over. You will recall that I initially listed 6 categories of foundation components (that is, its infrastructure) and the eHealth that are related to Dentistry and one of them was services and solutions will evolve and change as we and the e-Prescriptions. Electronic Transfer of Prescriptions (ETP) systems become more sophisticated. eHealth will impact on is a subset of e-Medication Management in which your your business and operational models for your dental practice Desktop Software creates and sends electronic prescription and at the moment issues like the PCEHR and secure message information (ePrescritpions). These electronic script copies delivery are what we need to get our thoughts around. What will be sent to a Prescription Exchange Service (PES) where eHealth can do for you is: they are stored and can be retrieved later by a dispenser at the time of dispensing. • reduce your time finding information When a prescriber (doctor, dentist etc.) generates an • make your consultations more efficient ePrescription two things happen: • potentially reduce duplication 1. an electronic copy of the prescription is submitted to the Prescription Exchange Service (PES), and • allow for better informed clinical decisions 2. a unique barcode is generated and printed on the paper • provide you with efficient access to health information prescription. that you did not already have. At the pharmacy the pharmacist scans the bar code on Our CEO, Gary Disher has penned an article on eHealth which the paper prescription and the prescription details are is on the College website for further information for you. Also automatically retrieved from the Prescription Exchange there are eHealth officers in each Medicare Local office that Service thus saving time and more importantly reducing the are available to help practices work through any issues. In likelihood of errors. addition to the above NEHTA has prepared a new edition of the “eHealth user guidance for General Practices and Private Specialist Practices”. Specific reference is also made to Allied Health and NEHTA sees us as fitting under that umbrella. (Of course our mantra is that dentistry is different and it should be Medicine, Dentistry and Allied Health but that’s politics for another day.) The reference for the NEHTA Guide is www.nehta.gov.au for- providers about-ehealth-guidance. The guide aims to assist you to navigate the complexities of eHealth (including the PCEHR) every step of the way from planning, preparation, registration and implementation through to meaningful use. Address for correspondence [email protected]

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 71-73 CONSTRUCTION OF FLUORIDE-CONTAINING PLLA NANOFIBRE SCAFFOLD FOR BONE REGENERATION Qingsong Ye* PhD, DDS, MSc, MOrth RCSEd Jia Xu PhD Yan He PhD, DDS, MSc Andrew Sandham PhD, DDS Qingsong Ye is Associate Professor of Orthodontics and Program Coordinator of Orthodontics at James Cook University. Jia Xu and Yan He are both Postdoctoral researchers at James Cook University. Professor Andrew Sandham is Head of Dentistry at James Cook University. ABSTRACT In this study, a novel material, fluoride-containing Poly (L-lactic acid) (PLLA) nanofibre scaffold was successfully constructed through electrospinning process. Scanning electron microscopy (SEM) image showed that the morphology of the fibres was uniform and smooth, and the average diameter of the fibres was about 300 nm. Transmission electron microscopy (TEM) proved that a lot of calcium fluoride (CaF2) nanoparticles with an average diameter of about 50 nm were well dispersed in the PLLA fibre matrix. Fluoride is one of the few inorganic ions which are able to stimulate osteoblasts (OB). This novel material seems to be a promising scaffold for bone tissue engineering. Keywords: Electrospinning; Fluoride; Nanofibre; PLLA; Tissue engineering INTRODUCTION MATERIALS AND METHODS Fluoride is one of the few inorganic ions which are able to Materials stimulate osteoblasts (OB). In 1983, Fareley et al.1 confirmed 2, 2, 2-trifluoroethanol (TFE) was obtained from Rhodia that fluoride could directly stimulate osteoblastic proliferation, Company Ltd.; Sodium fluoride (NaF) from Beijing Tongguang increase the activity of alkaline phosphatase (ALP) and Fine Chemicals Company; Calcium chloride (CaCl2) from promote the collagen synthesis. Dequcker2 believed that Beijing Chemicals Company and Poly (L-lactic acid) (PLLA, fluoride could increase the deposition rate and the number of Mw = 5000) from Changchun Institute of Applied Chemistry. OB by stimulating OB mitosis. Therefore, addition of fluoride into scaffold material was considered as a potential method Nanofibre construction and collection to enhance osteoblastic activities in the field of bone tissue CaCl2 (0.0500 g) and NaF (0.0378 g) were dissolved in 1 ml engineering. and 0.6 ml distilled water respectively and stirred vigorously for 30 min. Then, 4.5 ml TFE was added into the CaCl2 aqueous Poly (L-lactic acid) (PLLA)3 is a synthetic polyester with good solution and stirred vigorously for 30 min. PLLA (1.5848 g ) biocompatibility and biodegradability, its fibre fabric has was dissolved in the above solution and stirred vigorously for been widely used in biomedical fields, such as drug controlled 6 h at room temperature. NaF aqueous solution was added release and wound dressings, particularly as scaffolds in the into the above blended solution dropwise with vigorous field of engineering tissue. PLLA can also be used as a vehicle stirring. The mixture was then stirred at room temperature to deliver the bioactive molecules, e.g. growth factors, to for 6 h. The spinning liquid had been prepared. The apparatus instruct the tissue regeneration. for the electrospinning experiments was similar to previous report.8 At room temperature, the spinning liquid was placed However, the construction of bioactive scaffolds is quite into a glass syringe with the tip of inner diameter of 1 mm. complex and considered as the bottle neck for biomaterials A clamp connected with high voltage power supplier was and regenerative medicine. Recently, with the development attached to the glass syringe. As grounded collector, a piece of electrospinning technique,4 nanofibre products have of aluminum foil was placed towards the tip at the distance of been constructed and increasingly used as the scaffolding 15 cm. The membrane of CaF2/PLLA nanofibres was formed biomaterial in tissue engineering.5-7 However, its application on the aluminum foil at 16 kV. The membrane was then stored as a bioactive mediator delivering vehicle has not been in a vacuum oven for 24 h at 40 °C to remove residual solvent. investigated. Therefore, the current study was set out to explore the methods of constructing fluoride-containing Morphology and characterization PLLA nanofibre scaffold by electrospinning for bone tissue The morphology and the energy-dispersive X-ray engineering. spectroscopy (EDX) mapping of the electrospun fibres were observed under a SEM (SHIMADZU SSX-550). The TEM images and the electron diffraction studies were performed with on

72 a JEM-2000EX microscopy. FT-IR spectra were recorded on all fluoride salts can produce the ideal structure of PLLA a Nicolet Instruments Research series 5PC Fourier Transform nanofibre scaffold. In addition to the bioactive effects of Infrared spectrometer. fluoride in tissue engineering, calcium has also been shown to enhance the bone regeneration.11-13 Therefore Ca++ and RESULTS AND DISCUSSION F- (CaF2 ) seems to be the optimal combination for the nanofibre scaffold. Moreover, the PLLA nanofibre scaffold The current study has successfully constructed a bioactive can also be used for the delivery of multiple factors to assist scaffold through adding fluoride into nanofibres, for bone bone regeneration, and our research group has identified tissue engineering. The nanofibres were made of Poly (L-lactic some key regulatory pathways in this process.14-15 acid) (PLLA) which can be dissolved in many organic solvents. The technical difficulty for this project is that PLLA need to CONCLUSIONS be dissolved in a solvent which can also dissolve the inorganic fluoride salt. Our pilot studies have found that the hybrid The following conclusions can be made from the current solvent with 2, 2, 2-trifluoroethanol (TFE) and water can study: (1) fluoride was successfully introduced into PLLA dissolve calcium fluoride (CaF2) and PLLA to form a solution nanofibres by electrospinning; (2) CaF2 nanoparticles is for nanofibre electrospinning. The standard procedure of the optimal choice to construct the nanofibre scaffold with the spinning liquid and the nanofibres was mentioned in our average diameter about 50 nm well dispersed in the PLLA previous report.9 nanofibre matrix; and (3) fluoride contained PLLA nanofibre seems to be a very promising scaffolding biomaterial for the As is shown in the SEM mocrograph (Fig. 1), the morphology bone tissue engineering. of the CaF2/PLLA fibres was uniform and the average diameter of fibres was about 300 nm. This suggest that ACKNOWLEDGEMENT the desired nanofibre scaffold can be achieved through the electrospinning. TEM images (Fig. 2) further showed the The authors gratefully acknowledge the support of DECRE deposition of CaF2 on PLLA nanofibres. It could be seen grant (DE120101666, Dr. Ye) from Australian Research that some CaF2 nanoparticles with the average diameter Council, and JCU Rising Stars Program (Ye 2012). about 50 nm were well dispersed in the polymer fibre matrix. To determine the accurate structure for these CaF2 REFERENCES nanoparticles, electron diffraction (SAED) pattern of these CaF2 nanoparticles at the TEM-selected area was recorded 1. Fareley JR, Wergedal JE, Baylink DJ. Fluoride directly stimulates as shown in inset (Fig. 2). The diffraction pattern of the proliferation and alkaline phosphatase activity of bone-forming cells. nanoparticles in the polymer fibre matrix was consistent Science 1983;222:330–332. with single crystal CaF2 10, indicating that the CaF2 crystal nanopaticles have been indeed successfully introduced into 2. Dequeker J, Declerck K. Fluor in the treatment of osteoporosis. An the PLLA nanofibres. overview of thirty years clinical research. Schweiz Med Wochenschr 1993;123:2228–2234. Fig. 3 compares the flourier transform infrared spectroscopy (FT-IR) spectra of the electrospun pure PLLA fibres (curve A, 3. Zhang JF, Sun XZ. Mechanical Properties of Poly(lactic acid)/Starch black) and CaF2/ PLLA fibres (curve B, red). Curve A depicts Composites Compatibilized by Maleic Anhydride. Biomacromolecules characteristic absorption bands at 1759, 1185, 1130 and 1089 2004;5:1446–1451. cm− 1, which represent the backbone ester group of PLLA. 4. Li D, Xia Y. Electrospinning of Nanofibres:Reinventing the Wheel? Adv Interestingly, the peaks position of these spectra Curve Mater 2004;16:1151–1170. (CaF2/ PLLA fibres) almost the same as that of Curve A. This may be explained that the molecular interaction between 5. Chen ZG, Mo XM, Qing FL. Electrospinning of collagen–chitosan CaF2 and PLLA was weak. Therefore, the viscosity of PLLA complex. Mater Lett 2007;61:3490–3494. solution seems to be the main reason that CaF2 nanoparticles could be dispersed in spinning liquid homogeneously but not 6. Yang F, Murugan R, Wang S, Ramakrishna S, Electrospinning of nano/ accumulated into sediment. The distribution patterns of Ca++ micro scale poly(L-lactic acid) aligned fibres and their potential in element and F- element in the CaF2/PLLA nanofibre were neural tissue engineering. Biomaterials 2005;26:2603–2610. further tested using EDX mapping. It could be seen that Ca++ element and F- element were dispersed homogeneously in the 7. Nam J, Huang Y, Agarwal S, Lannutti J. Materials selection and residual scaffold. The result proved that the CaF2 nanoparticles can solvent retention in biodegradable electrospun fibres. J Appl Polym Sci be dispersed homogeneously in the PLLA nanofibre scaffold. 2008;107:1547–1554. Hence, we tested whether the same type of PLLA nanofibre 8. Badami AS, Kreke MR, Thompson MS, Riffle JS, Goldstein AS. Effect can be achieved by any fluoride salt. Sodium fluoride (NaF) of fibre diameter on spreading, proliferation, and differentiation was chosen as a control. NaF was also directly dissolved in of osteoblastic cells on electrospun poly (lactic acid) substrates. the hybrid solvent of TFE and water, and then PLLA was put Biomaterials 2006;27:596–606. into the solution for spinning. Fig. 4 showed the TEM image of a NaF/PLLA nanofibre prepared from above spinning liquid. 9. Xu J, Yan J, Gu Q, Li JF, Wang HY. Preparation of fluoride-containing It could be seen that some NaF nanoparticles were dispersed gelatin nanofibre scaffold. Mater Lett 2011;65:2404–2406. in the PLLA fibre matrix. However, comparing with CaF2 nanoparticles (Fig. 2), the size and shape of NaF nanoparticles 10. Zhao DH, Shen YL, Zhang YL, Wei DQ, Gao NY, Gao HW. Milli-sized were not unified. The reason for such a difference in CaF2 calcium alginate sorbent supporting the dye waste – calcium fluoride and NaF is not clear. However, it can be concluded that not hybrid for adsorption of organic contaminants. J Mater Chem 2010;20:3098–3106. 11. Barrère F, van Blitterswijk CA, de Groot K. Bone regeneration:molecular and cellular interactions with calcium phosphate ceramics. Int. J. Nanomedicine 2006;1:317. 12. Arinzeh TL, Tran T, Mcalary J, Daculsi G. A comparative study of biphasic calcium phosphate ceramics for human mesenchymal stem- cell-induced bone formation. Biomaterials 2005;26:3631-3638. 13. Lobo SE, Livingston AT. Biphasic calcium phosphate ceramics for bone regeneration and tissue engineering applications. Materials 2010;3:815-826. 14. Xing Q, Ye Q, Fan M, Zhou Y, Xu Q, Sandham A. Porphyromonas gingivalis lipopolysaccharide inhibits the osteoblastic differentiation of preosteoblasts by activating Notch1 signaling. J. cellular physiology 2010;225:106-114. 15. Chen X, Zhang T, Shi J, Xu P, Gu Z, Sandham A, Ye Q. Notch1 signaling regulates the proliferation and self-renewal of human dental follicle cells by modulating the G1/S phase transition and telomerase activity. PlosOne 2013;8:e69967.

73 Fig 1. SEM image of CaF2/PLLA Fig 2. TEM image of CaF2/PLLA Fig 3. FT-IR spectra: (A) pure PLLA nanofibres. nanofibres; Electron diffraction nanofibres and (B) CaF2/PLLA patterns of the nanoparticles in the nanofibres. PLLA nanofibre matrix shown in inset. Fig 4. TEM image (D) of NaF/PLLA nanofibre (control). Address for correspondence Assoc. Professor Qingsong Ye Office 218, D1 Building School of Medicine and Dentistry James Cook University (Cairns) P.O. Box 6811, Cairns QLD 4870, Australia [email protected]

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 74-76 REPLACEMENT OF LOST ANTERIOR TEETH IN YOUNG INDIVIDUALS: AUTOTRANSPLANTATION OF PREMOLARS: THE JOINT ROLE OF THE PAEDIATRIC DENTIST, ORAL SURGEON AND ORTHODONTIST Frances M. Andreasen, DDS, dr.odont. Since 1980, Dr Andreasen has been actively involved in dental trauma research, with approximately 100 scientific publications, related primarily to pulpal responses to acute injury, long-term prognosis after acute trauma and restoration of the traumatised dentition. ABSTRACT Autotransplantation of premolars for lost anterior incisor teeth in young patients is a safe and predictable procedure. Teeth which have been avulsed and replanted and with signs of ankylosis (replacement resorption) or late diagnosis of inflammatory/ infection-related root resorption with large defects on the root surface, intrusions, or with crown-root fracture, as well as teeth with dubious endodontic success may be suitable for autotransplantation with premolar teeth. Autotransplantation of premolars with incomplete root formation is an excellent tool for meeting this need, with a 10-year survival rate of 90% in the hands of experienced clinicians. The joint roles required of the paediatric/restorative dentist, oral surgeon and orthodontist is discussed. INTRODUCTION Fig 2. A photograph of a crown root fracture which Correct, standardized clinical and radiographic examination may have a poor outcome techniques are necessary to establish the diagnosis, prognosis if the root is retained. and appropriate treatment plan for the traumatized dentition. The clinical exami-nation begins superficially and works its way in to the oral cavity. In contrast, treatment of the den-tal/ oral injuries proceeds from the oral cavity, working its way exteriorly to ensure optimal access to the traumatised region. The radiographic technique employs film holders and multiple exposures to disclose possible tooth displacement, fractures of the alveolar process as well as horizontal root frac-tures.1-5 The clinical research done by Frances and Jens Andreasen, and co-workers have provided the clinician with a set of predictors for the fate of the dental pulp and periodontium following tooth luxation6-14 and tooth avulsion and subsequent replantation.15-18 The knowledge gained from these and other works have shown that candidates for tooth loss after injury can include: teeth which have been avulsed and replanted and with signs of ankylosis (replacement resorption) (Fig. 1) or late diag-nosis of inflammatory/infection-related root resorption with large defects on the root surface, intrusions (Fig. 2), or with crown-root fracture (Fig. 3), as well as teeth with dubious endodontic success. Fig 3. A photograph of an intrusive luxation injury where prognosis is known to be poorer than other luxation injuries. Fig 1. A radiograph of a central incisor with terminal ankylosis.

75 Research has shown us how to correctly deal with premolar. Research has shown that the optimal time for inflammatory/infection-based root resorption by the autotransplantation (i.e. optimal periodontal and pulpal introduction of calcium hydroxide (Ca(OH)2) into the healing post-operatively as well as optimal root length) is infected root canal chamber. With the ad-vent of MTA, when the donor tooth has achieved ¾ of its expected root treatment strategy has been changed. Among its many length.19 properties, calcium hydroxide is bacteriocidal and creates an environment conducive to hard tissue formation and will This implies intimate knowledge of long-term prognosis after arrest inflamma-tory root resorption. However, it has been injury so that the correct time of treat-ment is not passed shown that prolonged use of Ca(OH)2 can lead to brittle by while the clinician “waits and sees” if “something” will dentine and thereby weaken tooth structure. Therefore, happen. present treatment strategy advocates short-term use of Ca(OH)2 (i.e. 10-14 days.) followed by insertion of MTA as The orthodontist must be consulted with respect to the an apical plug. Thus, pulpal healing complications (i.e. pulp patient’s general treatment needs. Swedish studies have necrosis) can usually be treated with good long-term results.1 shown that there is an increased risk of severe anterior tooth injury with increasing over-jet.20,21 Thus, it is often such However, late periodontal healing complications can lead to patients who ultimately become candidates for traumatic tooth loss. To date there is no known treatment for replacement tooth loss and hence autotransplantation. The orthodontist’s resorption/ankylosis; so all treatment procedures should be duty is to assess occlusion, space relationships, optimal aimed at avoiding this complication. However, the question treatment timing, whether there are developing donor teeth remains: when ankylosis does occur, can we use its osteogenic present (i.e. no premolar agenesis) and whether the patient is potential to our advantage? Clinical experience has shown a candidate for premolar extraction. If the latter is relevant, that early tooth loss can lead to atrophy of the maxillary arch then instead of re-moving the first premolars as standard and serious aesthetic, restorative problems. The same is true procedure, the second premolar (due to root anatomy) from of ankylosis, if allowed to progress once infraocclusion of the the contralateral side is to be chosen for maxillary central ankylosed tooth is diagnosed, whereby root substance will incisors and mandibular first premolars for replacing lost be removed by osteoclastic activity and replaced by bone. maxillary lateral incisors. Presumably it is enam-el, which cannot be resorbed, that is the cause of arrested maxillary growth. However, if when In this connection, when premolar extraction is not indicated, in-fraocclusion is diagnosed and the clinical crown carefully it should be considered that an aesthetic tooth replacement removed surgically – leaving the resorbing root in place – more posteriorly in the dentition is more easily achieved clinical research has shown that maxillary dimensions can be than in the prior to the surgical procedure to accommodate stabilized, if not in-creased. the premolar root. With respect to space relationships, it is the orthodontist’s duty to determine whether there is In adults, an aesthetic treatment can usually be achieved space enough for the graft, or whether palatal ex-pansion is by fixed prosthetics of various forms includ-ing implants. necessary prior to transplantation. Moreover, harvesting of Osseointegration following implant insertion can be likened to the donor tooth should not be done at too early a stage of root ankylosis in the young patient; and in young patients can lead development, as this can result in arrested root development. to serious restorative and aesthetic problems, due to arrested maxillary growth containing the implant/ankylosed tooth The oral surgeon who is to perform the transplantation and growth in the parts of the jaw adjacent to the implant/ procedure should be very experienced in atraumatic tooth ankylosed tooth. For this reason implants are contraindicated extraction. The surgical procedures for autotransplantation in this patient group. Ortho-dontic space closure might be an differ in approach to e.g. third molar removal. When a third alternative solution; but treatment time can be protracted molar is to be removed, it is often necessary to section the and the aesthetic result less than optimal. tooth prior to removal to minimise bone loss. In contrast, when harvesting the donor tooth, bone must be gently Knowledge of the pathogenesis of the various resorption removed so that the tooth and follicle can be taken in toto. In processes (i.e. damage to the cellular layer most intimately this way the periodontal tissues surrounding the donor root related to the root surface) that can occur following acute are protected. Periodontal tissues have a known osteogenic dental injury can aid the clinician in delivering treatment capacity. Thus, even in the case of bony defects, successful that minimizes further trauma to the already traumatised autotransplantation will lead to restoration of sup-porting dentition. And in the long-run can allow us to replace lost bone. Surgical techniques include incision of the PDL with anterior teeth in young individuals, at an age where dental thin, specially formed scalpel blades that can slip between implants are directly contraindicated. bone and follicle to carefully remove the graft. AUTOTRANSPLANTATION OF PREMOLARS TO THE In case of bony defects, as from atrophy due to early tooth ANTERIOR REGION loss, a “sandwich graft” technique can be used. A gingival flap is raised. The labial bone plate is sectioned carefully from the Autotransplantation of premolars with incomplete root maxilla, leaving the palatal bone in place. It should be noted formation is an excellent tool for meeting this need, with a that all surgical procedures must be performed employ-ing 10-year survival rate of 90% in the hands of experienced burs and handpieces that are equipped with internal cooling, clinicians.19 With timely treat-ment planning and coordination not to heat the bone. The harvested bone is cut into strips between the paediatric dentist, orthodontist and oral with surgical scissors. Once the tooth graft is put into place surgeon, “planned dental trauma”can be performed, and stabilized with a silk suture at the neck of the tooth where an untreatable anterior tooth can be replaced by a and gingiva, strips of bone are laid loosely over the root. Trabecular bone, with its high vascular content is a source of osteoclasts which can participate in root resorption. To

76 minimize the risk of resorption, the bony strips are, therefore, REFERENCES placed with the compact bone placed facing the root surface and trabecular bone oriented facially. The gingival flap is 1. Andreasen FM, Kahler B. Pulpal response to acute dental injury in the now tested for re-laxed realignment over the tooth and bone permanent dentition: Clinical implications. A review. Dent Traumatol grafts. It is often necessary to incise the gingiva at its at- 2014: Submitted for publication. tachment to periosteum to achieve relaxed repositioning. 2. Andreasen JO, Bakland LK, Flores MT, Andreasen FM, Andersson L. With successful treatment, optimal root length, periodontal Traumatic Dental Injuries. A Manual (3rd ed.). Oxford: Wiley-Blackwell 2011. support and pulp vitality will be achieved. Three months after successful treatment, pulp canal obliteration (PCO) can be 3. Andreasen JO, Andreasen FM, Andersson L (eds.). Textbook and Color seen radiographically as a sign of pulp survival. The job of Atlas of Traumatic Injuries to the Teeth (4th ed.) Oxford: Blackwell the restorative dentist is now to transform premolar crown Munksgaard, 2007. anatomy to that of a central incisor either by resin composite build-up, porcelain veneers or crowns. However, the rapidly 4. Andreasen FM, Andreasen JO. Diagnosis of luxation injuries. The deposited post-operative tertiary dentine can present a risk importance of standardized clinical, radiographic and photographic for secondary pulp necrosis if soft tissue (i.e. pul tissue) techniques in clinical investigations. Endod Dent Traumatol 1985;1:160-9. inclusions are exposed in the grinding procedure. Hence prophy-lactic endodontic intervention might be advocated 5. Dental Trauma Guide. www.dentaltraumaguide.org. Accessed when root development has reached an optimal level. This 1.03.2014. will facilitate tooth preparation and eliminate the need for compromise with respect to porcelain restorations. Figure 6. Andreasen FM, Vestergaard Pedersen B. Prognosis of luxated 4 shows a successful case where autotransplantation of a permanent teeth - the development of pulp necrosis. Endod Dent premolar tooth into the site of avulsed incisor teeth. Following Traumatol 1985; 1:207-20. orthodontic movement and composite resin res-torations created a pleasing aesthetic appearance. 7. Andreasen FM. Pulpal healing after luxation injuries and root fracture in the permanent dentition. Thesis: Copenhagen University 1995. ISBN Fig 4a. Avulsion of maxillary right central and lateral no. 87-9855538-0-1. incisors. The teeth could not be retrieved and replanted at the time of injury. 8. Andreasen FM, YU Z, Thomsen BL, Andersen PK. The occurrence of pulp canal obliteration after luxation injuries in the permanent Fig 4b. After transplantation of the lower left first premolar dentition. Endod Dent Traumatol 1987; 3:103-15. to the upper right central incisor position, orthodontic movement of the upper right canine to the lateral incisor 9. Andreasen FM, Andreasen JO, Bayer T. Prognosis of root fractured position and slight rotation of the upper right first premolar. permanent incisors - predic¬tion of healing modalities. Endod Dent Traumatol 1989;5: 11-22. Fig 4c. The final result after composite resin build-up of the “central” and “lateral incisors” and moderate grinding of 10. Andreasen FM. Pulpal healing after luxation injuries and root fracture the “canine”. in the permanent dentition. Endod Dent Traumatol 1989; 5:111-131. CONCLUSION 11. Andreasen FM, Zhijie Y, Thomsen BL. Relationship between pulp dimensions and development of pulp necrosis after luxation injuries in In conclusion, autotransplantation of premolars for the permanent dentition. Endod Dent Traumatol 1986;2:90-8. replacement of lost anterior teeth in young patients can return the traumatised dentition to its original function 12. Andreasen FM, Andreasen JO, Bayer T. Prognosis of root-fractured and beauty. This requires a concerted effort by a team of permanent incisors–prediction of healing modalities. Endod Dent paediatric dentist, orthodontist and oral surgeon. Intimate Traumatol 1989; 5:11-22. knowledge of long-term prog-nosis after acute injury and correct timing of treatment are essential to ensure success. 13. Andreasen JO, Bakland LK, Andreasen FM. Traumatic intrusion of permanent teeth. Part 2. A clinical study of the effect of preinjury and injury factors, such as sex, age, stage of root development, tooth location, and extent of injury including number of intruded teeth on 140 intruded permanent teeth. Dent Traumatol 2006; 22:90-8. 14. Andreasen JO, Bakland LK, Andreasen FM. Traumatic intrusion of permanent teeth. Part 3. A clinical study of the effect of treatment variables such as treatment delay, method of repositioning, type of splint, length of splinting and antibiotics on 140 teeth. Dent Traumatol 2006; 22:99-111. 15. Andreasen JO, Borum MK, Andreasen FM. Replantation of 400 traumatically avulsed permanent incisors. I. Diagnosis of healing complications. Endod Dent Traumatol 1995; 11:51-8. 16. Andreasen JO, Borum MK, Andreasen FM. Replantation of 400 traumatically avulsed permanent incisors. II. Factors related to pulpal healing. Endod Dent Traumatol 1995; 11:59-68. 17. Andreasen JO, Borum MK, Andreasen FM. Replantation of 400 traumatically avulsed permanent incisors. III. Factors related to root growth. Endod Dent Traumatol 1995;11: 69-75. 18. Andreasen JO, Borum MK Andreasen, FM. Replantation of 400 traumatically avulsed permanent incisors. IV. Factors related to periodontal healing and root resorption. Endod Dent Traumatol 1995;11:76-89. 19. Andreasen JO. Atlas of Replantation and Transplantation of Teeth. Fribourg: Mediglobe SA, 1992. ISBN 2-88239-015-X. 20. Järvinen S. Incisal overjet and traumatic injuries to upper permanent incisors. A retrospective study. Acta Odontol Scand 1978;36:359-62. 21. Malmgren O, Malmgren B. Orthodontic Management of the Traumatized Dentition. In Andreasen JO, Andreasen FM, Andersson L (eds.). Textbook and Color Atlas of Traumatic Injuries to the Teeth (4th ed.) Oxford: Blackwell Munksgaard, 2007. Address for correspondence Specialist consultant in dental trauma Copenhagen, Denmark [email protected]

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 77-81 PLANNING EARLY ORTHODONTIC TREATMENT Dr John Fricker, OAM, MDSc Grad Dip Ed (Adult) MRACDS(Orth) FRACDS FADI FPFA FICD Dr Fricker is an orthodontist in private practice in Canberra, with a Consultant position at the Canberra Hospital Maxillo-Facial Unit. In 2010 Dr Fricker was awarded the Medal of the Order of Australia (OAM) for services to the dental profession. ABSTRACT This presentation introduces concepts of planning orthodontoc treatment during the mixed dentition phase of growth and development. Planning commences with an understanding of the nomal presentation of the dentition and follows of the possibilities of deviation from the normal. In this lecture, I will discuss occlusal abnormalities requiring early intervention as a preventive or interceptive approach to orthodontic treatment. PLANNING ORTHODONTIC TREATMENT buttons or belt buckles? But be discreet about the possibility of adoptions. Planning orthodontic treatment for the young child begins The assessment of the children begins as they come down when you see on your day sheet that you have a child booked the hall to you surgery or new patient room. Observe the in as a new patient. As you plan your day, make a note of the children, who is with them? Are the children comfortable age of the child and picture the child as he or she walks into with them? Are they well nourished? Check their gait and are your surgery. I am assuming that they are walking but it is they “funny looking kids” which warrants deeper questioning always possible they are disabled. about syndromes. Consider a case scenario of twins age 8 years. As you picture EXTRA ORAL EXAM the possible presentations of these children, I will move on to discuss possible orthodontic problems that indicate early The extra oral exam begins with assessing the skeletal treatment. Treatment options may be either preventive or relationships of maxilla to mandible, maxilla to cranial base interceptive. Preventive implies procedures that eliminate and mandible to cranial base (Fig. 1). Facial harmony and or factors that may lead to a malocclusion in an otherwise symmetry is assessed both in full face frontal and in profile. normally developing dentition. For example, controlling a digit sucking habit. Interceptive orthodontics relates to Fig 1. Cephalometric film showing key planes for facial procedures to limit a potential irregularity from progressing harmony. Blue lines: cranial base, palatal plane, mandibular to a more severe malocclusion. For example correction of a plane. Yellow line, anterior facial plane from Nasion to posterior cross bite. The aim is to allow normal growth and Menton (chin point). Pink line, aesthetic line, from nose tip to development of the dentition and minimise future orthodontic soft tissue chin point. treatment. The third permanent molars erupt between 18 and 30 years of age so planning requires thinking ahead at least ten years. Returning to the day sheet and our twins, what would you expect to see? Are they identical, mirror imaged or non identical. In this case they are brother and sister. At 8 years old you would expect mixed dentition, that is upper and lower permanent incisors, first permanent molars and deciduous canines and molars. However, does chronological age always match dental and skeletal age and would you expect the boy and the girl to have the same dentition? Planning early orthodontic treatment also requires careful history taking with specific questions related to growth and development, syndromes or history of trauma to the dentition, face and head. Family history includes where the children were born, and where they have lived for the last 8 years looking at exposure to disease and access to fluoride. Allergy to nickel is surprisingly common and many modern orthodontic wires contain nickel. So rather than just asking are the children allergic to anything? Be specific and ask if the children have ever had itchiness to metals such as earrings,

78 To assess facial balance I suggest sitting the patient in the Fig 2b. Intra-oral view of Fig. 2a showing deviation of tooth in an upright position. Stand behind him/her and look down 21 into the arch. over the top of the head and visualise a line from the midpoint between the eyes to the midpoint of the chin. Assess the left right symmetry while the teeth are in occlusion then follow with an assessment of opening and closing patterns. Begin the mouth as wide open as possible and rest your fingers lightly over each of the TMJ’s. Ask the patient to very slowly close to maximum occlusion and monitor for any lateral or anterior displacement on complete closure. Any lateral slide indicates a functional cross bite as does propping the mandible forward to move into an anterior cross bite. A functional slide into a cross bite is cause for early intervention and I will suggest options for treatment in a later section. An extra oral exam also includes an assessment of swallowing patterns and mentalis activity, which relate to habits such as lip biting or digit sucking. INTRA ORAL EXAM The dental relationship is then recorded with the teeth in occlusion. In the early mixed dentition the important thing is It may seem obvious, but the first thing is to count the teeth. to check for a normal overbite and overjet over a harmonious Identify the deciduous and permanent teeth and match this to skeletal base. An overbite refers to the degree of vertical the expected dentition for the age of the child. If the presentation overlap of the maxillary and mandibular incisors. An excessive does not match the expected for the age of the child then you overbite is one where the maxillary permanent incisors need to ask questions regarding absent teeth or supernumerary overlap the lower permanent incisors in the vertical direction teeth. What is the dental history and is there anything in the by more than fifty per cent. An excessive overbite can result in family history such as Ectodermal dysplasia which would account trauma to the soft tissue of the palate and is an indication for for multiple missing teeth? Conduct a caries and periodontal early treatment. Overjet refers to the horizontal relationship check and look for mottling of teeth. Again match this to the of the maxillary incisors to the mandibular incisors and history, Did the child grow up with fluoride? Was it too much may be positive or negative. A positive overjet greater than or not enough? Be aware of molar incisor hypomineralisation five millimetres may be related to a dental discrepancy due (MIH) which I will review later in this presentation. to linguoversion of the lower incisors combined with the labioversion of the upper incisors as a result of digit sucking With the teeth apart, check for ectopic positioning of teeth. or biting the lower lip. An excessive overjet may also indicate The maxillary first permanent molars drift mesially as they a skeletal discrepancy where the mandible is too small for erupt and are prone to getting caught under the distal of the the maxilla or retrognathic. Digit sucking can also lead to an second deciduous molars. The permanent incisors may also anterior open bite which describes the presentation of the erupt ectopically. The normal path of eruption for the lower anterior teeth where there is no vertical overlap. A negative incisors is lingual to the deciduous lower incisors and as the overjet is another way of describing cross bites. As mentioned deciduous incisors exfoliate the pressure from the tongue earlier, an anterior cross bite may be due to the ectopic guides the permanent teeth into alignment. Occasionally the position of the tooth but is also a common presentation of a deciduous incisors are retained and the lower permanent maxillary skeletal discrepancy. Cross bites of first permanent incisors remain in an ectopic position lingually. Simple removal molars present for the same reasons. of the deciduous precursor teeth is usually enough to allow the natural action of the tongue to align the permanent incisors. Malocclusions as a result of digit sucking or lip biting are reasons for early intervention as removal of the extraneous forces on The normal path of eruption of the maxillary permanent the dental development will usually allow the natural balance of incisors is labial to the deciduous incisors Lack of space due the lips and tongue muscles to restore the anterior relationships to a skeletal deficiency, trauma to the deciduous incisors to a normal pattern. Anterior or posterior cross bites in an eight or the presence of a mesiodens, can result in the ectopic year old without any functional slide on opening or closing do positioning of the permanent incisors. Clinically this may not require early intervention. However, where the extra-oral present as delayed eruption of the permanent incisor and or examination has revealed a slide to full occlusal interdigitation, ectopic eruption of the incisor into the arch (Fig. 2a and 2b). early intervention is warranted to remove occlusal interferences and allow the TMJ’s to develop harmoniously. Fig 2a. OPG with an unerupted supernumerary tooth in the maxillary midline (mesiodens).

79 TREATMENT OF CROSS BITES Anterior cross bites Fig 4b. Modified Hawley appliance with occlusal cover and Z Anterior cross bites may involve a single tooth or all for springs. incisors. A pseudo class III occurs when a child protrudes into an anterior cross bite to avoid occlusion interferences (Fig. Posterior cross bites 3). Treatment is usually simple and straight forward as often only tilting or proclining of the maxillary incisors is required. As stated earlier, correction of posterior cross bites is only A cross bite of a single tooth that is not in excessive overbite indicated where there is a functional slide to a unilateral cross can be corrected with a tongue blade or a lower inclined bite in full occlusion. There is a shift of the midline towards plane. A tongue blade or paddle pop stick is placed in the the side of normal buccal overjet and occlusal interdigitation. mouth vertically against the palatal surface of the tooth in This usually a reflection of a bilateral narrowing of the cross bite and over the labial surface of the lower incisors maxillary dental arch and this can be confirmed by guiding the and held against the chin. Instruct the child to bite against the child to slowly close together with the midlines co-incident. stick and count to 50 out loud as one apple, two apples, three If the buccal segments are edge to edge, bilateral expansion apples etc. Try to repeat this six times per day with at least 30 of the palate is indicated. Palatal expansion is possible with minute intervals. A lower inclined plane has a similar action both removable appliances or fixed appliances. The standard except it is fixed to the lower incisors This can be an acrylic removable appliance consists of a Hawley type retainer with overlay or simply building up the crowns of the lower incisors a mid palatal screw and occlusal cover over the deciduous to create an interference which restricts the functional slide and permanent molars to remove occlusal interferences. and proclines the tooth in cross bite. This expansion screw is then activated a quarter turn twice a week. The effectiveness of removable appliances on a young Fig 3. Anterior cross bite as a result of propping forward into patient are firstly compliance and secondly retention of the occlusion, hence pseudo class III. appliance. Compliance demands assistance from a third A cross bite of two or more incisors can generally be party to activate the palatal screw and refit it. Teeth can be corrected with an upper removable appliance fastened to the tender after each activation and as you cannot watch a child first permanent molars with Adams cribs. An anterior bite 24 hours per day the appliance can spend a lot of time in a platform of acrylic will reduce the vertical overlap (overbite) pocket rather than in the mouth. Retention is also difficult as of the teeth in cross bite and allow free passage as the tooth the deciduous molars have short clinical crowns and it is more is proclined. The active components are Z springs against the difficult to clasp these successfully than permanent teeth. palatal surfaces of the teeth in cross bite (Fig. 4a & 4b). Fixed appliances are more effective as they overcome the problems of compliance and retention while at the same time provide a more continuous expansion force on the dentition. The appliance of choice for bilateral palatal expansion in the young child is the quad helix (Fig. 5). This appliance consists of a transpalatal spring attached to cemented bands on the first permanent molars. Activation is once per month by the practitioner by expanding each of the four helices. Generally, the helices are expanded in the mouth with pliers and each third visit the appliance removed, adjusted and recemented. Ideally the cross bite should overcorrected to half the buco-lingual width of the lower molars each side and the appliance left in situ for three months before removing the appliance. The child should be able to close with the midlines co-incident and no lateral slide Fig 4a. Unilateral cross bite with a midline shift indicating a functional slide.

80 EXTRACTION OF FIRST PERMANENT MOLARS Gross caries or hypomineralisation of the first permanent molars can pose difficult dilemmas in treatment planning. Molar-Incisor hypomineralisation (MIH) is hypomineralisation of systemic origin that affects one to all of the first permanent molars and is often associated with affected permanent incisors. MIH molars are fragile, and characterised by rapid caries development. Often molars cannot be anaesthetised with local anaesthetics and combined with the fragility of the enamel, makes restoration of these teeth very difficult. Restoration of these teeth with stainless steel crowns under a general anaesthetic is usually the treatment of choice to provide a functional occlusion in the mixed dentition (Fig. 7). Fig 5. Quad helixfor slow maxillary expansion. SUPERNUMERARY TEETH Supernumerary teeth can present in any part of the dental arch and rarely in the deciduous dentition. The most frequent sites are the maxillary midline (mesiodens) or the third molars and less likely, lateral incisors or the mandibular premolars. If a supernumerary tooth obstructs the eruption of an adjacent tooth, which is the most likely cases with a mesiodens, the supernumerary should be removed as soon as possible. The risks facts need to be considered as with all dento-alveolar surgery before committing to the surgical removal. ECTOPIC ERUPTION OF FIRST PERMANENT MOLARS Fig 7. MIH molars restored with stainless steel crowns. Maxillary first permanent molars can impact against the distal The treatment of MIH is based on the long term prognosis of of the second deciduous molars. Where there is only a slight the first permanent molars and orthodontic considerations engagement between these teeth, simply slicing the distal into the future. The presence or absence of the third of the second deciduous molar will allow the spontaneous permanent molars may influence whether to extract the first eruption of the first permanent molars. Alternatively, placing permanent molars, however, even where the third permanent an orthodontic separating elastic at the distal of the second molars are absent, extraction of the first permanent molars deciduous molar may disimpact the first permanent molar. may be the best option for the long term goal of a functional Where the first permanent molar is severely impacted and occlusion with minimum maintenance. the distal of the second deciduous molar is resorbed, removal of the second deciduous molar is indicated to allow the first Before any extractions are confirmed, an OPG should be taken permanent molar to erupt into the arch (Fig. 6). Often space to confirm the presence of developing premolars and third regaining is then required to provide space for the future permanent molars. In an eight year old child an OPG may not eruption of the second premolar. A space regaining appliance show the development of the third permanent molars. That is can be fixed as in a sectional archwire supporting a coil spring not to say they are absent as they may show over the next two to open the space, or a removable appliance with distalising to three years. The ideal time for the extraction of the first springs mesial to the erupting first permanent molars. permanent molars is when the roots of the second permanent molars are just starting to form which suggests that where possible the first permanent molars should be preserved with stainless steel crowns until they are extracted at age 10. Orthodontics may be required once the second permanent molars erupt to detail the occlusion but the final occlusion is one of reduced maintenance (Fig. 8a & 8b). In crowding cases, it is interesting to note that where third molars are present, the chances of these erupting are approximately 90% when the first permanent molars are extracted as against 55% when premolars are extracted. Fig 6. OPG film showing resoption of teeth 55 and 65 and the ectopic eruption of teeth 16 and 26.

Fig 8a. Permanent dentition with stainless steel crowns on 81 16 26. SUMMARY Planning orthodontic treatment in the young child is looking ahead and forecasting where that child will be in 5, 10, 15 or 20 years. The development of the occlusion is theoretically complete when the third permanent molars have erupted, but the remodelling of the alveolar bone may continue into the late 20’s. Preservation of teeth is a primary goal, however the long term prognosis and the cost of maintenance must be reconciled with what can be done in the best interest of the child for a functional occlusion with minimal maintenance. REFERENCES 1. Fricker J, Kharbanda O, Dando J. Orthodontic diagnosis and treatment in the mixed dentition. In: Cameron AC, Widmer RP, Eds. Handbook of Pediatric Dentistry. Edinburgh: Mosby Elsevier, 2013:409-445. 2. Fitzpatrick L. First permanent molars with molar incisor hypomineralisation. J Irish Dent Assoc 2007;53:32-37. 3. Mahoney EK, Ismail FSM, Kilpatrick N & Swain M. Mechanical properties across hypomineralized/hypoplastic enamel of first permanent molar teeth. Eur J Oral Sci 2004;112:497-502. 4. Seddon J. Extraction of four first molars: A case for the general practitioner. J of Orthod 2004;31:80-85. Fig 8b. Maxillary arch following extraction of 16, 26 and orthodontics substituting the second permanent molars for the irst permanent molars.

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 82-85 GENES AND ENVIRONMENTAL INTERACTIONS IN ORAL AND OROPHARYNGEAL CANCER Professor Newell W Johnson, CMG, FMedSci, MDSc, PhD, FDSRCS (Eng), FRACDS, FRCPath (UK), FFOP(RCPA), FHEA(UK), FICD. Professor Newell Johnson is a long time educator of undergraduate and postgraduate students, and having served as former Dean of the Griffith School of Dentistry and Oral Health, he continues to be active in education research, especially in relation to health sciences and dentistry. ABSTRACT The dental profession has responsibility for the prevention and early diagnosis of cancer of the mouth and of the oropharynx, and is a major contributor to management of these devastating diseases. In Australia, cancer of the oral cavity itself is largely due to tobacco use and alcohol abuse, predisposed to by poor diets, and affects predominantly those in the lower socio-economic classes: the incidence is declining. On the other hand, cancer of the oropharynx is a completely different disease: the major risk factor is sustained infection by “high-risk” types of human papillomavirus; it tends to affect younger adults, and is associated with sexual activity. The approach to primary prevention is obvious in both situations. Secondary prevention by population screening is only viable in high risk populations. Cancer is a genetic disease. To a minor degree, the genes we inherit affect susceptibility. However it is the many types of genetic damage produced by our environment which is driving the growing epidemic of cancer worldwide. In all cancers, acquired defects in the structure and/or the expression of many genes drive uncontrolled cell proliferation, so that a malignant neoplasm spreads locally and throughout the body. The genes involved are those controlling cell division, cell death, cell nutrition, DNA repair, the supply of blood vessels to the neoplasm, and the immune response. Very many biochemical pathways are involved: it is rather like a map of the London Underground, but many times more complex. Defects in one or other of these pathways increase in number and complexity as the neoplasm “progresses”. Some of these aberrations are common to many/most patients with a cancer of the mouth or oropharynx: others specific to a subset of patients, or unique to an individual. The mainstay in managing head and neck cancer remains surgery, with adjunctive radiotherapy and chemotherapy. These are highly toxic and disfiguring. We are thus moving towards biotherapies which seek to correct or block the key abnormal pathways of the individual patient. There is no such thing as a single magic bullet which will cure all patients, but drugs, monoclonal antibodies, and interfering ribonucleic acids targeted on the genetic damage for a particular patient are increasingly coming to clinical trial. Successes with some cancers of the breast and colon, for example, encourage the drive to better individualised treatment of head and neck squamous cell carcinoma. Many will continue to suffer, and our role in prevention, early diagnosis and rehabilitation remains essential - and challenging.   Over the past two decades we have come to understand that “oral cancer” is not one, but many different diseases. Whilst INTRODUCTION the majority are squamous cell carcinomas, it has become apparent that the balance of the causes is substantially The dental profession has a particular responsibility for different between sub-sites of this anatomically complex cancers of the lips, mouth and oropharynx. This is the part of the human body: ultraviolet light and tobacco remain anatomical area of our patients which we observe in our daily important for cancer of the lip; tobacco, alcohol, poor nutrition work: We play the leading role in monitoring and promoting and “dental factors” for cancer within the oral cavity itself; the health of these tissues; we encourage primary prevention infection with oncogenic types of human papillomavirus for by helping our patients to be free of the major life-style risk the mouth in a minority of cases and for the majority of cases factors, and are responsible more than any other professional arising in the oropharynx. “Oral cancer” and “oropharyngeal group for early detection of suspicious lesions. It is incumbent cancer” are different diseases. on every clinician to inspect every square millimetre of the oral mucosa of these sites at intervals based on a rational KEY EPIDEMIOLOGICAL FACTS appraisal of the individual subject: at first appointment for every new patient; every time a patient reports suspicious These cancers are the 6th most common in the world.1,2,3 signs or symptoms; at recall intervals based on an assessment The major burden is in developing countries and, in South of the risk status of the individual. Asia, oral cancer alone is usually the leading cancer site amongst males (as in Sri Lanka); sometimes in females (Fig. For some, our role extends to the application of additional 1). According to Globocan4, Papua New Guinea has the highest diagnostic tools, to active therapy, and to rehabilitation after treatment. Managing this devastating disease – these diseases – requires teamwork, and dentists must play leadership roles.

83 rates in the world, although the data are extrapolated from damage our chromosomes and mutate our individual genes other populations: we are currently working with colleagues by exposure to environmental carcinogen. Our environment there to expand and audit Registry acquisitions. In India, can also silence some functions, these epigenetic events oral cancer remains a major public health problem with an arising predominantly from hypermethylation of a gene. inexorable rise in disease burden, partly due to population growth.5 In Australia, there are encouraging declines in oral How does this apply to oral and oropharyngeal cancer? There cancer, but rises in the oropharynx, with steadily increasing is, undoubtedly, a degree of inherited susceptibility, but this trends of 1.2% pa for men and 0.8% pa for women from is minor compared to environmental influences. Inherited 1982 to 2008, these rises attributed to HPV infections.6 In susceptibility arises mostly from polymorphisms in the many western countries cancer of the oropharynx is rising genes controlling detoxification of carcinogens: particularly substantially: fortunately it is well established that such the cytochrome p450 system in the liver; and the efficiency cases respond well to radiotherapy, so that treatment de- of DNA repair mechanisms.16,17 We know of no “oral cancer escalation is now possible with these particular cancers7 and gene” which confers major risk in the same way that carriage demonstration of the presence of oncogenic HPVs in oral and of BRCA 1 and/or BRCA 2 confers risk of familial breast cancer oropharyngeal cancer biopsy tissues is now a routine part of in women, for example. treatment planning.8 Further, the success of HPV vaccination in the prevention of cancer of the uterine cervix is now So what of genetic changes acquired from environmental beginning to be seen for HPV-related head and neck cancers.9 damage? This is what environmental carcinogens do. This is why the risk of developing cancer increases with age. There is MAJOR RISK FACTORS an explosion of knowledge and related publications. A global initiative to describe genetic changes associated with all of the The major role of behavioural or life style risk factors remain: common cancers is underway. The base for “oral cancer” is in tobacco – both smoked and unsmoked; areca [betel] nut; India and the database is publically accessible.18 It currently heavy alcohol use; all acting in an environment of diets poor contains descriptions of 242 genes associated in some way in essential vitamins and minerals which lower resistance, with these diseases which we lump as oral cancer. It is not especially the ability to scavenge free radical and reactive feasible to attempt a description of them all here, let alone oxygen species.1,2 The importance of human papillomaviruses to critically analyse their importance, or the biochemical is summarised above. The role of “dental factors” is receiving pathways they control. renewed attention. Chronic trauma from sharp teeth, restorations or appliances may focus the site at which chemical FROM PRECANCER TO CANCER carcinogens act, and a neoplasm arises within a much wider field of altered tissue. Associations with periodontal disease It is a common belief that “oral cancer” arises from long are often suggested:10 here it is likely that the common risk standing lesions of the involved mucous membranes. factor of heavy microbial load in the mouth contributes the Leukoplakia is the most common: erythroplakia; mixed risk, and there is a renewed understanding that chronic lesions and submucous fibrosis are also important. We inflammation itself contributes to carcinogenesis.11 now define these collectively as oral potentially malignant disorders – OPMD.19 The terminology is important: we use Heavy alcohol consumption – whatever the beverage, is the the term ‘condition’ in recognition that changes at the major risk factor in western populations.12 We know that molecular level are widespread, involving much of the upper oral micro-organisms – fungi and bacteria - can metabolise aero-digestive tract [the long-standing concept of “field alcohol,[which is not itself carcinogenic, to acetaldehyde, cancerisation”], if not the whole body [eg systemic changes in which is.13 This has given rise to concerns about the potential immune response]. These visible lesions are but the external dangers of alcohol containing mouthwashes, which has representation of a systemic condition in which the individual led to the withdrawal of most of these products from sale: has an increased potential to develop a cancer – most likely although there is a biological basis for these concerns, in but not necessarily at the site of the clinically visible lesion. practical terms the available epidemiological evidence does not indicate that the risk is significant.14 In cultures where use of areca nut and smokeless tobacco are common, and sometimes in heavy alcohol users, the There is renewed awareness of a possible role for bacterial majority of oral cancers do arise in and from a visible lesion infections within an oral neoplasm itself, perhaps causing of an OPMD. In the Western World, the majority of oral and of – and continuing to drive – the malignant process: modern oropharyngeal cancers arise without the patient or a clinician molecular techniques permit the recognition of a wide range being aware of a pre-existing lesion – which is not to say that of bacterial signatures, yet to be fully understood.15 [widespread] molecular lesions have not pre-existed. GENETIC ABERRATIONS So: the assumed natural history of normal mucosa progressing from hyperplasia, through increasingly severe grades of And so to genes! We are what is in our genes and in their dysplasia, to carcinoma in situ and to invasive carcinoma has behaviour. These we inherit from our biological parents, led to extensive study of a presumed sequence of genetic according to simple Mendelian genetics. Our genes events. Many linear models have been developed, and the programme the synthesis of proteins which are the building current state of the literature is very well reviewed by Dionne blocks of our cells and tissues, and of the enzyme systems et al. 2014.19 Many of the genetic changes described [Table 1] which control all functions. The structure of our genes may have value in prognosis – for groups of patients - but will is inherited: and efficiency of gene expression is partly not necessarily apply to a given individual: none so far have inherited and partly changed by our environment – we can proven therapeutic utility.

84 Such research is important in increasing our understanding. ACKNOWLEDGEMENTS However, in the opinion of this author, the models on which they are based are oversimplified: progression to cancer is not I acknowledge colleagues in many countries with whom it has a linear process and whereas some genetic aberrations may been a privilege to work over many years and especially my be more common than others, and there may be “common past and current PhD students who teach me so much. final pathway[s]”, findings from groups of patients will not necessarily apply to a particular individual. REFERENCES THE PROGRESSION OF CANCER 1. Johnson NW, Jayasekara P, Amarasinghe AA. Squamous cell carcinoma and precursor lesions of the oral cavity: epidemiology and aetiology. Sequencing of the genes of an individual, and screening for Periodontol 2000. 2011; 57:19-37. epigenetic changes, is becoming quicker and cheaper 20,21 but prudence is necessary in interpreting the massive amounts 2. Johnson NW, Amarasinghe AAHK. Epidemiology and Aetiology of of data thus generated, and applying this to patient care.22 Head and Neck Cancer. In: Bernier J ed. Head and Neck Cancer: Once a carcinoma of the upper aero-digestive tract has Multimodality Management. Springer / Humana Press, 2011:1-40. become irrevocably malignant, the cardinal (microscopically) visible stage being breach of the basement membrane of 3. Chaturvedi AK, Anderson WF, Lortet-Tieulent J, Curado MP, Ferlay J, the epithelium and the beginning of infiltration of malignant Franceschi S, Rosenberg PS, Bray F, Gillison ML. Worldwide trends in keratinocytes into the connective tissues, many other incidence rates for oral cavity and oropharyngeal cancers. J Clin Oncol. genetic aberrations follow. These affect a wide range of 2013;31:4550-9. essential biological processes [Table 2] which can be affected in any order and to any degree. Again these are not linear 4. http://globocan.iarc.fr/Default.aspx, accessed 16 March 2014. processes. The phenomenon of “tumour progression”, 5. Gupta B, Ariyawardana A, Johnson NW. Oral cancer in India continues whereby different clones of cells emerge with different properties, those conferring a growth advantage surviving in epidemic proportions: evidence base and policy initiatives. Int Dent best and damaging the host more, has long been accepted J. 2013;63:12-25. dogma. With head and neck squamous carcinomas this 6. Ariyawardana A, Johnson NW. Trends of lip, oral cavity and progression, the development of new branches to the stem oropharyngeal cancers in Australia 1982-2008: overall good news but or trunk of the original malignancy, behaves more like a with rising rates in the oropharynx. BMC Cancer. 2013;13:333. bush than a palm tree: multiple branches occur early with 7. Mirghani H, Amen F, Blanchard P, Moreau F, Guigay J, Hartl DM, Lacau increasing polyclonality and complexity. It may be necessary St Guily J. Treatment de-escalation in HPV-positive oropharyngeal to “correct” the function of many genes to achieve a complete carcinoma: ongoing trials, critical issues and perspectives. Int J Cancer. elimination of malignant cells and cure the patient. 2014;. doi: 10.1002/ijc.28847. [Epub ahead of print]. 8. Mirghani H, Amen F, Moreau F, Guigay J, Ferchiou M, Melkane AE, Hartl PATIENT BIOTHERAPIES DM, Lacau St Guily J. Human papilloma virus testing in oropharyngeal squamous cell carcinoma: what the clinician should know. Oral Oncol. Nevertheless, modern molecular science is delivering 2014;50:1-9. biotherapies, tailored to genetic aberrations present in a 9. HPV vaccine could also prevent oropharyngeal cancer, says IARC. [No particular patient, with mixed success. For head and neck authors listed] Cent Eur J Public Health. 2013;21:149,154. SCC the most studied so far are use of monoclonal antibodies 10. Wen BW, Tsai CS, Lin CL, Chang YJ, Lee CF, Hsu CH, Kao CH. Cancer risk to block overexpression of epithelial growth factor receptors among gingivitis and periodontitis patients: a nationwide cohort study. [EGFR] on the surface of malignant keratinocytes and the use QJM. 2013; [Epub ahead of print]. of gene therapy to replace mutant TP53 genes with the wild 11. Feller L, Altini M, Lemmer J. Inflammation in the context of oral cancer. type [normal] gene in the cancer of a patient with mutant p53. Oral Oncol. 2013;49:887-92. 12. Li Y, Mao Y, Zhang Y, Cai S, Chen G, Ding Y, Guo J, Chen K, Jin M. Commercial anti-EGFR monoclonal antibodies (mAbs), eg Alcohol drinking and upper aerodigestive tract cancer mortality: A Cetuximab,23 are currently the only molecular targeted systematic review and meta-analysisOral Oncol. 2014;50:269-75. therapy for head and neck cancers approved by regulatory 13. Gainza-Cirauqui ML, Nieminen MT, Novak Frazer L, Aguirre-Urizar JM, agencies worldwide to treat advanced disease. There are also Moragues MD, Rautemaa R. Production of carcinogenic acetaldehyde trials using this approach for chemoprevention.24 by Candida albicans from patients with potentially malignant oral mucosal disorders. J Oral Pathol Med. 2013;42:243-9. PRIORITY FOR PRIMARY PREVENTION AND EARLY 14. Gandini S, Negri E, Boffetta P, La Vecchia C, Boyle P. Mouthwash and DETECTION oral cancer risk quantitative meta-analysis of epidemiologic studies. Ann Agric Environ Med. 2012;19:173-80. It is self-evident that we will never reduce the global burden 15. Hooper SJ, Crean SJ, Fardy MJ, Lewis MA, Spratt DA, Wade WG, Wilson of oral and of oropharyngeal cancer by treatment of cases: no MJ. A molecular analysis of the bacteria present within oral squamous amount of brilliant robotic surgery or wonder biotherapy will cell carcinoma. J Med Microbiol. 2007;56:1651-9. do this on a population basis, any more than better air rotors 16. Lou Y, Peng WJ, Cao DS, Xie J, Li HH, Jiang ZX.DNA repair gene XRCC1 or restorative materials will impact the epidemiology of dental polymorphisms and head and neck cancer risk: an updated meta- caries. The present paper does not focus on prevention, but analysis including 16344 subjects. PLoS One. 2013;23;8:e74059. by a combination of public education and government action 17. Mondal P, Datta S, Maiti GP, Baral A, Jha GN, Panda CK, Chowdhury we must reduce the use of known risk factors in people S, Ghosh S, Roy B, Roychoudhury S. Comprehensive SNP scan of DNA throughout the world, and continue as a health profession to repair and DNA damage response genes reveal multiple susceptibility be vigilant in screening and advising our patients.25 loci conferring risk to tobacco associated leukoplakia and oral cancer. PLoS One. 2013;8:e56952. 18. http://www.actrec.gov.in/oralcancer/GeneHome.htm accessed 18 March 2014. 19. Dionne KR, Warnakulasuriya S, Zain RB, Cheong SC. Potentially malignant disorders of the oral cavity: current practice and future directions in the clinic and laboratory. Int J Cancer, 2014, in press. 20. Brunotto M, Zarate AM, Bono A, Barra JL, Berra S. Risk genes in head and neck cancer: A systematic review and meta-analysis of last 5years. Oral Oncol. 2014;50:178-188. 21. Jessri M, Farah CS. Next generation sequencing and its application in deciphering head and neck cancer. Oral Oncol. 2014;50:247-253. 22. Yokota T. Is biomarker research advancing in the era of personalized medicine for head and neck cancer? Int J Clin Oncol. 2014 Jan 21. [Epub ahead of print]. 23. http://www.cancerresearchuk.org/cancer-help/about-cancer/ treatment/cancer-drugs/cetuximab accessed 18 March 2014. 24. Mak MP, William WN Jr. Targeting the epidermal growth factor receptor for head and neck cancer chemoprevention. Oral Oncol. 2014 Jan 9. pii: S1368-8375(13)00812-9. doi: 10.1016/j.oraloncology.2013.12.024. [Epub ahead of print].

85 25. Johnson NW, Warnakulasuriya S, Gupta PC, Dimba E, Chindia M, Otoh EC, Sankaranarayanan R, Califano J, Kowalski L. Global oral health inequalities in incidence and outcomes for oral cancer: causes and solutions. Adv Dent Res. 2011;23:237-46. Genetic alterations which have been described in association with oral carcinogenesis. [Summary adapted from Dionne et al, 2014, op cit]. Associated with epithelial Associated with invasion/overt dysplasia malignancy Number of chromosomes Ploidy status per cell, usually an increase Loss of heterozygosity [aka ploidy status] [LOH] at chromosome sites 3p, 9p, and less frequently Altered genes at 8p, 11q, 13q, 17p hTERT Altered genes c-fos HIF-1 Cyclin D1 c-Jun EGFR CENP-F ABCG2 COX-2 ALDH1 TP53 CD133 TGF- MAGE-A CyclinD1 pRB EGFR DeltaNp63 Ki-67 CyclinD1 MCM-2 EGFR Mib-1 Ki-67 PDPN MMP1 p16 MCM2 MMP9 PDPN TP53 miR-21 miR-181b miR-34 mep16 p16 Table 1. Essential biological processes which malfunction in the progression of epithelial cancers. Control of: Within the epithelial component Interactions with and processes Fig 1. A Global incidence rates per 100,000 population per within connective tissues annum of cancer of the lip and mouth; B: Global mortality rates Cell proliferation from cancer of the lip and mouth; C: Global incidence of cancer Cell surface receptors and Integrity of basement of the pharynx [excluding nasopharynx]; D: Global mortality signaling membranes rates from cancer of the pharynx [exc nasopharynx].4 Immunogenicity Intercellular communication Angiogenesis and neo- Address for correspondence Cell differentiation and de- angiogenesis differentiation Emeritus Professor of Oral Health Sciences, King’s College Cell movement Epithelial cell migration London Programmed cell death Desquammation Homeostasis of collagen & Professor Emeritus, Griffith Health Institute, Griffith Secretion of cytokines and other fibres Homeostasis of University: Population and Social Health Research chemokines ground substance Programme - Lead for Population Oral Health; Infectious DNA repair Diseases and Cancer Research Groups The immune inflammatory response [email protected] Entry into blood vessels and lymphatics Metastastic processes Table 2.

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 86-87 ADULT ORTHODONTIC TREATMENT – A VIEWPOINT Brett Kerr, BDS (Lond), LDSRCS (Eng), MDSc (Syd) Dr. Kerr has over 30 years’ experience in the specialist practice of orthodontics. For more than 11 years he has taught orthodontics to undergraduate and post-graduate students at the University of Queensland School of Dentistry. INTRODUCTION communicating objectives and potential outcomes with patients and professional colleagues Orthodontic treatment in the non-growing patient presents its own challenges, rewards, and advantages. All orthodontic • “Mid-Course Correction”, giving the same flexibility as treatment relies heavily on patient understanding and co- with fixed braces to change treatment plans if required, operation, and commonly lasts one to three years, requiring or if treatment response is not ideal multiple appointments. • “Refinement” – multiple extra Aligners to correct In the pre-adolescent the patient is often passively involved; recalcitrant teeth in the adolescent they may become antagonistic during such a prolonged period; in adults it is to be hoped that any • “Optimised” attachments, for more precise control of treatment they undertake is done so voluntarily and with movements reasonable understanding of the processes and intended outcomes. • “Precision cuts” providing the ability to use elastic traction in all vectors This presentation does not attempt to cover the entire spectrum of post-adolescent orthodontics, but takes a • “Pontics” can be placed in the Aligners for edentulous pragmatic view of basic orthodontic treatment in the non- spaces. growing patient. RETENTION RATIONALE With any orthodontic treatment, retention is a prime concern and has to be addressed before treatment commences. Research shows1-5 that a malocclusion is not, by definition, Each form of retention has its own set of advantages and pathological and rarely becomes so. If left untreated most disadvantages. malocclusions will tend to worsen over time, but will not jeopardise the longevity of the dentition, assuming good Basically, retainers can be divided into bonded and removable dental care. types. Reports have suggested an unacceptably high failure rate for bonded retainers, although this is highly technique Extreme cases may require complex orthodontic treatment and operator specific. Failure rates of 35-50% over 6-24 and perhaps orthognathic surgery. Most patients seeks month studies are common.7-10 Who is responsible for their only an improvement in their appearance or their occlusion. long term care and maintenance? Is it the orthodontist, the As always each case has to be assessed individually, and patient, or the general dentist? For how long? all treatment options offered and explained. If treatment is undertaken it is important to explain the benefits, With removable appliances the balance can be shifted towards disadvantages and limitations of such treatment to ensure patient responsibility. The following protocol has served well the patient is able to reach an informed decision. for the past decade: TREATMENT At the end of treatment alginate impressions are taken, from which upper and lower “invisible” retainers are made from Until the turn of the century, adult orthodontic treatment Essix Ace 0.040” plastic (Dentsply Raintree Essix Glenroe; was limited to “traditional” appliances, whether removable or Sarasota, FL). These retainers are worn full time for a period, fixed. Recently, Invisalign6 has become a primary option for or night time only, as the individual patient’s status dictates. adults (and many teenagers), since it can now achieve similar This type of material tends to crack after a few months results to fixed appliances, whilst using an aesthetic, hygienic because of its stiffness and comfortable appliance. once initial stability has been achieved, polyvinylsiloxane There are several aspects of treatment with Invisalign that (PVS) impressions are taken in single-use plastic trays. From separate it from similar treatment modalities. These include: these a second set of retainers is made, using a more flexible, abrasion resistant plastic, such as Trutain 0.30” Coping (Tru- • “ClinCheck” software, which allows 3D analysis of Tain Orthodontic and Dental Supply, West Rochester, MN) or the occlusion, assessment of different treatment Essix 0.040” C+ (Dentsply Raintree Essix Glenroe). These alternatives and provides an excellent tool for retainers will commonly last for 3-5 years.

87 When the second set of retainers is fitted the patient is given REFERENCES the PVS impressions to keep. The patient now has two sets of retainers, plus their last set of Aligners, which they are 1. Järvinen S. Indexes for orthodontic treatment need. Am J Orthod advised to keep in different locations in case of accidents. Dentofacial Orthop 2001;120:237-239 They are instructed to wear them every night, 12 hours per night, ad infinitum. They are also told never to have less than 2. Sadowsky C, BeGole EA. Long-term effects of orthodontic treatment two sets of retainers. If a set of retainers is lost, damaged, or on periodontal health. Am J Orthod 1981;80:156-172. broken, the PVS impressions can be re-poured and a new set of retainers made to the end-of-treatment alignments. 3. Sadowsky C, Polson AM. Temporomandibular disorders and functional occlusion after orthodontic treatment: results of two long-term studies. SUMMARY Am J Orthod 1984;86:386-390. The key is communication. Patients need to be: 4. Helm S, Petersen PE. Causal relation between malocclusion and caries. Acta Odontol Scand1989;47:217-221. • given an outline of all logical treatment plans 5. Ackerman M. Evidence-based orthodontics for the 21st century. J Am • given any necessary information to decide on their Dent Assoc 2004;135:162-167. preferred treatment 6. www.invisalign.com/braces-for-adults-and-teens/adults [accessed 21 • given the opportunity to ask any questions December 2013] • advised before treatment commences that retention 7. Scheibe K, Ruf S. Lower bonded retainers: survival and failure rates will be forever, that they will be provided with these two particularly considering operator experience. J Orofac Orthop sets of retainers, and that the responsibility for wearing 2010;71:300-307. them is theirs and theirs alone. 8. Pandis N, Fleming PS, Kloukos D, Polychronopoulou A, Katsaros C, Eliades T. Survival of bonded lingual retainers with chemical or photo polymerization over a 2-year period: A single-center, randomized controlled clinical trial. Am J Orthod Dentofacial Orthop 2013;144:169- 175. 9. Taner T, Aksu M. A prospective clinical evaluation of mandibular lingual retainer survival. Eur J Orthod 2012;34:470-474. 10. Salehi P, Najafi HZ, Roeinpeikar, SM. Comparison of survival time between two types of orthodontic fixed retainer: a prospective randomized clinical trial. Prog Orthod 2013;14:1-6. Address for correspondence [email protected]

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 88-90 ORAL HEALTH IN THE FIRST HALF OF LIFE: AN UPDATE ON THE DUNEDIN STUDY Dr Jonathan M. Broadbent, BDS PGDipComDent PhD, University of Otago Prof W. Murray Thomson, BSc BDS MA MComDent PhD, University of Otago, Prof Richie Poulton, MSc PGDipClPs(Otago) PhD(NSW) FRSNZ, University of Otago J.M. Broadbent is a senior lecturer in Preventive and Restorative Dentistry in the Department of Oral Rehabilitation at the University of Otago. W.M. Thomson is Professor of Dental Epidemiology and Public Health in the Department of Oral Sciences at the University of Otago. R. Poulton is Professor and Director of the Dunedin Multidisciplinary Health and Development Research Unit in the Department of Preventive and Social Medicine, University of Otago. ABSTRACT The Dunedin Multidisciplinary Health and Development Study is a lifecourse study of health and development in a cohort of children born in Dunedin between 1 April 1972 and 31 March 1973. The Study members were assessed at birth and ages 3, 5, 7, 9, 11, 13, 15, 18, 21, 26, 32, and most recently at age 38, when 95.4% of the surviving Study members participated. The Dunedin Study dataset contains a broad range of health data, including oral health information. The oral health-related research publications of the Dunedin study over the past 40 years have included discussion of the social determinants of health, dental neglect, use of dental services, aetiology of developmental defects of dental enamel, epidemiology of dry mouth, and risk factors for periodontal disease, dental caries, and poor oral health-related quality of life. The Dunedin Multidisciplinary Health and Development Study old offspring of Dunedin Study members and investigates (Dunedin Study) is a prospective observational study of a whether lifestyles, behaviours, attitudes and health differ cohort: 1037 babies born between 1st April 1972 and 31st March from original Study Members when they were aged 15. 1973.1 Study members were assessed at birth and ages 3, 5, 7, 9, 11, 13, 15, 18, 21, 26, 32, and 38 years. Age 38 assessments An international team of researchers from a range of were completed in March 2012. Dental examinations were disciplines supports the research activity of the Dunedin conducted using WHO methods at ages 5, 9, 15, 18, 26, 32, and Study, and more than 750 peer-reviewed journal articles 38. The high participation rate in the Dunedin Study (Figure 1) have been published to date using the findings. Other is a strength, due to the minimisation of non-participation bias. contributions include monographs/books (51), book chapters (84), theses (53) and unpublished reports (69). The Study is Fig 1. Participation in the Dunedin Multidisciplinary Study by age multidisciplinary, and key areas of research have included Sub-studies in the Dunedin Study include: the Family Health cardiovascular health, respiratory health, oral health, mental History Study, which involved the parents of Dunedin Study health, sexual and reproductive health, and psychosocial members to find out about the health of family members functioning, together with a number of other areas of health. (2003-2006); the on-going Parenting Study, which focuses The study has been able to elucidate many of the factors on the first three-year-old child of each Study member; that impact upon the development of a person from infancy, and the Next Generation Study, which involves the 15-year- through childhood and adolescence, and into the adult years (an example being the influence of social position during childhood on adult general and dental health).2 A considerable range of dental information is available to Dunedin Study researchers, including tooth surface-level caries data, site-specific periodontal disease data, plaque quantification, plaque samples (ages 32 and 38), enamel developmental defect data (ages 9 and 15), dental interview data (all ages), dental photographs (at age 15 years) and panoramic radiographs (at age 18 years). Family dental health data are also available, including (1) the self-reported dental health of the parents of Study members (when the latter were 5 years old and again when they were 32), and (2) dental examination and interview data for Study members’ children at age 15 (as part of the Next Generation Study). Patterns of dental caries experience and progression rates are very similar among populations,3 and previous caries experience is a strong predictor for future caries development.4 The disease progresses with age at a relatively

89 constant rate right through adulthood.5 Intergenerational 7. Shearer DM, Thomson WM, Broadbent JM, Poulton R. Maternal oral continuity in poor oral health also occurs, most notably with health predicts their children’s caries experience in adulthood. J Dent periodontal disease,6 dental caries and tooth loss.7 Res 2011;90:672-7. The determinants of social inequalities in oral health have long 8. Evans RW, Beck DJ, Brown RH, Silva PA. Relationship between been a focus of research in the Dunedin Study, ever since early fluoridation and socioeconomic status on dental caries experience research considered the role of community water fluoridation in 5-year-old New Zealand children. Community Dent Oral Epidemiol in minimising social inequalities in dental caries experience.8 1984;12:5-9. Social class in childhood can have profound effects on adult dental health,9 and the inequality gap in the experience of dental 9. Thomson WM, Poulton R, Milne BJ, Caspi A, Broughton JR, Ayers KMS. caries widens with age (Figure 2).10 In the Dunedin Study, tooth Socioeconomic inequalities in oral health in childhood and adulthood in loss due to dental caries was rare prior to the ending of the free a birth cohort. Community Dent Oral Epidemiol 2004;32:345-53. dental care entitlement at age 18, but, in the 20 years since then, social inequalities in tooth loss have widened dramatically,11 10. Broadbent JM. Oral health inequalities to the fourth decade of life. PhD whether considering social class of origin (Figure 3) or personal thesis. Dunedin: University of Otago; 2010. educational achievements (Figure 4). This has profound policy implications, and highlights the need to address oral health 11. Thomson WM. Social inequality in oral health. Community Dent Oral inequalities through early life preventive care and through the Epidemiol 2012;40 Suppl 2:28-32. minimisation of deprivation and advantage among children and in access to education. A user-pays, treatment-oriented dental 12. Watt R, Sheiham A. Inequalities in oral health: a review of the evidence healthcare service results in profound differences in the health and recommendations for action. Br Dent J 1999;187:6-12. and treatment provision between those who are deprived and those who are not.12 Address for correspondence Current work on dental-related Dunedin Study research [email protected] includes: investigations into dental plaque characterisation; possible links between DNA telomere length and periodontal disease; purported non-dental health effects of community water fluoridation; further work on early-life risk for developmental defects of enamel; characterisation of oral bacteria through gene-sequencing; the aetiology of temporomandibular dysfunction; (importantly) clarifying links between caries/periodontitis and general health risks; and continuation of the oral health inequalities research. ACKNOWLEDGEMENTS AND FUNDING Fig 2. Mean cumulative count of decayed, missing, and filled tooth surfaces (DMFS) by childhood socio-economic status from We are indebted to previous researchers for collecting the ages 9 to 32 years dental data prior to age 26 and thank Study founder Dr Phil Silva. The Dunedin Study would not be possible but for the ongoing participation of the Study members, their families and friends. The Dunedin Study is funded by the Health Research Council of New Zealand, with additional support from the US National Institutes of Health and the UK Medical Research Council. Early data collection phases were also supported by the New Zealand Department of Education, the New Zealand Department of Health, and the National Children’s Health Research Foundation. REFERENCES Fig 3. Prevalence of caries-associated tooth loss by social class in childhood 1. Silva PA, Stanton WR. From child to adult: the Dunedin Multidisciplinary Health and Development Study. Auckland: Oxford University Press; 1996. 2. Poulton R, Caspi A, Milne BJ, Thomson WM, Taylor A, Sears MR, Moffitt TE. Association between children’s experience of socioeconomic disadvantage and adult health: a life-course study. Lancet 2002;360:1640-5. 3. Sheiham A, Sabbah W. Using universal patterns of caries for planning and evaluating dental care. Caries Res 2010;44:141-50. 4. Broadbent JM, Thomson WM, Poulton R. Trajectory patterns of dental caries experience in the permanent dentition to the fourth decade of life. J Dent Res 2008;87(1):69-72. 5. Broadbent JM, Page LA, Thomson WM, Poulton R. Permanent dentition caries through the first half of life. Br Dent J 2013;215:E12. 6. Shearer DM, Thomson WM, Caspi A, Moffitt TE, Broadbent JM, Poulton R. Inter-generational continuity in periodontal health: findings from the Dunedin family history study. J Clin Periodontol 2011;38:301-9.

90 Fig 4. Prevalence of caries-associated tooth loss by educational achievements of Dunedin Study members Fig 5.

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 91-95 THIRD MOLARS: INDICATIONS FOR INTERVENTION Dylan M Hyam, BDS (Hons), MBBS (Hons), FRACDS (OMS) Dr Hyam began his career serving in the Royal Australian Army before taking up his first residency post at Westmead Hospital, Sydney. Dr Hyam trained in Sydney, Canberra and the United Kingdom and is currently Director of the Oral and Maxillofacial Surgery Unit at The Canberra Hospital. ABSTRACT The management of third molars remains a skill and art. Evidence is still developing to help guide clinicians in their decision making. This article provides clinicians with a decision matrix which allows them to tailor a solution to the individual patient’s needs. The matrix articulates the need to identify the indication for surgery, then modify the surgical plan to account for; surgical risk, the patients current medical status, their future medical needs, and their social and financial circumstances. An examination is made of the evidence for different indications for intervention, an assessment protocol for surgical planning, and a review of the common medical issues which might impact upon the surgical decision matrix. The decision to commit a patient to the removal of a third values and preferences in order to make decisions concerning molar can be complex and challenging. No clinician wishes the treatment of individuals in their care.” Given the lack of to expose the patient to surgical risk, pain and discomfort strong evidence a decision making matrix is necessary. during recovery, and the financial burden of surgery, unless there is an identifiable benefit to the patient. Every oral CLASSIFICATION OF THIRD MOLARS surgeon faces this dilemma on a daily basis. Over recent years the indications to remove third molars have expanded The concept of classification of third molars has matured as our understanding of periodontal disease and the systemic over the last ten years. Third molars were originally classified effects of transient oral bacteraemia have increased. The as either being symptomatic or asymptomatic, impacted or clinician faces the challenge of deciding if and when and non-impacted, erupted, partially erupted, or un-erupted. intervention is required, along with the duty to minimise A more suitable classification system has developed in the morbidity and risk. recent literature.4 This classification describes third molars as being symptomatic or asymptomatic and disease free or It is possible that the issue of third molars and their removal disease positive. It can also classify third molars as being is becoming an increasingly important question for teenagers visible at the line of occlusion, visible not at the line of and young adults. Previously, many people had had occlusion, or not visible. This classification can be utilized to extractions by the time they reached late puberty, and this describe third molars as being one of four categories (Table may have facilitated the eruption of third molars late into the 1). The decision to remove a symptom positive and disease dental arch into a functional position. As oral hygiene around positive third molar is straight forward. This decision would the world has improved, and orthodontists increasingly utilize only be modified by a significant patient contraindication. a non-extraction treatment plan, the prevalence of impacted The decision to remove a symptom positive disease negative third molars may rise in the future. Studies1 have shown that tooth is generally received favourably by both the surgical at least 96% of the population have a third molar. Up to 36% community and patient’s alike. There is now considerable of young people may have an impacted third molar.2 Where evidence to support the removal of symptom free, disease more than a third of the population faces this decision about positive third molars in young adults. This evidence will be how best to manage impacted teeth, this places a significant reviewed later in this paper. burden on the healthcare sector. A challenging decision must be made for patients on how to Much time and effort has previously been given to reviewing manage the symptom free and disease free third molar that literature in order to determine what evidence is available is either at the line, or not at the line of occlusion. This is the and what quality evidence can be utilized in the decision intervention dilemma which causes clinician’s the most angst. making process. The Cochrane3 review in 2012 found “there is This paper aims to provide a decision matrix that clinicians no evidence from random controlled trials, that prophylactic can use to identify the thought processes, patient factors, removal of asymptomatic third molars prevents painful and/ indications, contraindications, and financial factors, that all or infection complications arising from the retention of these combine to influence the decision to remove a third molar. third molars.” The review also found that there was only a single randomized controlled trial which could be classified WHAT IS “EARLY INTERVENTION”? of being sufficient rigor to provide evidence in this issue. This trial showed no evidence of a difference in retention or There is no consensus within the literature about what removal. The Cochrane review summarized its findings by constitutes early intervention. Early might be defined “asking clinician’s to rely on clinical experience and patient

92 according to the chronological age of the patient as being The local progression theory of periodontitis identifies that younger than 18 years or younger than 21 years. Early could 38% of people with periodontal disease around a third molar also be defined according to tooth development, particularly have disease progression within two years. The systemic regarding whether the crown formation is complete or the effects of periodontal disease have been associated with root formation is complete. Another option for the definition periodontal disease progression during pregnancy and pre- of early would be whether the tooth has developed symptoms term birth. The associations between periodontal disease or disease. and transient bacteraemia are proving harder to quantify for researchers. Clinicians are often inclined to intervene “early” for patients with the belief that this may reduce; The role of prophylactic removal of third molars to prevent the development of pathology such as dental cysts seems • Post operative pain and suffering5 limited. Whist it is agreed that pathology can form,9,10 the number needed to treat to achieve a meaningful benefit may • That early intervention may increase the patient’s be too high. quality of life6 Food trapping around a third molar is an obvious clinical • That it may reduce the financial burden indicator of reduced or deficient oral hygiene. Very little research exists as to what risk ratios food trapping around • That it may maximize oral health a third molar confers in terms of caries experience in the upcoming years. Most clinician’s would agree that a third • That it may prevent the complications of long term molar that has issues with oral hygiene and maintenance is at retention of non functional third molars. high risk of developing caries in the short term. This paper confines its discussion regarding intervention to External root resorption is a common concern amongst the surgical removal of teeth. There are other alternative patient’s, family members, and clinician’s. Research has treatments such as medications, oral hygiene adjuncts, confirmed that up to 7.5% of 21 – 30-year-olds have evidence operculectomy, and coronectomy which are not considered. of external root resorption in at least one site in the dental arch.11 This appears to have a 3:1 male preponderance. The decision matrix (Fig. 1) for the removal of the third molars Interestingly, once root formation appears to be complete and should always begin with an indication. Indications for removal the patient has reached 30 years of age, the root resorption of third molars are summarized in figure two according to does not seem to continue. This would seem to confer some disease status and symptom status. Once an indication has protection against root resorption by the removal of impacted been identified, the decision to proceed to surgery will be third molars up until the age of 30 years but very little benefit modified by the procedural risk associated with the surgical after this point. removal. The patient’s current health will then modify the decision further. The clinician’s expectations for the patient’s One of the most contentious areas in the decision making future health are an additional modifier. The final modifying process for the removal of third molars is the issue of post factor should include the patient’s social support mechanisms orthodontic stability. There is limited evidence of clinical use and financial capacities. This decision matrix is summarized in in this area.12-15 The one paper which met the eligibility criteria figure three. for the Cochrane review had a relatively small sample size and was vulnerable to bias.15 This paper still found no difference INDICATIONS FOR REMOVAL between the retention and removal of third molars in the orthodontic patient. In the orthodontic patient, regarding The indication for the removal of third molars are outlined lower anterior crowing. There are several concepts worth in Table 2. The indications for removal of third molars where considering which currently have little to no suitable evidence the patient is both symptom positive and disease positive available for discussion. Some of the previous research are relatively straight forward and will not be considered regarding this topic was conducted on patient’s who had had further. The indications where the patient is symptom free pre molar extractions as a component of their orthodontic but disease positive are worth further examination. There are plans. Significant numbers of modern orthodontic patients also indications where the patient is both symptom negative are having non extraction orthodontics and this may be and disease negative (i.e., prophylactic removal) which will be increasing the rate of impaction of lower molars. Another reviewed further. important concept is that a vertically impacted third molar can still impart horizontal force vectors during its eruption Recent research has identified periodontitis associated with phase. Also of importance in managing the post orthodontic third molars as a key contributor to reduction in oral health.7, 8 patient is the assessment of the third molar and its current stage of root formation. The key concepts regarding periodontitis and third molars are: The decision to prophylactically remove third molars in • A potential periodontal reservoir the post orthodontic patient remains a purely clinical and patient preference derived decision. The evidence one way • Local periodontal progression or another is lacking and unclear. Many parent’s in western countries who have access to quality healthcare consider it • The systemic effects of periodontal disease a reasonable risk to remove the potentially impacted lower third molars both to help ensure against orthodontic relapse The reservoir theory has been confirmed by research which and protect the long term prognosis for the lower second shows that a third molar which has a periodontal probing molar against external resorption and distal root caries. depth of 4mm or greater is likely to experience an increase in that probing depth over time. That patient is also likely to develop clinically significant periodontal probing depths in the anterior dental arch if they have a pre existing periodontal defect at a third molar.

93 This currently remains a personal preference decision for anatomy of the inferior alveolar nerve as it passes the apex of patient’s, their families, and their clinician’s. the roots particularly in the context of more modern imaging techniques such as cone beam computerized tomography. The prophylactic removal of third molars can be divided into six main groups. These include: CURRENT HEALTH MODIFIERS • Sport or military patients Current health modifiers for patients include things such as »» Contact sports16 cardiac state, whether immunocompromised, coagulation »» P eak performance patients function, medications such as bisphosphonates and denosumab, respiratory function, the patient’s fitness for • Physical dexterity anaesthetic/sedation/local anaesthesia, and the patient’s »» Tremors pregnancy status. If any of these conditions are present in »» Neuromuscular disease a significant manner it is likely that the decision to remove the third molar will be given both more consideration and will • Mental capacity require a higher potential health benefit to proceed. »» Dementia »» Cognitive development FUTURE HEALTH MODIFIERS • Pre-medication Future health modifiers are difficult in some instances »» Bisphosphonates for clinician’s to predict. In other instances patients can »» Anticoagulants specifically attend for an examination of their third molars because they are aware that they are about to commence • Pre-treatment medication, have a tissue transfer procedure, or become »» Radiotherapy pregnant. In these situations the clinician must try to predict »» Chemotherapy the likelihood of the third molar acquiring either symptoms or disease within a specified period and balance this against • Immunomodifiers the potential for morbidity following the surgical removal of »» Bacteraemia the tooth. »» Tissue transfer patients SOCIAL AND FINANCIAL MODIFIERS In the patients where prophylactic removal is being considered the clinician must attempt to judge the likelihood that this Social modifiers of note for patients include access to tooth will need removal or acquire disease or symptoms care and support post surgery. The patient’s level of within a particular future period. They must then balance this understanding and capacity to communicate along with their risk against the risks of surgical removal. The clinician must manual dexterity must also be considered. Many patients feel that the patient will be better for having had surgery have specific personal desires and this can be intimately tied at this time and then for having had surgery at a later time in with their mental health and their religious background. where the procedure may be more complex the recovery Issues such as transport and home help can also be major more tenuous and the complication rate may be higher. modifiers in the decision to proceed to surgery. SURGICAL ASSESSMENT For many patients in western culture financial modifiers are also an important component of the health care decision. Once the clinician has decided that there is an indication for When have access to insurance plans for specific periods the removal of a tooth, they must then decide on the relative whilst in employment, or are under family access plans, importance of the modifying factors, a surgical risk, the they will often be more inclined to remove third molars at patient’s current health, future health and social and financial an earlier stage. Also of importance to many young people support structures. is the potential to limit loss of income due to the retention of third molars (from time lost from work through pain) versus Classically third molars have been considered with various a specified period of loss of income during a relatively short classifications to describe the difficulty and risk associated period of recovery following surgery. Another example of with their surgical extraction. Classifications such as Pell and a financial modifier might be the decision to remove one Gregory17,18 or Winter’s classification19 have largely fallen into symptomatic third molar along with three asymptomatic third disuse. A more common system for examining and predicting molars for patients who only wish to undergo one period of the difficulty of removal of third molars is the WHARFE recovery rather than four separate episodes of recovery over system.20 This considers: the next 10 years. W – Winter’s lines CASE STUDY H – Height of mandible Fig. 4 shows a case study of a 17-year-old male who has Fragile X syndrome and lives in institutional care. He has limited A – Angulation support from his elderly mother and is engaged within her health plan for another year until he turns 18 years of age. R – Root form The patient has presented with the tooth 38 partially erupted but symptom free. There is a 3-mm periodontal pocket at the F – Size of follicular sec mesial aspect. E – Exit pathway of tooth This allows for a more thorough examination of the tooth and its radiology prior to its removal. Also of significance is the

94 The decision matrix shows that this is a symptom negative Classification systems (Dodson)4 and disease negative tooth. The procedural risk for the removal of this tooth is relatively low. The patient’s current Disease Positive Disease Negative health modifiers may make the surgeon less likely to remove the tooth given the patient’s poor understanding and capacity Symptom Positive S+/D+ S+/D- to consent to the procedure. The patient’s future health modifiers may increase the inclination towards surgery, a Symptom Negative S-/D+ S-/D- trend multiplied by the patient’s relatively poor oral hygiene which is not likely to improve in the future. The patient’s social Table 1. modifiers may also increase the inclination towards surgery given that the patient has current access to social, family, and financial support. The decision to remove this asymptomatic and disease free third molar may end up being made for largely non-clinical but very significant social and financial factors. This is a common example of why the decision to remove a third molar remains a highly tailored process where the individual’s desires and needs are considered on a case by case basis. INTERNATIONAL VIEWS Indication for the removal of third molars grouped according to symptom and disease status The international experience regarding the decision making process for the removal of third molars is interesting. In the Pain Periodontitis Fracture United Kingdom’s National Health Service (NHS), the National Caries Pathology Institute for Clinical Excellence (NICE) has recommended that Peri-apical pathology Unrestorable impacted third molars that are free from disease should not Pericoronitis Food Trapping (subgingival be operated on.21 They have recommended that patients who Odontogenic infection margins) have impacted third molars that are asymptomatic should Root visit their dentist for their usual checkups and that only resorption Orthognathic patients who have diseased third molars or other problems Surgery with their mouth should have their third molars removed. This guideline essentially excludes the third fourth and fifth Orthodontic (current health modifiers, current future modifiers, and social and financial modifiers) elements from the decision matrix. Prosthetic This may be because the guidelines were produced before the need onset of significant events such as bisphosphonate related osteonecrosis of the jaw, or because the NHS funds the Tumour majority of third molars surgery so that financial decisions resection are less of a factor in treatment planning. Facilitate The American Association of Maxillofacial Surgeon’s (AAOMS) access to recommends that ‘treatment decisions regarding why, when, adjacent teeth or how, to treat third molar teeth are extremely complex. (7’s) There is no pat answer, cookbook recipe, or flow chart that is universally accepted regarding the decision making Occlusal process’.22 The AAOMS clearly identifies the need to tailor the interference decision matrix to the needs and desires of the individual. Orthodontic Australia has neither such guidelines nor clinical stability recommendations. The majority of Australian surgeons would use a model similar to this decision matrix to decide In conjunction for each patient. The risk of post surgical morbidity, long with another term neurosensory complication, pain and suffering due oral surgery to retention of third molars, and the social and financial procedure implications of both retention and removal of third molars would typically be a factor in most Australian surgeon’s Prophylactic decision-making process. Hopefully, this decision matrix removal illustrates a repeatable consideration process for clinicians. There is as yet insufficient evidence for specific indications a. Sport such as post orthodontic stability or prophylactic removal to assist the new clinician in this decision making process. Many b. Military of these decisions are made based on previous experience and patient desire. This continues to be a reasonable method c. Pre provided consideration is made across the broad concepts medication outlined in this article. d. Pre geriatric e. Bacteraemia Key: Symptom (S), Disease (D) Table 2.

95 Fig 1. Decision Matrix for Third Molars  REFERENCES 13. Lindqvist B, Thilander B. Extraction of third molars in cases of anticipated crowding in the lower jaw. Am J Orthod 1982;81:130-39 1. Kruger E, Thomson WM, Konthasinghe P. Third molar outcomes from age 18 to 26: Findings from a population-based New Zealand 14. Richardson ME. Orthodontic Implications of lower third molar longitudinal study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod development. Dental Update 1996;23:96-102 2001;92:150. 15. Harradine NW, Pearson MH, Toth B. The effect of extraction of third 2. Celikoglu M, Miloglu O, Kazanci F. Frequency of agenesis, impaction, molars on late lower incisor crowding: a randomized controlled trial. Br angulation, and related pathologic changes of third molar teeth in J Orthod 1998;25:117–22. orthodontic patients. J Oral Maxillofac Surg 2010;68:990-995 16. Tevepaugh DB. Dodson TB. Are mandibular third molars a risk factor 3. Surgical removal versus retention for the management of for angle fractures? A retrospective cohort study. J Oral Maxillofac asymptomatic impacted wisdom teeth (Review). Cochrane 2012 Surg 1995;53:646-9; discussion 649-50 http://summaries.cochrane.org/CD003879/surgical-removal-versus- retention-for-the-management-of-asymptomatic-impacted-wisdom- 17. Pell GJ, Gregory BT: Impacted mandibular third molars: Classification teeth. Accessed 14 April 2014 and modified techniques for removal. Dent Digest 1933;39:330 4. Dodson TB. How many patients have third molars and how many have 18. García-García A, Gude-Sanpedro F, Gandara-Rey J, et al. Pell-Gregory one or more asymptomatic, disease-free third molars? J Oral Maxillofac classification is unreliable as a predictor of difficulty in extracting Surg 2012 Sep;70(9 Suppl 1):S4-7. doi: 10.1016/j.joms.2012.04.038. impacted lower third molars. Br J Oral Maxillofac Surg 2000;38:585-7 5. Bui CH, Selodin EB, Dodson TB. Types, frequencies and risk factors 19. Winter GB: Principles of Exodontia as Applied to the Impacted Third for complications after third molar extraction. J Oral Maxillofac Surg Molar. St Louis, MO, American Medical Books, 1926 2003;61:1379 20. MacGregor AJ. The Impacted lower wisdom tooth. Oxford Medical 6. Slade GD, Foy SP, Shugars DA, et al. The impact of third molar Publications 1985 symptoms, pain and swelling, on oral health-related quality of life. J Oral Maxillofac Surg 2004;62:1118-24 21. National Institute for Health and Clinical Excellence. Wisdom teeth – removal. December 2010. Technology appraisal 1. Available at http:// 7. Blakey GH, Hull DJ, Haug RH et al. The changes in third molar and non- www.nice.org.uk/TA1 Accessed 14 April 2014 third molar periodontal pathology over time. J Oral Maxillofac Surg 2007;65:1577-84 22. Evidence Based Third Molar Surgery. AAOMS. Available at www.aaoms. org/docs/evidence_based_third_molar_surgery.pdf Accessed 14 April 8. Moss KL, Ruvo AT, Offenbacher S et al; Third molars and progression 2014 of periodontal disease during pregnancy. J Oral Maxillofac Surg 2007;65:1065-69 Address for correspondence 9. Guven O, Keskin A, Akal UK. The incidence of cysts and tumors around Director, Oral & Maxillofacial Surgery, The Canberra Hospital impacted third molars. Int J Oral Maxillofac Surg 2000;29:131-5 Lecturer, Australian National University 10. Glosser JW, Campbell JH. Pathologic change in soft tissues associated [email protected] with radiographically normal third molar impaction. Br J Oral Maxillofac Surg 1999;37:259-60 11. 11. Nitzan D, Keren T, Marmary Y. Does an impacted tooth cause resorption of the adjacent one? Oral Med Oral Surg Oral Path 1982;51:221-225. 12. Schwarze CW. The influence of third molar germectomy – A comparative long term study. Transactions of the Third International Orthodontic Congress, London 1975: 551-555

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 96-97 MAJOR SURGERY IN THE ELDERLY. DOTTING THE Is AND CROSSING THE Ts. Dr Martin D Batstone, MBBS, BDSc(Hons), MPhil(Surg), FRACDS(OMS), FRCS(OMFS) Martin is a full time staff specialist in the Maxillofacial Surgery Department of the Royal Brisbane Hospital. His principle interests are the surgical management of Head and Neck Cancer and associated reconstructive surgery. Research topics cover head and neck oncology, microvascular reconstructive surgery and the management of facial trauma. NTRODUCTION CARDIOVASCULAR DISEASE The theme of this conference is “From the genome to the Cardiovascular disease (heart and blood vessel; peripheral nursing home: Everything under the sun”. Whilst population and central) remains the leading cause of death in Australia. predictions are difficult and the rate of fertility and overseas Of all the common medical complaints it probably has the migration can only be estimated, one prediction holds true greatest impact on surgical management and dentistry. across all models of projection - ageing of the population. Ischaemic heart disease (angina and myocardial infarctions) Improvements in nutrition, sanitation and health care have lead to chest pain and the propensity to heart attacks, and led to a marked increase in the median life expectancy of the subsequently to cardiac failure (shortness of breath, ankle Australian population to 74.4 years for boys and 80.3 years swelling, reduced exercise tolerance). Well controlled angina for girls (at birth). is not a contraindication to dental treatment per se but patients with uncontrolled angina should be treated with The increasing cost of health care is already straining state caution. In addition, the medications used to manage cardiac and federal budgets. This is only going to increase in time disease frequently affect blood clotting, which can have and from a health economic perspective the only rational major implications for dentistry. response to this is an expansion in primary care. What does that mean for dentistry? More and more patients will have As a general rule there are no anticoagulants which prevent to be treated in the community, in your practices, and under the use of local anaesthetic and non-surgical dentistry (e.g., local anaesthetic. restorative treatment, fixed prosthodontics, endodontics). Lignocaine is probably preferred as bupivicaine is more Sensible practitioners will take a pro-active approach to this cardiotoxic. As always, the appropriate dose should be used. change and embrace it as an opportunity. Dentistry in the Care should be taken when undertaking surgical dentistry elderly will no longer be a new set of dentures every 10 years. (oral surgery, periodontal debridement with flaps, implant Rather the full spectrum of treatment is desired by these placement, apical surgery). patients and with attention to detail is entirely deliverable. Major surgery in elderly patients provides a good basis Warfarin: if the patients International Normalised Ratio to explain a systematic approach to the management of (INR) is less than 4.0, then extractions are possible1 but use medical co-morbidities. Employing an approach that covers haemostasis, haemostatic sponge in the sockets and suture the major organ systems adversely affected by ageing over the top. Place local pressure after extraction. will allow safe treatment of even extremely compromised patients. Aspirin: treat as normal, but use local pressure, haemostatic sponge and sutures. RESPIRATORY FUNCTION Clopidogrel: treat as normal with local haemostatic measures as above. Respiratory dysfunction in older age is common condition particularly in smokers or chronic asthmatics. Its impact Aspirin + clopidogrel: routine-non invasive dentistry should can manifest as mild shortness of breath on exertion, all present no problems. the way through to dependence on home oxygen. Infective exacerbations of respiratory disease can lead to reversible Liaise with the patients cardiologist and ask if clopidogrel deteriorations. Exercise tolerance questioning provides very can be ceased for the duration of therapy, should invasive useful information about functional reserve. Fortunately dentistry be required. A recent study suggested no increased other than patients’ dependant on home oxygen, the impact bleeding risk with single antiplatelet therapy but an increased of respiratory disease on dental treatment under local risk with dual therapy and suggested the use of local anaesthetic is minimal. Those who are dependant on oxygen haemostasis in all patients.2 should keep using it during treatment, and avoidance of naked flames is obviously important. The airway should not Newer anticoagulants: liaise with the patients cardiologist be impeded if at all possible (e.g., no dental dam). before performing invasive dentistry.

97 RENAL DYSFUNCTION IMMUNE SUPPRESSANTS Renal dysfunction (kidney failure) is manifest as an inability Autoimmune diseases such as rheumatoid arthritis, to clear waste products and problems with fluid management. ulcerative colitis and Sjogren’s disease may involve treatment Its implications for local anaesthetic dentistry are minimal, with immune suppressants. Again, restorative dentistry is however it can have a major impact on large surgical preferred and can be undertaken without great concern. procedures where extensive fluid shifts are expected. Surgical procedures carry a higher risk of postoperative Dialysed patients should be treated in conjunction with their infection which can be managed by prophylactic antibiotics schedule and in all patients with renal failure care should be and close follow up. taken when dosing with antibiotics. Gentamycin and other nephrotoxic drugs should be avoided. If in doubt, consult with SUMMARY the patient’s renal physician. Elderly and potentially unwell people are going to be an METABOLIC ORDERS increasing proportion of dental patients. Co-morbidities are common but rarely contra-indicate outpatient dental Diabetes (Type II greater than Type I) is probably the most treatment. The approach to managing these co-morbidities common metabolic disorder affecting the elderly. It will have can be extrapolated from major surgical procedures and an adverse impact on cardiovascular function and peripheral should follow a systematic approach dealing with each vascular disease and can also affect renal function. The organ system in turn. Consultation with the patients medical management of those organ systems is listed above. In treating team will be necessary as will an understanding of addition, diabetes adversely affects the immune system common mediations and their effects. and wound healing. This can manifest as an increased predisposition to local infections and wound healing REFERENCES problems. Management should involve optimisation of blood sugar control if possible and occasionally increased usage of 1. Bacci C, Maglione M, Favero L, Perini A, Di Lenarda R, Berengo M, antibiotic prophylaxis. Zanon E.Management of dental extraction in patients undergoing anticoagulant treatment. Results from a large, multicentre, MEDICATION prospective, case-control study. Thromb Haemost 2010;104:972-5 Bisphosphonates 2. Lillis T, Ziakas A, Koskinas K, Tsirlis A, Giannoglou G. Safety of dental extractions during uninterrupted single or dual antiplatelet treatment. The management of patient on bisphosphonates is a topic Am J Cardiol. 2011;108:964-7 in itself, however some general principles can be applied. Restorative therapy, including endodontics and coronal 3. Lo JC, O’Ryan FS, Gordon NP, Yang J, Hui RL, Martin D, Hutchinson restorations, are preferred to extractions. Restorative M, Lathon PV, Sanchez G, Silver P, Chandra M, McCloskey CA, Staffa therapy can be undertaken in patients on both oral and JA, Willy M, Selby JV, Go AS. Prevalence of osteonecrosis of the jaw iv bisphosphonates. The risks of Bisphosphonate-Related in patients with oral bisphosphonate exposure. Predicting Risk of Osteonecrosis of the Jaws (BRONJ) following dental Osteonecrosis of the Jaw with Oral Bisphosphonate Exposure (PROBE) extractions or surgical dentistry which exposes the bone Investigators. J Oral Maxillofac Surg. 2010;68:243-53. in patients with oral bisphosphonates is only very low and should not prevent extractions in general practice, however Address for correspondence informed consent is important.3 Intravenous bisphosphonates pose greater risks and consultation with a surgical colleague Senior Staff Specialist is probably appropriate. Royal Brisbane and Women’s Hospital Herston Road Herston QLD 4029 University of Queensland Upland Road St Lucia QLD 4067 [email protected]

ANN ROY AUSTRALAS COLL DENT SURG 2014; 22: 98-101 PREPARING MALAYSIAN DENTAL GRADUATES TO PROVIDE CARE FOR PATIENTS WITH SPECIAL HEALTH CARE NEEDS - HOW DO WE COMPARE WITH AUSTRALIA? EDUCATION SPECIAL NEEDS DENTISTRY IN MALAYSIA Mas S Ahmad, BDS1,2; Ishak A Razak, PhD3; Gelsomina L Borromeo, PhD2 1 Universiti Teknologi MARA, Shah Alam, Malaysia. 2 University of Melbourne, Victoria, Australia 3 Vinayaka Missions International University College, Petaling Jaya, Malaysia Dr. Mas Ahmad is currently undertaking a joint Doctor of Clinical Dentistry (Special Needs Dentistry) and PhD at the Melbourne Dental School which is funded by the Malaysian Ministry of Education. She holds an academic position at the Universiti Teknologi MARA Malaysia. Her area of interest is in dental education, community dentistry and oral health care for people with special healthcare needs. ABSTRACT Changing trends in population health suggests a rise in the number of people living with special health care needs (SHCN) indicating increasing needs and demands for oral health care amongst this patient cohort. This paper focused on the role of undergraduate education in preparing graduates to become competent in managing patients with SHCN, thus bridging the gap in access to oral health care. It will discuss the findings of a study on teaching and learning in Special Needs Dentistry (SND) in Malaysia, a developing country with increasing awareness in health and welfare for people living with SHCN. The level of undergraduate education in SND in Malaysian dental schools was compared with Australian counterparts. The study compared the educational experience between the two countries, leading to identification of areas that can be developed in the dental undergraduate curriculum in Malaysia. The study also obtained information pertaining to how Malaysian undergraduate dental students’ perceive those with SHCN. Baseline information obtained can direct global development of dental education in an effort to reduce oral health inequalities and improve oral health status of those with SHCN. Keywords special care dentistry; special needs dentistry; dental education; disability; special health care needs. Introduction Methods People with special healthcare needs (SHCN) include those Comparison of dental curriculum in relation to SND with any congenital, developmental or acquired forms of physical, developmental, mental, sensory, behavioural, Deans of Malaysian Public Dental Schools (n=6) and Heads cognitive or emotional impairment as well as having a limiting of Australian Dental Schools (n=9) were invited to complete condition that requires medical attention and specialised a postal survey on their perception of the current training management in healthcare and daily routine.1 These in SND. The questionnaire, developed based on the existing individuals may have limitations creating barriers to quality literature,7-11 consisted of 3 sections: didactic and clinical of life including aspects of oral health. 2,3 teaching and undergraduate education in SND. Training oral health professionals to provide care for Investigation of dental students’ knowledge, attitude and comfort patients with SHCN, a specialty area under the auspices of levels when treating patients with SHCN together with their perception Special Needs Dentistry (SND), has been related to improved of SND education. attitudes, knowledge, comfort and quality of care amongst students and qualified oral health care practitioners.4-6 It was A self-administered questionnaire was conducted with final reported that poor oral health outcomes for these patients year undergraduate Malaysian public dental students. It was linked to inadequate training in SND, suggesting the need was developed based on a study conducted previously on to improve the amount of teaching and learning in this area. 3 Australian samples12, and consisted socio-demographic characteristics, perception of SND, perception of patients The study aims to compare undergraduate education in SND with SHCN, and training programmes for SND. between Malaysian and Australian dental schools together with assessing Malaysian students understanding around this Students ability to define SND was categorised according discipline. Aspects of SND such as acceptance as a specialty to the definition set by the Royal Australasian College of and its future direction will aid further development of this Dental Surgeons (RACDS)13, which identified four SND patient dental field at both local and international levels. categories including those with intellectual disabilities, complex medical conditions, physical disabilities, and psychiatric issues. Students who were able to identify two or more categories were classified as having ‘adequate’


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