the recipient site are typically made along the ridge Treatment Complications and Failures with Dental Implants 325 crest. As blood vessels facial to the ridge do not cross over to the palatal or lingual regions, a crestal incision This allows a better evaluation of the requirements of maintains vascular supply to the flaps (Whetzel and the bone repair and minimizes the time from bone Sanders 1997) (see Figure 9.43a–z1). harvest to graft placement. Harvesting the block from the donor site first may risk obtaining a bone graft The bone defect and graft recipient site are usually that is too small. An accurate graft size should be exposed and prepared prior to a bone graft harvest. ascertained by CBCT preoperatively (see Figures 9.44a, b and 9.45a, b). (a) (b) (c) (d) (e) (f) (g) (h) (i) Figure 9.43 (a) Six months post restorative implant failure along with the grafted bone, (b) and (c) Clinical view showing the resultant osseous defect both facially and incisally, (d–f ) CBCT scan images showing lost both labial and palatal plates of bone, (g) Intraoperative view showing the defect with the flap reflected, (h) Monocortical allograft is stabilized both labially and palatally, (i) Incisal view of the grafted plates.
326 Advances in Esthetic Implant Dentistry (l) (o) (j) (k) (m) (n) (p) (q) (r) (s) (t) (u) Figure 9.43 (j) and (k) Voids filled with particulated graft, (l) Collagen membrane is placed and stabilized to cover the grafted bone, (m) Connective tissue graft is sutured on top, (n) Flap sutured, (o) One week post healing, (p–r) CBCT views showing grafts in position, (s) CAD/ CAM surgical guide in place for implant insertion, (t) Intraoperative view showing the implant in place, (u) CBCT view showing implant position within the two plates of bone.
Treatment Complications and Failures with Dental Implants 327 (v) (w) (x) (y) (z) (z1) Figure 9.43 (v–x) Attempting to place a connective tissue graft to enhance the labial contour from the cervical area, (y) Final tissue healing and maturation, contour regain. (z) Incisal view with the final restoration in place showing the completed treatment. (z1) Facial view of the case finalized. (a) (b) (a) (b) Figure 9.44 (a) and (b) Examples of insufficient graft size. Figure 9.45 (a) and (b) CBCT views showing the faulty position (inside the natural tooth root) of the titanium screw. 9.4.3 Complications with Allographs preparation are not always consistent (Lavernia et al. 2004). Cadaver bone has been transplanted with consid- Bone allograft transplants are now being widely used erable success since the beginning of the twentieth cen- by dental practitioners more than any other bone aug- tury and in large n umbers for the past few decades. To mentation material. This is probably due to the ease of obtain optimal results with grafting procedures and to use and preparation, and the availability of allografts safeguard recipients, the clinician must possess full from many networks of tissue banks (Tomford et al. knowledge of the biologic properties of allograft bone 1983; Kozak, Heilman and O’Brien 1994). Regretfully, (see Figure 9.46a–c). the source of these grafts and the means of their
328 Advances in Esthetic Implant Dentistry (a) (b) (c) Figure 9.46 (a) An Implant is placed showing labial bone dehiscence, (b) The bone defect was grafted with particulated autogenous bone mix and covered with PDLLA membrane and stabilized with resorbable screws (KLS Martin, GmbH, Tuttilngen, Germany, SonicWeld), (c) Final case restored showing enhanced soft tissue contours with the complete restoration of labial profile. The biologic properties and safety of allograft bone Bone allografts can be obtained and prepared in sev- was demonstrated by Hyatt and Butler (1957) and Kreuz eral ways. There is comprehensive donor screening and et al. (1951); the demand for allogeneic bone increased rigorous disease surveillance using donor medical his- precipitously. This resulted in an increase in the number tory, advanced laboratory methods, blood and marrow of tissue banks, which had substantial variations in tech- culture testing, and post-mortem examination. Using niques for allograft excision and preparation. The accu- these measures minimizes the risk of transmitting rate and strict control of tissue banks for monitoring the d isease to the recipient (see Figure 9.47a–h). processing of allografts worldwide is not consistent with the prevention of disease transmission. (a) (b) (c) (d) (e) (f) Figure 9.47 (a) and (b) CBCT scan showing deficient buccolingual width of the alveolar ridge, (c) Two implants placed leaving labial dehiscence, (d) and (e) Allograft particles were placed, stabilized and covered with collagen membrane and two membrane tacs (Auto Tac, BioHorizons, Birmingham, AL, USA), (f ) Case restored.
(g) (h) Treatment Complications and Failures with Dental Implants 329 Figure 9.47 (g) and (h) Pre and post grafting picture with one a higher osteogenic potential than particles smaller than year follow-up showing no bone formed labial to the implant 125 μm. Optimal particle size appears to be between 100 surface in spite the fact that the grafting procedure were and 300 μm. This may be due to a combined effect of sur- optimal which indicates the lack of the predictability of using face area and packing density (Schwartz et al. 1996). Very allografts alone. small DFDBA particles elicit a macrophage response and are rapidly resorbed with little or no new bone forma- 9.4.3.1 Inconsistent Regenerative Outcome tion. Tissue banks providing DFDBA usually have the and Questionable Osteoinduction graft material in various particle sizes, and they offer a The effectiveness of demineralized bone grafts may dif- range with variable particle size. Particle size from 250 to fer depending on the age and gender of the donor, the 750 μm is the most frequently available. Glowacki and residual mineral, the particle size, or the preparation Mulliken (1985) developed the technology of preparing method. According to Salyer et al. (1992), the success demineralized bone implants in powder form. Powder and safety of demineralized bone implants as well as dif- provides the maximum surface area necessary for ferent characteristics of the product, including its oste- interaction with recipient target cells, which stimulates oinductive potential, depend on the technological endochondral proliferation. Glowacki et al. (1981) dem- process used to produce them. Studies have examined onstrated that the extent of bone induction is a function the ability of commercial demineralized freeze‐dried of the surface area of the implanted bone. bone allografts (DFDBA) to induce new bone formation to assess whether the broad variation in clinical response Gendler (1986) introduced micro perforations in the was due to differences in the preparations or due to vari- demineralized bone, which, according to his long‐term ations in the host response. It was found that wide experience, are centers of new bone formation. He variations in commercial bone bank preparations of assumed that the mechanism of osteoinduction of DFDBA do exist, including the ability to induce new demineralized perforated bone is similar to that described bone formation, even within the same bank (Committee for other forms of demineralized bone matrix although on Research, Science and Therapy of the American the micro perforations, in his opinion, enhance osteoin- Academy of Periodontology 2001); however, the com- duction. Thus, the presence of micro perforations in mittee did not offer a solid statement on the osteogenic demineralized bone allograft also affects the osteogenic capacity of DFDBA. Commercial bone banks do not ver- potential of the graft. It is the author’s opinion that the ify the specific amount of BMPs or any level of inductive use of the allograft particles alone does not give the capacity in any graft material they sell. Therefore, graft required osteogenic response because the bone particles quality cannot be considered standard. Delaying the pro- go through a series of processes that probably lose their curement of donor bone after death, improper storage osteogenicity. As there is no proof of the presence of conditions, or other processing factors may play a sig- bone morphogenic proteins inside the graft particles is nificant role in the bioactivity of an allograft that makes questionable and requires further research to confirm it. its way to the clinician’s office (Holtzclaw et al. 2008). The clinician must understand the capacity and the clini- cal outcome of all the grafting materials used and be able If DFDBA particles remain in the site for longer than a to make the right choice for a long-term successful out- year acting as a bone matrix, they may weaken the host come. Usually after the placement of the allogeneic bone and delay normal bone formation, possibly by grafts, there is no second re‐entry to check bone forma- interfering with the osteoclast’s ability to resorb the tion. In other words, clinicians do not perform another DFDBA particles (Grover et al. 2011). When DFDBA is surgical re-entry to check graft viability, they only check used in particulate form, particle size also appears to with the radiographs. The presence of radio opacity in be an important variable in its success as a bone induc- the radiographic view does not confirm the viability of tive material. Particles in the range 125–1000 μm possess the grafted bone. Some researchers suggest that irradia- tion interferes with osteoinduction (Singh, Singh and Singh 2016), others suggest that a dose of radiation (2.5 Mrad) used by most tissue banks for the sterilization of bone tissue does not destroy the bone induction prop- erties of allografts (Tallentire and IAEA 1990). Therefore, sterilization processing may be an important contributor to variability in the osteoinductive properties of DFDBAs. There are two major concerns regarding the use of bone allografts: antigenicity, and the risk of disease transmis- sion (see Figures 9.48a–e and 9.49a–f ).
(a) (b) (c) (d) (e) Figure 9.48 (a) Deficient vertical bone height, (b) Successful bone grafting procedure, (c) The regain of natural tissue architecture, (d) Final restoration in place, (e) Graft resorption and disintegration two years post restorative due to the poor systemic condition of the patient (uncontrolled diabetes). (a) (b) (c) (d) (e) (f) Figure 9.49 (a) Mucopreosetal flap reflected and teeth were extracted revealing bone deficiencies, (b) Two implants (Spline, Sulzer Medica, Carlesbad, CA, USA) bone allograft (Mineross, BioHorizons, Birmingham, AL, USA) was placed and a collagen membrane (Biomend, Sulzer Medica, Carlesbad, CA, USA) and tacked with membrane tacs (Auto Tac, BioHorizons, Birmingham, AL, USA), (c) and (d) Frontal and incisor view for the case finally restored with two PFM crowns at the year 2002, (e) Post insertion view at 2002 and three years later 2005 showing gingival recession, (f ) Radiographic view at the time of implant placement 2002 and three years later showing advanced bone loss.
Because of the increased risk of disease transmis- Treatment Complications and Failures with Dental Implants 331 sion, gamma irradiation or ethylene oxide is used to s econdarily sterilize the allografts. Residuals due to inad- (a) (b) (c) equate evacuation following ethylene oxide or radiation sterilization may also contribute to the variability in the Figure 9.50 (a) Clinical view showing soft tissue swelling three graft response. Residual levels of ethylene oxide in the weeks post implant placement as a result of infection, (b) and graft have been shown to be toxic to fibroblasts and (c) Radiographic views showing sever bone resorption related to appear to cause morphologic changes in fibroblasts that both implants. may or may not be reversible (Buck et al. 1989). Ethylene oxide may produce inflammation and impair healing, implanted materials from other human donors. However, unless it or its byproducts are removed from the graft. the possible immune reaction is considerably diminished More infections were found with the use of non‐resorb- with allografts but still remains a factor to consider, as able membrane for the GBR procedure compared with a does the risk of disease transmission such as HIV. Smith, bioabsorbable membrane over a bovine bone in a xeno- Young and Kearney (1996) showed that, even at doses at graft study (Friedmann et al. 2011). Selection of a suita- which tissue quality begins to be compromised (1.5– ble membrane and proper timing of membrane removal 2.5 Mrads), irradiation failed to be virucidal for HIV type may reduce the risk of infection. Contamination with 1 (see Figures 9.51a–c and 9.52a–f). oral saliva is probably a major factor leading to bone graft infection (Glaser et al. 2004) (see Figure 9.50a–c). With the use of allografts, antigenicity poses particular health risks that involve an exaggerated host response to (a) (b) (c) Figure 9.51 (a) The resultant osseous defect is grafted with allograft, (b) The graft is covered with collagen membrane, (c) Bone allograft failure as a result of immunologic reaction. (a) (b) (c) Figure 9.52 (a) Cancellous allograft is trimmed and stabilized to treat 3D osseous defect, (b) Collagen membrane covering the graft, (c) Two weeks postoperative healing.
332 Advances in Esthetic Implant Dentistry (d) (e) (f) Figure 9.52 (d) Pus oozing from the side indicating infection, (e) Flap reflection showing resorption of the graft, (f ) Graft removal. Another form of allograft is the block form, which are alveolar ridges augmented with cancellous bone‐block available as monocortical blocks, corticocancellous blocks, allografts were treated. Recipient site complications asso- also known as the J blocks, and the cancellous blocks. Due ciated with block g rafting (infection, membrane exposure, to the large size of the graft, the sterilization process is incision line opening, and perforation of mucosa over the probably questioned more than the particle size. In a study grafted bone, partial graft failure, total graft failure, and by Chaushu et al. (2010) a total of 101 consecutive patients implant failure) were recorded. Partial and total bone‐ (62 females and 39 males; mean age 44 ± 17 years) with block graft failure occurred in 10 (7%) and 11 (8%) of 137 implant‐supported restoration of 137 severe atrophic augmented sites, respectively (see Figure 9.53a–d). (a) (b) (c) (d) Figure 9.53 (a) Fourmonths post grafting showing marked redness and screw exfoliation, (b) Mucopreosteal flap reflected, (c) Bone graft removed due to morbidity, (d) Resultant osseous defect. The implant failure rate was 12 (4.4%) of 271. Soft tis- from the apical to the coronal portions, with a more lacu- sue complications included membrane exposure (42 nae in the apical portion and fewer vessels in the coronal (30.7%) of 137), incision line opening (41 (30%) of 137), portion than in the autograft group. Thus it was con- and perforation of the mucosa over the grafted bone (19 cluded that fresh‐frozen allografts cannot be considered (14%) of 137). Infection of the grafted site occurred in 18 as successful and safe in alveolar bone reconstruction as (13%) of 137 bone blocks. Therefore it was concluded autogenous bone grafting. that the alveolar ridge deficiency location had a statisti- cally significant effect on the outcome of recipient site In yet another recent study, Deluiz et al. (2016) analyzed complications. More complications were noted in the adverse events associated with placement of fresh‐frozen mandible compared to the maxilla. Failures caused by bone allografts (FFBAs) during alveolar ridge augmenta- complications were rarely noted in association with can- tion and to assess one‐year survival of dental implants cellous block grafting. placed in reconstructed sites. They enrolled 58 c onsecutive patients (15 males and 43 females, aged 38–76 years; mean In another histologic and histomorphometric study, age: 58 ± 9.2 years) requiring maxillary bone reconstruc- Dellavia et al. (2016) treated 20 partially edentulous tion prior to implant placement. A total of 268 implants patients either with iliac crest fresh‐frozen allograft was subsequently placed in sites reconstructed with fresh‐ blocks (14 patients) and with autografts (6 patients). The frozen bone allografts. Infection occurred in six (10.34%) results revealed a decreasing proportion of blood vessels individuals, dehiscence in five (8.62%), and mucosal
perforation in seven (12.07%). Adverse outcomes catego- Treatment Complications and Failures with Dental Implants 333 rized as partial and total graft loss occurred in four (6.90%) and three (5.17%) patients, respectively. The implant fail- (20.70%) of 58 patients. The study concluded that infec- ure rate was 16 (5.97%) of the 268 fixtures placed in 12 tion and suture dehiscence are significantly correlated with graft loss in a maxillary FFBA augmentation (see Figure 9.54a–r). (a) (b) (c) (d) (e) (f) (g) (h) (i) (j) (k) Figure 9.54 (a) Preoperative view of horizontally deficient anterior lower mandible, (b) Meuco periosteal flap is reflected revealing severe horizontal osseous deficiency, (c) Two allograft cortico‐cancellus blocks (Puros Allograft, Zimmer dental, Carlesbad, CA, USA) stabilized by titanium microscrews (KLS Martin,GmbH, Tuttilngen, Germany), (d) Four month post‐surgery revealing the integration of the bone blocks to recipient bed, (e) and (f ) Trephine core is being harvested to confirm the nature of regenerated bone, (g–i) A histological decalcified H & E stained section showing multiple bone trabeculea (Woven bone). Rhythmic pattern of bone formation (resting lines) highly cellular, (j) Two implants are placed, (k) Final prostheses in place.
334 Advances in Esthetic Implant Dentistry (l) (m) (n) (o) (p) (q) (r) Figure 9.54 (l) and (m) One year post grafting showing graft morbidity and exfoliation, (n) The exfoliated graft, (o) The resultant defect at the time of graft removal, (p) One week post graft removal, (q) and (r) Radiographic view showing the resultant osseous defect. 9.4.4 Complications with Alloplasts Figure 9.55 Signs and symptoms of bone graft infection. Alloplastic bone graft materials are synthetic materials developed to overcome the inherent problems associated variety of forms: porous non‐resorbable, solid non‐ with allografts (Hench 1998). The major advantages of resorbable, and resorbable (non‐ceramic, porous) alloplastic materials include their high abundance rela- (Sheikh et al. 2015b; Tevlin et al. 2014). However, HA tive to natural materials, no risk of disease transmission have limited in vivo resorption and remodeling capacity and very low antigenicity (Shetty and Han 1991). and although unsuitable for bone augmentation, it is a Alloplastic materials have an osteoconductive character rather good for space making and defect filling (Petrovic without any potential for osteoinduction, and are mainly et al. 2012) (see Figure 9.56a–d). used as a filler in osseous defects and as a matrix for new bone formation. Numerous alloplastic materials and forms are available such as tri‐calcium phosphate which is a porous form of calcium phosphate. TCP has two crystallographic forms, α‐TCP and β‐TCP (Hashimoto‐ Uoshima et al. 1995); another form of TCP is dicalcium phosphate dihydrate (DCPD) called Brushite that claimed to offer (partial osteogenesis) generation of varying amounts of woven bone and fibrovascular tissue (Bauer and Muschler 2000) (see Figure 9.55). Another new form called biphasic calcium phosphate (BCP) is a mixture of HA and Ca3(PO4). Another alloplastic material, synthetic HA, has been used for a long time in bone regeneration for use in a
Treatment Complications and Failures with Dental Implants 335 (a) (b) (c) (d) Figure 9.56 (a) Loss of the labial plate of bone that mandates grafting, (b) Alloplast material was used to graft the defect, (c) Collagen membrane was used to cover the graft material, (d) Two years CBCT scan showing the total absence of the grafted material which indicates the lack of predictability of the alloplasts. Bioactive glass is also another form that gained popu- that include retarding epithelial down‐growth to the larity in the past decade; it is available in several p article site (Hallman and Thor 2008; Stanley et al. 1997; Wilson sizes and is composed of silicon dioxide (45%), calcium 1993). Another form of osteoconductive material, oxide (24.5%), sodium oxide (24.5%), and phosphorus Bioceramics, has been claimed to possess degradation pentoxide (6%) (Schepers et al. 1991). Studies claimed and progressive replacement by lamellar true bone that bioactive glass has several clinical benefits (Barinov et al. 2006) (see Figures 9.57a–c and 9.58a–c). (a) (b) (c) Figure 9.57 (a) and (b) Five years post maxillary sinus grafting with alloplastic showing adhesion of the particles to the periosteum, (c) Retained alloplastic bone graft particles in the gingival crevices for over two years. (a) (b) (c) Figure 9.58 (a) Bone dehiscence around an implant, (b) Alloplast material is placed to treat the defect, (c) Three months post‐operative showing complete resorption of the alloplast material.
336 Advances in Esthetic Implant Dentistry type of defects, the host, the systemic condition impact, the operator’s skills, and soft tissue condition at closure. The best clinical outcome of the osteoconductive vari- Many other commercially driven studies question the ants is the better understanding of its function and merit reality behind the use of alloplasts and most studies have of use, most of the osteoconductive materials (alloplasts) evaluation periods of one or two years, which is consid- is used only as a filler to fresh extraction site or limited to ered limited for the overall assessment of the material filling cup shaped osseous defects or offering a scaffold. (see Figure 9.59a–d). The efficacies of grafting materials are variable. Most of the conducted studies have many variables, such as the (a) (b) (c) (d) Figure 9.59 (a) Two implants placed (Tapered Internal, BioHorizons, Birmingham, AL, USA), (b) The labial bone defect is grafted with osteoplast material, (c) Collagen membrane is placed and secured with the cover screw, (d) Four months post grafting showing the poor regenerative outcome of the osteoplast. There have been many attempts to enhance the clinical failure if the mesh became exposed. Titanium has been outcome of alloplasts, like adding platelet‐rich plasma used extensively in numerous surgical applications (PRP) to tri‐calcium phosphate ß‐TCP, the osseous regen- because of its many inherent physical benefits: its low erating capacity was increased to 38%. Nevertheless, a d ensity and corresponding low weight, its ability to with- resorption rate of 32–43% was reported, where the type stand high temperatures and its resistance to corrosion. and quality of the crystal content of the graft material was The low density of titanium provides both high‐strength a dominant factor controlling the rate of resorption and lightweight dental materials (Artzi et al. 2003; Von (Cabezas‐Mojón et al. 2012; Reinhardt and Kreusser 2000). Arx and Kurt 1999). It has been used in guided tissue regeneration methods. Titanium‐reinforced non‐resorb- It is the author’s long‐term clinical assessment of the able membranes retain their three‐dimensional shape use of alloplasts that they have a questionable efficacy for with a specific height and width overcoming the main bone regeneration; it is the author’s opinion that allo- inherent problem with regular occlusive or non‐occlusive plastic materials may only be used as adjuncts to more barriers (Lekholm et al. 1993), space making, with tita- osteogenic autogenous grafting materials. They cannot nium mesh; the regenerative space is completely pre- be depended on purely and entirely as having bone‐ served by the physical geometry of the mesh. Since that forming potential. Alloplasts should be approached with time, numerous studies have reported the success of this caution and should not be overestimated as an osteo- technique in achieving a significant amount of osseous genic material. The short‐term assessment of the allo- regeneration in implant site development procedures plast materials has mislead many practitioners to use it (Longoni et al. 2007; Proussaefs and Lozada 2006) (see for regenerative purpose, but most of the studies did not Figure 9.60a–d and 9.61a–b). offer a long term assessment of the material, and most practitioners assessed the efficacy of the materials radio- Proussaefs and Lozada (2006) in a histomorphomet- graphically, which in reality does not reflect the osteo- ric study used titanium mesh for localized alveolar genic potential of the material. ridge augmentation. An equal mixture of autogenous bone graft and inorganic bovine mineral was used. 9.4.5 Complications with Titanium Mesh Titanium mesh was submerged for 8.47 months. Out of Boyne et al. (1985) introduced the concept of a titanium 17 patients, early mesh exposure (two weeks) was mesh scaffold to be used as an alternative to traditional observed in two patients and late exposure (>3 months) barrier membranes. The advantage purported at the time was observed in four patients. The histomorphometric was the ability to offer significantly increased and contin- evaluation concluded that the average area of all 17 core ued space maintenance during the healing phase to allow sections occupied by new bone was 36.47%, which bone regeneration to occur with fewer concerns about makes the amount of bone regenerated look complete to the clinician’s eye, but under the microscope, the
Treatment Complications and Failures with Dental Implants 337 (a) (b) (c) (d) Figure 9.60 (a) Dendunudation of soft tissue on top of previously placed titanium mesh, (b) Disinfecting the site with iodine solution, (c) Freshening the wound edges (removing the epithelial margins), (d) Flap closure. (a) (b) bone formed constitutes almost one third of the formed mass under the mesh. In order to overcome such limita- Figure 9.61 (a) Late mesh exposure (Three months), (b) Note the tions, the use of deproteinized inorganic bovine bone very poor regenerative outcome due to the mesh exposure. has been developed as a xenogeneic graft material that can be mixed with autogenous bone graft. The rationale of mixing autogenous bone with the graft is to combine the scaffold properties of the x enograft with the osteo- genic and osteoinductive properties of the autograft (Misch and Dietsh 1993) (see Figures 9.62a, b, 9.63a, b, and 9.64a, b). (a) (b) (a) (b) Figure 9.62 (a) Three months post healing showing the titanium Figure 9.64 (a) One week post‐surgery picture showing early soft mesh in place, (b) Frontal view showing poor regenerated bone tissue dehiscence, (b) Rotated palatal flap is used to correct the underneath the mesh. dehiscence. (a) (b) The majority of mesh exposure cases occurred in patients with thin tissue phenotypes; this was Figure 9.63 (a) Titanium membrane (Frios Bone Shields, Dentsply related to the increased thickness of the pseudo‐ Friadent, Mannheim, Germany) was tacked apically with (Auto Tac, periosteum layer observed under the mesh and the BioHorizons, Birmingham, AL, USA) and inciosally with the cover lower bone quality in the area of exposure (Poli et al. screw, note that the edges of the membrane is close to the flap 2014). Buser et al. (1990) stated that the predictabi edges which indicates the improper flap design as well as the lity of guided bone regeneration is significantly com faulty application of the titanium mesh around the neck of a promised by infection of membrane sites, and the non‐submerged implant fixture, (b) The Clinical outcome that retention of the shape cannot be anticipated (see indicates the failure of the bone grafting procedure with no bone Figure 9.65a and b). regeneration due to the exposure of the titanium mesh. In fact, the use of titanium mesh involved numerous complications, that included soft tissue dehiscence on top of the mesh; blockage of the periosteal blood sup- ply by ingrowth of the angiogenic cells, resulting in slow healing; and poor quality bone regenerated under- neath the mesh. Rominger and Triplett (1994) docu- mented 14% of infections in (nine membranes) and
338 Advances in Esthetic Implant Dentistry 14% of dehiscence with exposure of the mesh. These findings were also confirmed by a study by Maiorana (a) (b) et al. (2001), in which exposure of titanium mesh led to early graft resorption in the exposed area of about Figure 9.65 (a) A titanium mesh is being placed exceeding the 15–25%. Clinical management of titanium mesh expo- biological original ridge size, (b) Severe soft tissue sloughing due sure includes the complete removal of the exposed to suture rupture. mesh when the soft tissue is thin, and the exposure area is large, decontamination of the implant surface, and re‐grafting along with soft tissue modification for complete coverage of the area (see Figures 9.66a–c and 9.67a, b). (a) (b) (c) Figure 9.66 (a) Titanium mesh is stabilized with two micro screws (KLS Martin, GmbH, Tuttilngen, Germany), (b) One month post healing showing soft tissue dehiscence exposing the titanium mesh to the oral environment, the soft tissue opening was maintained with clorohexdine daily, (c) Four months post grafting showing reduced amount of regenerated bone due to the exposure of the titanium mesh to the oral environment. (a) (b) importance, once the nature of the defect is identified, whether a cup-shaped defect or a two‐dimensional Figure 9.67 (a) and (b) Late titanium mesh exposure and underlying defect, or a three-dimensional defect. Methods to soft tissue adhesions. amend the ridge are now proposed according to the known limitations and success rate of each method, Levine et al. (2014) presented part of a large, consecu- grafting materials are chosen accordingly, the selection tive series study on the use of a titanium mesh scaffold according to the speed of resorption of the material or for GBR. They concluded that complications related to the particle size etc. The identification of the local early exposure and early removal of the barrier mem- bone type (the bone density) standpoint will also pre- brane make this technique less predictable when signifi- dict the treatment outcome and mandates special cant regeneration is required, while soft tissue adhesion materials and techniques to be elected. The ability of makes titanium mesh more difficult to remove. the clinician to identify the tissue phenotype involved 9.4.6 Predictable Guidelines for Regenerative in the surgical approach is highly important and will Procedure definitely contribute to the fate of the regenerative pro- In the following section, some clinical guidelines are cedures immensely. detailed to offer a reliable regenerative outcome and to maximize the treatment outcome. Therefore, acquaintance with the currently available 9.4.6.1 Identify the Nature of the Defect classifications related to alveolar ridge defect has The accurate identification and understanding of the become mandatory. Lekholm and Zarb (1985) have nature of the osseous defect to be grafted is of great classified a five‐degree scale for alveolar bone resorp- tion status (A to E) and jaw bone quality on a four‐ degree scale (1–4). Cawood and Howell (1988) offered a classification system of the edentulous jaws based on the assumption that gradual atrophy follows the loss of teeth. The edentulous maxilla is classified as class 1–6. The key factors in achieving implant stability are bone quantity and bone quality. Friberg, Jemt and Lekholm (1991) showed an overall implant failure rate of 38% in edentulous maxillary type 4 bone and a 7% failure rate of 7 mm long implants compared to less than 1% in
implants longer than 10 mm. The impact of bone struc- Treatment Complications and Failures with Dental Implants 339 ture on implant stability was also shown by Jaffin and Berman (1991) with a failure rate of 44% in type 4 bone and type of the bone defect present is of high value as compared to 3.6% in types 1–3 (see Figures 9.68a–d and each individual osseous defect requires its own predict- 9.69a–i). The ability of the clinician to detect the nature able approach and treatment alternatives, which allows the clinician to anticipate the fate of the procedure prior to starting and convey it to the patient. (a) (b) (c) (d) Figure 9.68 (a–d) Cup shape osseous defect that gives high predictability to bone grafting procedures outcome. (a) (b) (c) (d) (e) (f) (g) (h) (i) Figure 9.69 (a) and (b) Clinical and radiological views showing severe vertical ridge deficiency which indicates a different unusual treatment approach. (c) Mobilized osteotomy performed, (d) Titanium microplates are used to stabilize the mobilized block, (e) CBCT four months post‐surgery for planning the future implants position, (f ) CAD‐CAM surgical guide in place, (g) Two months post implant placement healing, (h) CBCT showing Implants in place, (i) Final screw‐retained prosthesis in place.
340 Advances in Esthetic Implant Dentistry Figure 9.70 The phenotype (the quality of the soft and hard tissues) dictates the decision making and the operative approach On the other hand, cells within cancellous bone are to a great extent. responsible for at least 60% of the patient’s bone healing capacity. The periosteum in a young, healthy patient contributes an additional 30%. Cells in the cortical bone are responsible for only 10% of bone healing (Sandberg and Aspenberg 2016). As the cancellous compartment decreases, the reservoir for osteoblasts does as well. Computerized tomography can reveal the ratio of can- cellous bone to cortical bone at the recipient site prior to surgery (see Figure 9.70). 9.4.6.2 Predict the Host Response Many systemic inflictions to the patient’s health could directly impact the overall success of surgery, for exam- ple, diabetes, blood pressure, depression, osteoporosis etc. A reduction in mandible bone mass has been weakly correlated to cortical bone reduction in other parts of the skeleton, but no relationship to maxillary bone mass has been shown (see Figure 9.71a–o). (a) (b) (c) (d) (e) (f) Figure 9.71 (a) Two month post‐surgery showing after the peri‐implant tissue profiling. (b) CBCT scan showing loss of the labial plate of bone and failed bone graft as a result of smoking. (c) Intra operative view showing the failed implant supported restoration, (d) Implant removed and bone is cleaned, degranulated, (e) A new implant fixture is placed, (f ) Mono‐cortical allograft is placed and stabilized with micro titanium screws.
Treatment Complications and Failures with Dental Implants 341 (g) (h) (i) (j) (k) (l) (m) (n) (o) Figure 9.71 (g) Connective tissue graft is stabilized, (h) Flap closure attempted around the healing collar, (i) Immediate post op CBCT showing the graft is in place, (j) Two month post grafting, a clinical picture shows exposure of the bone graft, indicates its failure, (k) Pocketing along the graft surface and lack of epithelial attachment, (l) Vestibular incision is made to void crestal incision that might induce recession, the allograft cortical sheet is removed easily, (m) Connective tissue graft is positioned and flap closed, (n) Final healing one week post‐operative, (o) Final case restored. Patients are urged to reveal any ongoing medical treat- be approached with caution. Some of the patients seen ment and/or any medications they are taking as well as daily could be already contraindicated to implant ther- any influencing habits. It highlights contraindications or apy, some of them should be well controlled before the important areas of concern for dental implant therapy treatment, and others should be postponed for some (Sabes et al. 1970), it can also provide useful information time. Therefore, the complete understanding of the on the potential prognosis of implant treatment (Halstead medical background of the patients prior to surgery 1982; Misch 1982). The following areas of medical risks becomes mandatory. The clinician should have an idea of (Wakley and Baylink 1988) associated with dental the health profile of the patient just by gathering data implant placement can be evaluated through a detailed from the patient him/herself, and should any suspicious medical history or physical and laboratory examination, symptoms exists, then the patient should be referred to as dealing with medically compromised patients should his/her physician to investigate the condition and deliver
342 Advances in Esthetic Implant Dentistry due to thrombocytopenia. The treatment plan should shift towards a more conservative approach when deal- a clear report. Following this protocol could save patients ing with leukocytic disorders. Vitamin D is yet another from many of the potential complications during the factor considered to be influential to implant therapy; it course of the treatment. is synthesized in the liver, skin, kidney, intestine, and par- athyroid gland. It helps to increase absorption of calcium Renal disease is a major concern to dental implant and phosphate from the intestine and kidney. Deficiency therapy, which should be carefully evaluated initially of vitamin D is called ‘osteomalacia.’ Oral findings of through the medical history, because epinephrine and osteomalacia are a decrease in t rabecular bone, indistinct norepinephrine are naturally produced in the medulla of lamina dura, and an increase in the tendency to chronic the kidney and are responsible for the regulation of blood periodontal disease. Hyperparathyroidism also has dis- pressure, myocardial contraction, and excitability. tinctive oral findings including loss of lamina dura, loos- Glucocorticoids from the cortex is responsible for regu- ening of the teeth, and altered trabecular bone pattern lation of carbohydrates, fat, and protein metabolism. (ground glass appearance). Central and peripheral giant Hypo‐function of the adrenal gland may lead to Addison’s cell tumors may develop. Implants are relatively con- disease, which is manifested by weight loss, hypotension, traindicated in cases of hyperparathyroidism. Patients and nausea with or without vomiting. Oral manifestation with severely compromised immune systems, and severe is hyper‐pigmentation of lips and gingiva. The hyper‐ gastrointestinal diseases (e.g. hepatitis, malabsorption, function causes Cushing’s syndrome, manifested by a etc.) should also be excluded from any surgical interven- moon face, hypertension, and decreased collagen pro- tion for dental implant installation. Patients with muscu- duction. Patients s uffer from poor wound healing, osteo- loskeletal diseases (e.g. osteoporosis, osteopetrosis, and porosis and an increased risk of infection. Normal osteitis deformas (Paget’s disease)) that show a slowly creatinine levels are 0.7–1.5 mg 100 ml−1 and any distur- progressive bone disease due to increased osteoblastic bance may indicate kidney dysfunction and warrants activity, are usually marked by increased serum alkaline further investigation; if ignored it may lead to osteoporo- phosphates and calcium levels. Bony enlargement could sis and decreased bone healing. Patients that have any be palpated and appears radiographically as cotton wool chronic renal problems should receive additional s teroids shape. The patient is therefore predisposed to osteosar- prescribed by an experienced physician. Blood dyscra- coma. In such conditions, dental implants are totally sias such as anemia, leukemia, bleeding/clotting disor- contraindicated. Osteoporosis is a common oral bone ders, etc., also have an impact on dental implants. Mild disease that influences implant placement; the problem anemia has many intra-oral symptoms; fatigue, anxiety, arises from an imbalance between the rates of bone and sleeplessness, while chronic anemia is characterized resorption and formation. The resorption process domi- by shortening of breath, abdominal pain, bone pain, tin- nates, the cortical plates become thinner, the trabecular gling of the extremities, muscular weakness, headache, bone pattern more discrete, and advanced demineraliza- fainting, change in heart rhythm, and nausea. Oral symp- tion occurs. Osteoporosis affects females twice as much toms of anemia include a sore, painful, smooth reddish as males, especially after the menopausal period (Elaskary tongue, loss of taste sensation, and paresthesia of oral tis- 2008). It does not constitute an absolute contraindication sues. Anemia might have some further complications for dental implants, but it influences the treatment path. including impaired bone maturation and development, Precautions should include: estrogen therapy intake, die- while a faint large trabecular pattern of bone may appear tary calcium intake, progressive bone loading, and radiographically, which indicates a 25–40% loss of tra- implant designs should be greater in width and coated becular pattern (Elaskary 2008). with hydroxyapatite to increase bone contact (Wakley and Baylink 1988). Decreased bone density affects the initial implant placement and may influence the initial amount of Some situations or predicaments preclude the success mature lamellar bone forming at the interface of osseoin- of implant therapy because they compromise the body’s tegrated implants. Preoperative and postoperative anti- health either generally or locally. Pregnancy, persistent biotics should be administered and hygiene appointments oral infections, AIDS, neurologic disorders (e.g. stroke, should be scheduled more frequently. The anemic condi- palsy, mental retardation, etc.) which may render a tion should be corrected. On the other hand, the blood patient incapable of maintaining adequate oral hygiene leukocytic disorders entails leukocytosis, which is either on a daily basis, and malignancies are examples of such due leukemia, neoplasm, acute hemorrhage and/or dis- contraindicating situations for dental implant therapy eases associated with acute inflammation, necrosis or (Smiler 1987). leukopenia, which may accompany certain infections (e.g. hepatitis), or bone marrow damage (from irradiation Smoking is increasingly cited in the literature as a risk therapy). Both conditions may cause complications that factor in soft tissue healing (Rees et al. 1984), periodontal compromise the success of dental implant therapy, as infection, edema, and bleeding can be a common event
health, and implant therapy (Bergström and Preber 1994). Treatment Complications and Failures with Dental Implants 343 There are several controversial points of views concern- ing smoking in relation to dental implant failure; modern osteoclast stimulation may, in part, explain the increased science has proven that there is a potential increased risk rapidity of periodontal bone loss and refractory disease of smoking on the long- and short‐term success of dental incidence in patients who smoke (Elaskary 2008). implants (Gorman et al. 1994). A study by Persson, Bergström and Gustafsson (2003) evaluated the soft tis- Allergies are yet another source of concern. A thorough sue response towards smoking and they stated that medical and dental history is important in identifying aller- tobacco smoking has considerable negative effects on the gies that could dictate the use or avoidance of certain drugs outcome of periodontal treatment. The reason might be of other substances in dental implant therapy. Due to its related to altered neutrophil activity in terms of elastase high passivity and biocompatibility, no allergies to titanium and/or matrix metalloproteinase‐8 (MMP‐8), as well as or titanium alloy have been reported in the dental literature in the protease inhibitor alpha‐1‐antitrypsin (a‐1‐AT) (Bezzon 1993; Latta, McDougal and Bowles 1993). and alpha‐2‐ macroglobulin (a‐2‐MG) activities. The However, allergies to denture was reported (Hansen and study included 15 smoking and 15 non‐smoking patients West 1997) and restorative base metals such as chromium with moderate to severe periodontitis receiving surgical cobalt, nickel, and palladium‐copper‐gold alloys have treatment. Clinical examinations and collection of GCF appeared in research abstracts (Fieding and Hild 1993). were carried out prior to surgery and one and five weeks following treatment. The elastase activity was measured Patients with artificial joints may develop bacteremia with a chromogenic low‐molecular substrate and the lev- due to implant surgery that can cause hematogenous els of a‐1‐AT, a‐2‐MG, and MMP‐8 with enzyme‐linked seeding at the joint implants. It was hypothesized immunosorbent assay. Results showed unaltered levels of that bacteria may seed the prosthesis and cause a‐1‐AT, a‐2‐MG, and MMP‐8 in smokers following sur- infection due to dental procedures. Antibiotic coverage gery. In non‐smokers, the levels of a‐1‐AT and a‐2‐MG is preoperatively being highly indicated. The salivary increased, whereas MMP‐8 levels decreased. The levels glands and ducts must be inspected for any obstruction of elastase remained in both smokers and non‐smokers. that may hinder normal salivary flow and intra-oral The results indicated that in the presence of smoking, the lubrication to any oral prosthesis and may mandate a levels of a‐1‐AT, a‐2‐MG, and MMP‐8 remained unal- change in the proposed prosthodontic plan. Liver func- tered during the recovery period following surgical treat- tion should be assessed because liver cirrhosis causes ment. This is interpreted as a possible interference of reduction in the synthesis of clotting factors, abnormal smoking with the treatment response and may, in part, synthesis of fibrinogen and clotting proteins, vitamin K explain the clinical evidence of poor treatment outcome deficiency, enhanced fibrinolytic activity, and quantita- in patients who smoke. That probably explains the state- tive and qualitative platelet deficiency. Two of the more ment that excludes smokers from periodontal and important functions of the liver that are influential to implantology treatment till they follow a strict cessation implantology procedures are the synthesis of clotting protocol. Another study (Henemyre et al. 2003) deter- factors and the ability to detoxify drugs. Bilirubin altered mined the effect of physiologically relevant nicotine lev- range (total: 0.7 mg 100 ml−1) indicates liver disease that els on porcine osteoclast function as measured by affects tissue healing, drug pharmacokinetics, and long‐ resorption of calcium phosphate. The study used pure term overall health of the patient. In minor procedures, nicotine that was diluted in medium to the following con- postoperative control of bleeding should be applied by centrations: 0.03, 0.15, 0.30, 0.60, and 1.50 μM. Porcine using bovine collagen and additional sutures (Elaskary osteoclasts were seeded onto calcium phosphate multi‐ 2008). Advanced surgical procedures require hospitali- test slides and incubated at 37 °C with half media changes zation to control hemorrhage. Any history of osteomy- every 24 hours. Cells received 0, 0.15, 0.30, 0.60, and elitis or irradiation therapy in the region of the proposed implant receptor site should be well investigated; the 1.50 μM nicotine, or 25 nM parathyroid hormone (PTH). relationship between dental implant failure and Osteoclast resorption was quantified by measuring the irradiation therapy is not quite clear. Irradiation for the resorbed surface area of the calcium phosphate substrate. treatment of oral cancer does not seem to reduce the The study showed an increased number of osteoclasts was survival rate of implants as compared to those placed in directly related to an increasing nicotine c oncentrations; the non‐irradiated jaws; the main problem with irradi- ated patients is decreased salivary flow (xerostomia) however, no correlation was found between osteoclast (Jisaander et al. 1997), the liability for infection due to number and the amount of resorption. It was concluded the decrease in blood supply, and the possibility of osteo that nicotine appears to stimulate o steoclast differentia- radionecrosis (Marx and Johnson 1987). tion and the resorption of calcium phosphate, which is The complication of radiation starts when the dose the major component of bone. Nicotine‐modulated exceeds 64 Gy (Murray et al. 1980). Some authors stated that the maxilla is more liable to failure with dental implants after irradiation therapy. The waiting period
344 Advances in Esthetic Implant Dentistry excessive hypoglycemic drugs, or inadequate food intake. Its symptoms include: weakness, nervousness, tremor, between the end of radiation therapy and implant palpitations, and/or sweating, and in worse cases, confu- p lacement is not definite. Some authors suggest three to sion and agitation to seizure; coma is the final fate. six months (King, Casarett and Weber 1979). Others Diabetes mellitus does not directly affect the failure of suggest six months, because after six months fibrosis dental implants. A consensus expressed that the place- is expected to begin in the irradiated tissues as a ment of implants in patients with metabolically controlled result of reduced cell reproducibility and progressive diabetes mellitus does not result in a greater risk of failure ischemia. Others recommend a 12 month waiting period than in the general population; but a group study stated (Albrektsson 1988). It seems that the failure rate of den- that patients with diabetes experience more infection in tal implants after oral radiotherapy is minimal; but it is clean wounds than patients without diabetes (Goodson recommended to wait for a longer healing period and to and Hunt 1979). The liability of infection is probably due use hyperbaric oxygen therapy especially in the maxilla, to the thinning and fragility of the blood vessels, which to improve the healing capacity and avoid soft tissue alters the blood supply. In conclusion, current surgical ulceration as well as reducing fibrous tissue formation opinion is that patients with well‐controlled diabetes (Keller 1997). (below 250 mg dl−1) probably do not encounter inordinate operative risks, while patients with poorly controlled dia- Physical conditions and symptoms are not the only betes or high-risk patients (more than 250 mg dl−1) may aspects an oral surgeon should evaluate and assess. frequently experience wound failure; therefore, patients A patient’s psychological ability to commit to long-term with poorly controlled diabetes present more difficult treatment and maintenance programs must be an inte- management problems and postponement of the surgery gral part of the examination and selection process. is recommended until better control is achieved (Smith During the consultation, the clinician should determine et al. 1992). whether the patient is psychologically capable of making the necessary long‐term commitment. For example, Alcohol consumption is detrimental to the success of phobic or highly anxious individuals may have low pain dental implantology procedures (Sampson et al. 1996) thresholds and refuse to present for treatment follow‐ because it contributes negatively to osteoporosis, osteo- ups. On the other hand, patients whose dental com- penia. This statement is supported by the studies which plaints stem from somatization disorders will probably suggested that alcohol intake leads to a negative bone not be satisfied with the results of implant therapy balance effect and progressive bone loss (Lindholm (Melamed 1989). et al. 1991). This in turn may lead to insufficient bone volume for the application of dental implants. A study It is unfortunate that not every person may be consid- by Bombonato et al. (2004) evaluated the possible effect ered mentally, psychologically, physically, and emotion- of alcoholic beverage administration on reparative bone ally sound. As a result, some cases may contraindicate for formation around hydroxyapatite tri‐calcium phos- dental implant therapy. Persons afflicted with acute phate implants inside the alveolar socket in rats. The psychiatric or psychological disorder are one such exam- study confirmed that a significant delay in reparative ple. These disorders may be subdivided into (1) inability bone formation was detected in the alveolus of alcoholic to understand information, follow instructions, or make rats by using a histometric differential point counting reasonable decision (e.g. psychotic syndromes, severe method. A thorough physical examination prior to neurotic conditions, or character disorders, etc.); (2) implant placement is imperative to assess the patient’s impaired memory or motor coordination necessary for present health status and to detect early signs of any routine oral hygiene (e.g. cerebral lesion syndromes, pre‐ undiagnosed disease. Bi‐digital palpation of the lips, senile dementia, etc.); and (3) chronic, severe drug addic- buccal mucosa, hard and soft palates, the oral pharynx tion, because of a high propensity for poor motivation, and the submental, submandibular, and cervical lymph inadequate nutrition, and lack of compliance with oral nodes should be made to assess the presence of any hygiene regimen (Smith, Silverman, Auclert 1989). As masses (Smith, Silverman, Auclert 1989). By gently always, it is best to select candidates whose level of under- grasping and lifting the tongue forward, upward and lat- standing and cooperation is superior, for that guarantees erally, the floor of the mouth and the tongue can also be a successful end result (Elaskary 2008). Endocrine examined. Registering information and taking notes on systemic diseases (e.g. uncontrolled diabetes, hyperthy- past history are only one aspect of the presurgical stage roidism, pituitary/adrenal disorders, etc.), should be of implant therapy. Recording the patient’s vital signs approached with caution, as 75% of patients with diabetes (pulse, blood pressure, respiratory rate, and tempera- mellitus exhibit increased alveolar bone loss and inflam- ture) can be important in assessing the patient’s present matory gingival changes that might affect osseointegra- overall health. Other medical tests and/or consultations tion negatively. ‘Hypoglycemia’ is the most serious complication for diabetic patients during any dental pro- cedure; it occurs as a result of excessive insulin levels,
with the patient’s physician may be necessary when Treatment Complications and Failures with Dental Implants 345 compromised medical conditions exist or are suspected. It is important to note that the literature s uggests evalu- a patient‐by‐patient basis, as compromised medical ating medically compromised implant candidates on status alone is not necessarily indicative of implant failure (Elaskary 2008; Elaskary et al. 1999a, b) (see Figure 9.72a–r). (a) (b) (c) (d) (e) (f) (g) (h) (i) Figure 9.72 (a) Vertical bone loss related to maxillary left central incisor that requires a highly osteogenic grafting material, (b) CBCT scan showing complete loss of both labial and lingual plates of bone, (c) Inter‐operative view showing the severity of the bone loss, (d) The black markings showing the incision line (inverted V letter), (e) Approximation of the wound edges, (f ) Suturing of wound edges of the double papillary approximation flap, (g) Autogenous bone block harvested from the chin is stabilized with titanium screws (KLS Martin,GmbH, Tuttilngen, Germany), (h) 3.8 × 15 mm laser lock implant being inserted (Laser‐lock, BioHorizons, Birmingham, AL, USA), (i) Collagen membrane (Mem‐Lock, BioHorizons, Birmingham, AL,USA) is being stabilized by two membrane tacs (Auto Tac, BioHorizons, Birmingham, AL, USA).
346 Advances in Esthetic Implant Dentistry (l) (j) (k) (m) (n) (o) (p) (q) (r) Figure 9.72 (j) Rotated pedicle connective tissue graft from the palate is positioned along the crest of the ridge to ensure maximum tissue volume and better quality of keratinize tissue, (k) Intraoperative view of flap sutured, (l) CBCT postoperative view showing regain of both lingual and buccal contour, (m) Post healing result, (n) De‐epithelization the defective ridge, (o) Onlay keratinized graft is used to enhance the soft tissue condition, (p) One month post healing, (q) Final restoration inserted. 9.4.6.3 Optimal Soft Tissue Management and Closure that have been listed to manage oral soft tissues should be It is the author’s personal opinion that optimizing soft carefully taken into consideration. The author’s personal tissue management is more important than the bone opinion is that when performing regenerative therapy, the graft procedure itself, in the understanding that the bone clinician should start with soft tissue management and then graft fails easily when the overlying soft tissue fails; there- commence with bone therapy, because in cases where the fore, the success of the bone graft is strictly linked to the soft tissue is inadequate, or failed, then the regenerative status of the soft tissue. The movement of the flap during procedure should be aborted. Start the regenerative proce- the healing phase will cause fibrous tissues and epithelial dure by managing the soft tissue first, thus e nsuring that cells to fill the defect and invade the graft, leaving much scar this soft tissue will protect and cover the regenerative mate- and fibrous tissue in place. All of the previous guidelines rial with no or few potential complications (see Figure 9.73).
Figure 9.73 Removal of the inflammatory tissue is important prior Treatment Complications and Failures with Dental Implants 347 to any grafting procedure, it controls to a great extent the success of the grafting procedure. 9.4.6.4 Stability and Space Making for Graft Material Figure 9.74 Delicate periosteal reflection, minimal tissue trauma, One of the most important steps in regenerative therapy tension free sutures, and avoiding tissue laceration are all is to stabilize all the graft components, whether it is important factors to the success of any grafting procedure. autogenous grafts, alloplasts or allografts. Placing the bone graft then covering it with a collagen membrane without stabilization is no longer an acceptable treat- ment modality; the graft must be stabilized to protect the coagulum underneath and to counteract against the healing pressure from the periosteum and minimize fibroblast invasion to the graft. When the graft particles are not stable following soft tissue closure, the particles become dispersed throughout the site via muscular movement or chewing. Fixation devices like bone screws, membrane tacs, wires, etc., must be used all the time with no exception. The fact that guided bone regen- eration is based on isolating the grafted site from the surrounding soft tissue shows the value of stabilization. The GBR membrane keeps the faster growing tissues like epithelium, fibrous tissue, or gingival connective tis- sue out of the defect, allowing controlled regeneration to occur with vital bone formation. The application of bone graft material into the defect prevents the collapse of the collagen membrane and acts as a place holder for new regenerating bone and an osteoconductive scaffold for the growth of blood vessels and osteoblasts. The stability of the grafting complex is one of the most important factors currently being overlooked by many clinicians. Stability of the grafting complex becomes a prior value to any regenerative procedure (see Figure 9.74). By stabilizing the graft, sufficient space is preserved, and an adequate vascular supply ensured (see Figure 9.75a–c). Once you enable a space that is protected for the bone graft components, the regenerative procedure starts normally. Space making is an old topic that has been detailed by many authors over the years. Since the induction of the osteopromotion theory, it remains one of the most implant prerequisites in the field of regenerative dentistry. (a) (b) (c) Figure 9.75 (a–c) Achieve stability of the grafted complex via using either membrane tacs or fixating screws is an absolute necessity for stabilizing the coagulum underneath the membrane.
348 Advances in Esthetic Implant Dentistry is definitely different than those used for socket preserva- tion, which explains the value of the selection of the best 9.4.6.5 Selection of Suitable Regenerative grafting material. Approach & Material The correct selection of the grating materials and tech- The author suggests a grafting recipe that may ensure nique used, depends on several factors that should be a high predictability outcome of the regenerative proce- accounted for; the osteogenic potential of the graft com- dure, the optimal particulated mix (OPM) is composed ponents; the graft should attain certain osteogenic capac- of a combination of two thirds of autograft bone chips ity; the graft matrix must contain or encourage population and one third of deproteinized inorganic bovine bone by osteoblasts; the economic condition of the patient; the (DBBM), preferably of equine origin. The bone graft mix ability of the clinician to use the materials selected; and the is formed of autogenous bone chips harvested from the readiness of the materials in the office. A vast array of operating site using any commercially available bone choices are now available to clinicians for a graft to be suc- scrapers and DBBM grafting material of an average cessful. Bone grafting is regeneration not repair, the term p article size of 300 M (see Figure 9.76a–c). The reason ‘repair’ implies the regaining of lost tissue; regeneration is for using autogenous bone is to ensure a high osteogenic a biologic process where not only is the tissue regained but potential of the graft and the rest is used as a filler to also its form and function. The blood clot serves as the maintain a good body bulk of the graft, to ensure mini- initial matrix where cells migrate and then serves as mal graft remodeling postoperatively, and to minimize anchorage for the osteoblasts, therefore the need to stabi- the postoperative graft reapportion with minimal or no lize the blood clot is also important. Numerous grafting antigenicity or possible tissue reaction. The primary data materials and techniques are available in the marketplace. from the use of the OPM indicates a minimal remodeling It is the clinician’s responsibilty to select the best material rate, high regeneration capacity, ease of use, and less and technique that will provide the optimal treatment out- discomfort to the patient. come. The materials used for vertical bone augmentation (a) (b) (c) Figure 9.76 (a–c) Examples of space making. Harvesting autogenous chips from donor sites can be 75% Autogenous bone ships 25% DBBM accomplished using drills, piezoelectric curettes, bone scrapers, and manual curettes. Autogenous bone chips Figure 9.77 An optimal grafting mixture is proposed by the can also be harvested from an intra‐oral donor site, author that consists of 75% of autogenous bone chips and 25% of such as the maxillary tuberosity, mandibular retromolar deprotinized inorganic xenograft for less resorption and providing area, and the symphysis (Kainulainen et al. 2002, 2003) bulk to the body of the graft. (see Figure 9.77). The reasons behind selecting the bone chips as the pre- ferred method of autogenous bone use is supported by the work conducted by Miron et al. (2011), who evaluated the ability of the graft to promote an osteogenic response in osteoblast cultures, with cell proliferation measured at one, two, three, and five days, in an in vitro study (pigs). They compared four types of autograft forms: (1) milled block grafts, (2) bone chips harvested via a bone scraper, (3) bone
slurry harvested using a bone trap, and (4) bone harvested Treatment Complications and Failures with Dental Implants 349 via piezosurgery. The study concluded that osteoblasts seeded on bone mill and bone scraper samples exhibited In conclusion, there is no specific recipe that can be significantly higher levels of collagen, osteocalcin, and implemented in all clinical situations, because this is not osterix and produced more mineralized tissue, which applicable in the oral cavity due to the many variables explains the value of using the chips (see Figure 9.78a–c). that exist. The clinician should learn the benefits and side effects of each method along with its clinical pre- Bone collectors should not be used for this purpose, as dictability, using the previously mentioned guidelines as it has a high potential for contaminating the bone (Young a reference for any regenerative procedure that has been et al. 2002b) (see Figure 9.79a–c). found to be highly advantageous and leads to a highly predicable regenerative outcome (see Figure 9.80 a–c). (a) (b) (c) Figure 9.78 (a) Tools for autogenous bone chips harvesting Drills, Curettes, Scrapers, Peizzo surgery respectively, (b) and (c) an example of the right particulated bone grafting mixture that includes 75% of autogenous bone chips harvested with bone scrapper. (a) (b) (c) Figure 9.79 (a) Horizontal osseous defect in the anterior region, simultaneous Dental implants placement attempted along with non‐ staged grafting approach, (b) The defect was grafted with a particulate bone graft produced from harvested bone chips and mixed with one third alloplastic material, all covered with PDLLA membrane, (c) and (d) Incisal and frontal clinical views of the case finally restored. (a) (b) (c) Figure 9.80 (a) Preoperative view missing osseous contours and missing central and lateral incisors, (b) The local defect is rafted with a particulate bone graft produced from harvested bone chips and mixed with one third alloplastic material, all covered with PDLLA membrane, (c) Final case restored.
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359 Index Page locators in bold indicate tables. Page locators in italics indicate figures. The index uses letter‐by‐letter alphabetization. 3D see three‐dimensional resorption 38 BCP see biphasic calcium phosphate ridge augmentation 96–97 BF see bone fill a ridge preservation 143 bioactive glass 335 treatment complications and Bioceramics 335, 335 ABB see anorganic bovine bone biofilm 93 acellular dermal matrix (ADM) 233, failures 308–309, 313, 328 Bio‐HPP 6 amoxicillin 92, 117 Bio‐Oss collagen® 96–97 318, 318 anaerobic bacteria 149 bioresorbable membranes 110–117, adhesive bridges 15 anesthesia 307 ADM see acellular dermal matrix ankylosis 270 110–117 ADSD see Aesthetic Digital Smile anodontia 4 biphasic calcium phosphate (BCP) anorganic bovine bone (ABB) 201, Design 55–56, 334 advancement flaps 199–201, 200 206, 211, 216, 219, 226–227, bone fill (BF) 58–60, 58 Aesthetic Digital Smile Design 234–237 bone graft fracture 323–325, antibiotics 89–93, 102–103, 117 (ADSD) 33 apical repositioning flap 273 323–327 age 41–43, 41–42 Atrisorb® 114 bone loss allografts atrophic maxilla 218 autografts guided implant placement 247 guided bone regeneration guided bone regeneration implant positioning 293 234–235 201–202, 206, 211–219, 223, peri‐implant tissue stability 226, 233–234 immediately placed and loaded immediately placed and loaded 141, 142, 146, 149–150, implants 95–97, 106, implants 74, 80, 83, 88, 93, 156–157, 161 106–110, 127 98–100 treatment complications and peri‐implant tissue stability 147, failures 303, 308–309 peri‐implant tissue stability 147, 157–160, 159–160, bone modeling/remodeling 171, 177 166–169, 167–178, 171–177, immediately placed and loaded 178–179 implants 55, 71, 77, 83 treatment complications and treatment complications and peri‐implant tissue stability 143, failures 327–333, 328–334 failures 318–325, 319–327, 146–147, 147, 150 348–349, 348–349 treatment complications and alloplasts axial implant positioning 286–288, failures 321, 321 guided bone regeneration 237 286–287 bone quality treatment complications and guided implant placement 251 failures 332–338, b restorative space 283–284 333–338 treatment complications and bacterial endotoxins 149 failures 301 alveolar ridge BBP see buccal bone plates bone ring allograft 127, 177 distraction osteogenesis 276, bony window preparation 219 283–285 Brocken allograft sheet 109 guided implant placement 251 immediately placed and loaded implants 51–53 peri‐implant tissue stability 138, 141, 146–147 Advances in Esthetic Implant Dentistry, First Edition. Abdelsalam Elaskary. © 2019 John Wiley & Sons Ltd. Published 2019 by John Wiley & Sons Ltd. Companion website: www.wiley.com/go/elaskary/esthetic
360 Index composite resin 15 corticocancellous bone graft computed tomography (CT/CBCT) immediately placed and loaded buccal bone plates (BBP) 49–53, implants 74, 80, 83, 49–52, 52, 55, 60–61 3D planning with CAD/CAM 98–100, 103 2–4, 6–7 peri‐implant tissue stability 162, buccal pouch 210 162, 175, 180 buccal ridge defect 206, 209 computer‐assisted surgery 6–8, 7 treatment complications and buccolingual implant guided bone regeneration failures 320–321, 320, 323–325, 325, 332–333, 333 positioning 51–53 218, 221 bundle bone 141, 146–147 guided implant placement 248, crestal bone loss see bone loss Burstone line 38 crestal bone‐to‐implant interface 3 251, 256 criticized tissue band 85 c immediately placed and loaded cross‐linked collagen membrane CAD/CAM see Computer Aided implants 62, 63, 63, 65 207, 209, 214, 216, 219–220, Design/Manufacture arbitrary flapless implant fixture 232–233 crown lengthening 273–275, CAF see coronal advanced flap installation 84, 86–88, 273–275 calcium sulfate 83 90–94 CTG see connective tissue graft calcium sulfate–platelet rich novel concepts to treat defective cupid smile 31 labial plate of bone 100–103, plasma 83 101–112, 117, 117–119, d cancellous block allograft 331, 332 121–122, 123–125, 126–128 CBCT see computed tomography treatment complications DBBM see decalcified bovine bone CEJ see cementoenamel junction 71–75, 72–79, 78, 81–84 mineral; deproteinized cell adhesion/proliferation 151 modern trends in esthetic implant inorganic bovine bone cellular dermal graft 82 therapy 2–4, 4–5, 6–9 cementoenamel junction (CEJ) peri‐implant tissue stability DCPD see dicalcium phosphate 140–141, 156, 159, 160–161, dihydrate modern trends in esthetic implant 162–164, 171–176, 181–182 therapy 12 restorative space 276–277, decalcified bovine bone mineral 290–292 (DBBM) 96–97 peri‐implant tissue stability treatment complications and 138, 140 failures 306–307, 319, dehiscence‐type defect 206, 209, 325–328 236–237 restorative space 264, 280, Computer Aided Design/ 287–288 Manufacture (CAD/CAM) demineralized freeze‐dried bone modern trends in esthetic implant allograft (DFDBA) 234–235, cementum 12, 77 therapy 2–4, 6–7 329, 330 ceramic restorations 6–7, 63, 65 restorative space 276–277 chin block grafts 74, 80 treatment complications and dense‐polytetrafluoroethylene chlorhexidine gluconate 62, 117 failures 326 (d‐PTFE) 202, 211, 223, chronic periapical computer‐assisted surgery 6–8 226–227, 230, 238–239 computerized navigation periodontitis 91–93 surgery 277–278 dental analysis 34 cleidocranial dysostosis syndrome 4 cone‐beam computed tomography dentolabial analysis 34 CO2 laser 9–10 (CBCT) see computed deproteinized inorganic bovine bone coDiagnostiXTM 7–8 tomography collagen fibers 12 connective tissue graft (CTG) (DBBM) 348 collagen fibrils 145 immediately placed and loaded DFDBA see demineralized freeze‐ collagen membrane implants 107, 127 peri‐implant tissue stability dried bone allograft guided bone regeneration 207, 157–160, 159–160, 166–169, dicalcium phosphate dihydrate 209, 214, 216, 219–220, 167–178, 171–177 230–233, 239 coronal advanced flap (CAF) 167 (DCPD) 334 coronoapical positioning 55–60, DICOM format files 251, 256 immediately placed and loaded 56–59, 57, 58 digital dentistry 7–9, 33–34, 33 implants 74–76, 80, 83, coronoplasty 265, 266 Digital Smile Design tool 33–34 85, 91, 93, 94, 96, 114, cortical perforations 201, 202 distraction osteogenesis 275–276 123, 127 double papillary flap approximation peri‐implant tissue stability 172, 170–178, 170–177, 178–179 177, 180, 180–185 d‐PTFE see restorative space 267, 290, 294 dense‐polytetrafluoroethylene treatment complications and dropped facial contours 71–72, 71 dysesthesia 307 failures 321, 328, 331, 336 commissure smile 31 complex smile 31
e FPD see fixed partial dentures Index 361 free gingival grafts (FGG) 157–158, enameloplasty 265, 266 resorbable membranes endosteum 308 212, 224–225 206–210, 208–209, 213–222, enjoyment smile 30 freeze‐dried bone allograft (FDBA) 230–233, 239 Epi‐Guide® Bioresorbable Barrier 95–97, 234–235 revisiting barrier membranes Matrix 114 frenum/frenectomy 230–233, 231 e‐PTFE see expanded immediately placed and loaded revisiting bone grafts 233–237 polytetrafluoroethylene implants 84, 106 xenografts 235–237 ethics 20 bony window preparation 219 expanded polytetrafluoroethylene peri‐implant tissue stability buccal ridge defect 206, 209 147–148, 147–148 complications 238–239 (e‐PTFE) conclusion and guided bone regeneration 197, fresh‐frozen bone allografts (FFBA) 332–333, 333 recommendations 239 230, 233–234, 237, 238–239 cortical perforations 201, 202 immediately placed and loaded g creation of buccal pouch 210 dehiscence‐type defect 206, 209, implants 96 gap filling extraoral clinical outcomes 27–48 immediately placed and loaded 236–237 implants 55–60, 56–59, final prosthesis insertion/post‐ digital dentistry 33–34, 33 57, 58 human face 28–29 peri‐implant tissue stability insertion 205–206, 210, 213, intercommissure line 34–35, 35 146, 180 215, 218, 227 lip influence 37–40, 38–40 flap advancement 199–201, 200 preoperative and postoperative GBR see guided bone regeneration flap design 198–201, 199, 200 gender 43, 43 harvesting of free gingival results 27–28 generalized aggressive grafts 212, 224–225 smile arc 35–36, 35–36 horizontal ridge defect 206, 211, smile art 29–30 periodontitis 92–93 213, 216, 236–237 smile design 32–34, 32–33 Gibson’s smile exercise program 30 immediately placed and loaded smile landmarks 34–37 gingival analysis 34 implants 110–114, 110–113 smile pattern 30–32, 30–31 gingival bleeding 149 impressions 208 symmetry 44–46, 45–46 gingival display incisions at the adjacent teeth 199 teeth morphology 40–44, 41–44 incisions at the edentulous tooth loss 29, 29 extraoral clinical outcomes 30, site 198–199, 199 value of a smile to human beings 32, 40–42 mid‐crestal incision 198 slightly palatal incision 27–29 restorative space 284–285 198–199 vestibular reveal 36–37, 36–37 gingival recession see peri‐implant slightly vestibular incision 199 introduction 197 f tissue stability neurological complications 239 gingival zenith 286–288 peri‐implant tissue stability 147, facial analysis 34 growth factors 117, 237 161–163 facial anatomy 28–29 guided bone regeneration (GBR) recipient site preparation facial recession 71 201–208, 201–202 FDBA see freeze‐dried bone allograft 197–246 removal of bone overgrowth FFBA see fresh‐frozen bone allografts atrophic maxilla 218 204, 207 FGG see free gingival grafts biological rationale and historic sinus grafting 227–228 fibroblasts 145 soft tissue corrections after GBR in financial resolution 20–21 overview 197–198 the esthetic zone 237–238 fitted autogenous bone veneers bone graft and membrane soft tissue healing 203–205, 212, 214, 217–218, 223–226 100–105, 100–105 placement 201–208, stabilization of membrane fixed partial dentures (FPD) 21 208–229 214, 216 flap advancement 199–201, 200 allografts 234–235 surgical protocol and considerations flapless surgery alloplasts 237 for the esthetic zone 198–230 autogenous bone grafts sutures 204, 208–212, 223–228, guided implant placement 251 201–202, 206, 211–219, 223, 229–230, 229 immediately placed and loaded 226, 233–234 combining different bone implants 49–51, 49–52, 52, substitutes 237 61, 62 growth factors 237 labial plate of bone 73, 84–95, non‐resorbable membranes 86–95 201–206, 208, 211–213, 230, 238–239
362 Index i peri‐implant tissue stability 146–147, 150–151, 151–152, guided bone regeneration ICA see irradiated cancellous 158–161, 159–162 (GBR) (cont’d) allograft poor esthetics and tissue temporary crown insertion and ice‐cream cone technique 109 discoloration 72, 72 emergence profile 203–205, ICL see intercommissure line 215, 217 image guided implantology preclinical evidence 49–60 presence and thickness of the three‐dimensional ridge defect 277–278 209, 213, 216, 223, 227 immediately placed and loaded buccal bone plate 60 reasons for inconsistent outcome treatment complications and implants 49–68 failures 331, 337–338, 347 accuracy of implant 72–83 reduction of treatment time 70 vertical releasing incisions 199 positioning 78 restorative space 284 vertical ridge defect 211, 213, arbitrary flapless implant fixture risk assessment and classification 216, 226, 236–237 installation 84–95, 86–95 93–95 wound dehiscence and material block autografts 74, 80, 98–100 risk factors 82–83, 82–84 buccolingual implant positioning socket morphology classification exposure 238–239 guided implant placement 247–262 51–53 98–100 clinical evidence 60–65, 61–65 socket preservation therapy bone quality 251 composite grafts 117–125, conventional guided implant 95–97, 95 118–125 socket related pathology 89–93, placement 248–254 diagnostic skills and tools 72–75, pre‐surgical and virtual planning 89–93 72–76 Socket Repair Kit 114–117, 248–253, 250, 252 dropped facial contours 71–72, 71 surgical procedure 253–254, facial recession 71 114–117 fitted autogenous bone veneers socket trauma 82–83, 82–86 253–255 treatment benefits in the esthetic cumulative survival rates in 100–105, 100–105 flapless extraction surgery 49–51, zone 69–71, 69 selected studies 249 treatment complications 71–72 immediately placed and loaded 49–52, 52, 61, 62 implant morphology and design gap filling and implant labial plate of bone restoration implants 254, 255 introduction 247–248 coronoapical positioning 79–81, 80–82 model casts 256–258, 257 55–60, 56–59, 57, 58 restorative space 278–280, post‐extractive guided implant guided implant placement 254, 255 278, 287 placement 255–259 guided tissue regeneration see also implant surface pre‐surgical and virtual 110–114, 110–113 implant positioning implant fixture diameter 79–81, accuracy of implant planning 256–258, 256, 257 80–82 surgical procedure 258–259, improved esthetics 70–71, 70 positioning 78 introduction 69 accuracy of surgical guide 258–259 jumping gap and implant software development and surface 53, 54–55 276–277, 277 labial plate of bone axial positioning 286–288, products 248 restoration 69–135 three‐dimensional diagnostic level of technical skill 76–77, 286–287 76–78 buccolingual implant positioning imaging 248, 251, 252 loading protocol 88–89, 88 Guidor® Matrix Barrier 113 monocortical allografts 106, 51–53 106–110 computerized navigation surgery h nature of the labial plate of bone 78–79, 79 277–278 HA see hydroxyapatite novel concepts to treat defective gap filling and coronoapical hemorrhage 306–307 labial plate of bone 98–125, high‐performance polymeric 98–125 positioning 55–60, 56–59, patient expectations/ 57, 58 restorations 6–7 satisfaction 70 grip 276 horizontal ridge defect 206, 211, implant angulation 282–286, 282–285, 289–291 213, 216, 236–237 implant morphology and design hydroxyapatite (HA) 278–280, 278 mesiodistal position 281–282, immediately placed and loaded 281, 283, 288–289, 293 implants 96, 114 restorative space 279–280 treatment complications and failures 334 hyperalgesia 307
peri‐implant tissue stability International Team of Implantology Index 363 148–149, 148 (ITI) 255 improved esthetics 70–71, 70 positioning devices 277 IPS e‐max PRESS 7 introduction 69 rationale 280–288, 281–287 irradiated cancellous allograft level of technical skill 76–77, restorative space 263, 276–288 sharpness of cutting flutes of (ICA) 96 76–78 ISQ see Implant Stability Quotient loading protocol 88–89, 88 drills 277 iTeroTM 9 monocortical allografts 106, treatment complications and ITI see International Team of 106–110 failures 306 Implantology nature of the labial plate of treatment of malposed implants j bone 78–79, 79 288–296, 288–296 novel concepts to treat defective Implant Stability Quotient (ISQ) jumping gap 53, 54–55 labial plate of bone 98–125, 86–87 k 98–125 Implant Studio® 8 patient expectations/ implant‐supported restorations keratinized soft tissue satisfaction 70 guided bone regeneration 198, peri‐implant tissue stability 140– 40, 42 199, 225–227, 237–238 141, 141, 149, 162–164, 169 implant surface immediately placed and loaded poor esthetics and tissue implants 83, 86, 101, 107, discoloration 72, 72 immediately placed and loaded 109, 117–123, 119–122, reasons for inconsistent outcome implants 53, 54–55 125–126 with immediate implant modern trends in esthetic implant placement 72–83 peri‐implant tissue stability therapy 10–12 reduction of treatment time 70 149–150, 150, 156, 156 peri‐implant tissue stability risk assessment and classification 142–143, 144, 147, 152–153, 93–95 restorative space 279–280 165, 167, 169, 181–183 risk factors 82–83, 82–84 impressions restorative space 291, 292, 294 socket morphology classification treatment complications and 98–100 guided bone regeneration 208 failures 309–311, 310, 312, socket preservation therapy guided implant placement 254 315, 318, 322, 346 95–97, 95 modern trends in esthetic implant socket related pathology 89–93, l 89–93 therapy 14 Socket Repair Kit 114–117, infections labial plate of bone 114–117 accuracy of implant socket trauma 82–83, 82–86 guided bone regeneration 228 positioning 78 treatment benefits of immediate labial plate of bone restoration arbitrary flapless implant fixture implant placement in the installation 84–95, 86–95 esthetic zone 69–71, 69 89–93, 89–93 block autografts 74, 80, 98–100 treatment complications with peri‐implant tissue stability 149 composite grafts 117–125, immediate implant treatment complications and 118–125 placement 71–72 conclusion and recommendations labial profiles 82 failures 313–317, 320–321, 126, 126–128 labial tissue volume 157–164, 320, 331, 332, 334, 337–338 diagnostic skills and tools 72–75, 158–163 inferior alveolar nerve 307 72–76 labiopalatal positioning 283–285 inflammation dropped facial contours 71–72, 71 lamellar bone sheet 162–163, guided bone regeneration 228, facial recession 71 162, 174 231–232 fitted autogenous bone veneers laser surgery 9–10 peri‐implant tissue stability 100–105, 100–105 lingual bone plates (LBP) 49–51, 144, 149 guided tissue regeneration 49–50 treatment complications and failures 110–114, 110–113 lingual nerve 307 302–305, 309–310, 347 immediately placed and loaded lip augmentation therapy 40, 40 insurance 21 implants 69–135 lips 37–40, 38–40 intercommissure line (ICL) implant fixture diameter 79–81, lithium disilicate crown 205, 218 34–35, 35 80–82 loading protocol 88–89, 88 interdental papilla 12–13, 145 interim restorations adhesive bridges 15 modern trends in esthetic implant therapy 13–15 removable partial dentures 14 using or modifying an existing prosthesis 14
364 Index restorative space 292 optimizing deficient horizontal treatment complications and space 266–269, 268–269 m failures 319, 321, 323, 332 optimizing vertical space malocclusion 83 Morse Cone connection implant 57, insufficiency 269–273, mandibular fracture 305 270–273 mandibular ramus 161–162 60, 61 mandibular symphysis 161–162 mucoperiosteal flap rapid extrusion movement 270 material exposure 238–239 screw‐retained abutments maxillary canines 44, 44 guided bone regeneration 199–201 maxillary central incisor 41–43 immediately placed and loaded 273, 273 maxillary/mandibular smile orthopantomography (OPG) 250 implants 80, 82, 91–92, 96, osseoconductive grafting classification 30, 31 101, 124 maxillary sinusitis 294 peri‐implant tissue stability material 91 maxillary sinus membrane 145–146, 162 osseous crest management 275, 275 treatment complications and ostectomy 274 perforation 294 failures 311, 311, 317–318, osteoblasts 308, 348 maxillofacial trauma 82–83, 82–86 317–318, 330, 332–333 osteoclasts 146, 150, 308, 329 mental nerve 307 osteoconductive materials 335–336 mesiodistal position 281–282, 281, n osteocytes 308 osteoid matrix (OM) 56 283, 288–289, 293 nanomodified implant surfaces osteoperiosteal flap (OPF) 186 microrough implant surfaces 54–55, 54–55 osteoplasty 274 osteoprogenitor cells 144–145, 308 150, 150, 156, 156, 279–280 narrow diameter implants (NDI) osteoradionecrosis 343 microsurgery 9 266, 267 overdentures 302, 306 mid‐crestal incision 198, 199 overeruption 265, 265, 274 miniscrew implants 271–272, 272 NaviENT & Micron Tracker 9 model casts 256–258, 257 navigation systems 9 p modern trends in esthetic implant NDI see narrow diameter implants necrotic tissue pain 307 therapy 1–25 palatal flap 201 3D planning with CAD/CAM necrotic bone 317, 320 palatal rotational flap 81 peri‐implant tissue stability 179 papilla height measurement 3 2–4, 6–7 treatment complications and paresthesia 307 CO2 laser 9–10 particulated bone graft computer‐assisted surgery 6–8 failures 310, 315–316, current context 4–10 316, 324 guided bone regeneration digital impression systems 8–9 neurological complications 239 233–234, 236–237 digital scanning technologies 8 neurosensory alterations 307–308 historical context 2–4 NobelClinicianTM 8 immediately placed and loaded innovative prosthetic implants 75, 83, 84–85, 107, o 109, 124 materials 6–7 interim restorations 13–15 occlusion 83 peri‐implant tissue stability 161, microsurgery 9 OM see osteoid matrix 164, 172–173, 175, 181 navigation systems 9 onlay autogenous grafts 178–180, patient expectations/satisfaction restorative space 294 180–183 treatment complications and 18–21 OPF see osteoperiosteal flap patient records 15–16, 16–17 OPG see orthopantomography failures 328, 348–349, peri‐implant soft tissue optimal particulated mix (OPM) 348–349 patient–clinician relationship 18–19 optimization 10–11 348, 348 patient expectations/satisfaction predictability of esthetic implant oral hygiene extraoral clinical outcomes 29, 42–43 therapy 1–2 peri‐implant tissue stability 149, financial resolution 20–21 soft‐tissue bio‐characterization and 152–153 hazardous effects of poor dental practice 19–20 influence 11–13 treatment complications and immediately placed and loaded team members and collaboration failures 301–302, 305 implants 70, 86 modern trends in esthetic implant 16–17 orthodontics therapy 18–21 monocortical bone graft deficient vertical space 271–272, 272 immediately placed and loaded excessive vertical space implants 76, 106, 106–110 269–271, 271 extraoral clinical outcomes 46 peri‐implant tissue stability 162, 171, 180
patient–clinician relationship prevalence of implant related tissue Index 365 18–19 migration 138–139 personality 43–44, 44 restorative space 263 provisional and prosthetic design philtrum 38 patient records 15–16, 16–17 150–151, 151–152 phonetic analysis 34, 37 PDGF see platelet‐derived growth photodynamic therapy 9–10 recession scoring template piezoelectric surgery 102 factor 154–155, 155, 175–176, piezosurgery 180 PDL see periodontal ligament 184–185 pigmentation 10 PDLLA see poly‐D‐lactic, L‐lactic plaque regenerative techniques 147, 147 acid scalloping 139, 140, 141, peri‐implant tissue stability 153 pedicled periosteal flap 200–201 treatment complications and periapical infection 89–93, 89–93 143–144, 143 pericardium collagen membrane six years follow‐up showing failures 301, 305, 313 platelet‐derived growth factor 231–232 gingival recession 139 peri‐implantitis 293, 302–305, staged/non‐staged surgical (PDGF) 117 platelet‐rich plasma (PRP) 336 303–304 approach 143–144 platform‐switched implants peri‐implant mucositis 303–305, 303 technical factors 137–138, peri‐implant tissue stability 137–195 157, 158 148–153, 148, 150–152 PLGA see poly‐L‐lactic‐co‐glycolide chronological follow‐up for apical teeth morphologies 152, 152 tissue migration over three tissue phenotype 137–139, acid years 138 PLLA see poly‐L‐lactic acid 141–144, 141–144, 157–158 PMN see polymorphonuclear classification of implant‐related treatment of implant‐related gingival recession 153–154, leukocytes 153–154, 154 gingival recession 155–186 pneumatized left maxillary class I recession 165–169, conclusion and sinus 227 recommendations 187 165–169 pocketing 82, 88, 303 class II recession 169–178, poly‐D‐lactic, L‐lactic acid (PDLLA) factors leading to implant‐related gingival recession 137–138, 170–177, 178–179, 179–180 membranes 139–153 class III recession 178–186, immediately placed and loaded immediate implant placement and 180–186 implants 85, 111–117, 111, alveolar bone remodeling innovative implant‐related 113–117 146–147 peri‐implant tissue stability 160, designs 155–157, 156 172–173, 175, 181 immediately placed and loaded preventive treatment options treatment complications and implants 62–65, 64 failures 328, 349 155–165, 156, 158–164 poly‐L‐lactic acid (PLLA) membranes implant collar design subcrestal implant 110–114 149–150, 150 poly‐L‐lactic‐co‐glycolide acid placement 165 (PLGA) membranes implant positioning errors thickness doubling of labial tissue 110–114 148–149, 148 polymorphonuclear leukocytes volume 157–164, 158–163 (PMN) 11 interproximal recession 139 see also treatment complications positioning devices 277 introduction 137–138 preliminary orthopantomography labial plate of bone 140–141, and failures (OPG) 250 periodontal disease 90 Prettau® 6 141, 149 periodontal ligament (PDL) 50–51, provisional restorations see interim mid‐facial recession 139 restorations modern trends in esthetic implant 77, 282 PRP see platelet‐rich plasma periodontitis 11, 91–95 therapy 10–11 periodontium r muscle pull at frenum/ modern trends in esthetic implant radiography frenectomy 147–148, therapy 11–13 guided bone regeneration 215, 147–148 218, 220, 226–228 one year follow‐up showing peri‐implant tissue stability guided implant placement 250, gingival recession 137 141, 152 254–255, 256, 259 oral hygiene 149, 152–153 periodontium 141, 152 restorative space 281 periosteum 144–146, 145 periosteum physiologic factors 137, 140–147, 141–145, 147 immediately placed and loaded implants 50 peri‐implant tissue stability 144–146, 145 treatment complications and failures 308, 311
366 Index horizontal space component Schneiderian membrane 306 264–265, 264 screw loosening 279, 291, 302 radiography (cont’d) screw‐retained abutments 264, 273, immediately placed and loaded vertical space component implants 61, 63, 65, 72, 265, 265 273, 285–286 72–73, 91, 93–94, 102, SCTG see subepithelial connective 116–117, 119 optimizing deficient horizontal modern trends in esthetic implant space 265–269 tissue grafts therapy 3–4 SDA see solvent‐dehydrated allograft peri‐implant tissue stability enameloplasty/coronoplasty segmental osteotomy 292 163–164, 174, 176, 185 265, 266 SGS see Straumann Guided Surgery restorative space 267–269, 281, Sharpey’s fibers 141 283, 288 narrow diameter implants sinus grafting 227–228 treatment complications and 266, 267 sinus tract fistula 228 failures 304, 307–308, 324, slightly palatal incision 198–199, 199 329–331, 334 orthodontic movement slightly vestibular incision 199, 199 266–269, 268–269 smile arc 35–36, 35–36 ramus block bone grafting (RBG) 147 smile design 32–34, 32–33 rapid extrusion movement 270 optimizing vertical space smile landmarks 34–37 RBG see ramus block bone grafting insufficiency 269–276 smile line 31 recession scoring template 154–155, smile pattern 30–32, 30–31 crown lengthening 273–275, smoking 294, 302, 302, 305, 155, 175–176, 184–185 273–275 recombinant human platelet‐derived 309, 314 distraction osteogenesis social smile 30 growth factor (rhPDGF) 312 275–276 socket morphology classification removable partial dentures 14 residual cement 144, 304 orthodontic management 98–100 residual gap (RG) 58–60 269–273, 270–273 socket preservation therapy residual graft particles (RGP) 56 resin cements 144 osseous crest management 95–97, 95 Resolut® 113–114 275, 275 Socket Repair Kit 114–117, restorative crowns 61–65, 62–63 restorative space 263–300 treatment complications and 114–117 failures 347, 347–348 socket trauma 82–83, 82–86 assessment and management of soft tissue stability see peri‐implant restorative space 263 retrograde peri‐implantitis 293 reverse buttress thread 279 tissue stability implant positioning 263, 276–288 RG see residual gap soft tissue thinning 322, 322–323 accuracy of surgical guide RGP see residual graft particles solvent‐dehydrated allograft 276–277, 277 rhPDGF see recombinant human axial positioning 286–288, (SDA) 96 286–287 platelet‐derived growth factor split‐thickness envelope computerized navigation surgery Ricketts E‐plane 38 277–278 ridge‐lap design 284 technique 63 grip 276 root avulsion 83 Steiner S line 38 implant angulation 282–286, root‐form implants 279–280 Straumann® Guided Surgery (SGS) 282–285, 289–291 rotated palatal pedicle flap 85 implant morphology and rotated palatal subepithelial system 7–8 design 278–280, 278 subcrestal implant placement 165 mesiodistal position 281–282, connective tissue graft subepithelial connective tissue grafts 281, 283, 288–289, 293 (RPSCTG) 318 positioning devices 277 rule of thirds 46 (SCTG) 157–160, 159–160, rationale 280–288, 281–287 rupture of the Schneiderian 166–169, 167–178, 171–177 sharpness of cutting flutes of membrane 306 subepithelial pedicle connective drills 277 tissue graft 107 treatment of malposed implants s supernumerary teeth 4 288–296, 288–296 surface hydrophilicity 151 sandwich osteotomy symmetry 44–46, 45–46 loss of restorative space peri‐implant tissue stability synthetic bone grafts 55–56 263–264, 264 180–186, 183–186 restorative space 292, 293 t magnitude of restorative space scalloping TCP see tricalcium phosphate modern trends in esthetic implant teeth morphology therapy 3, 12–13 peri‐implant tissue stability 139, age 41–43, 41–42 140, 141, 143–144, 143, 158 restorative space 281 scar tissue 310, 310, 311
extraoral clinical outcomes inconsistent regenerative outcome Index 367 40–44, 41–44 and questionable osteoinduction 329–333, vertical crestal bone resorption gender 43, 43 330–334 (VCBR) 56, 57, 58, 60 personality 43–44, 44 tetracycline slurry 123, 124, 171 infections 313–317, 320–321, vertical releasing incisions 199 thread depth/geometry 279 320, 331, 332, 334, 337–338 vertical ridge defect 211, 213, 216, three‐dimensional (3D) diagnostic introduction 301–305 226, 236–237 imaging 248, 251, 252 neurosensory alterations 307–308 vestibular reveal 36–37, 36–37 three‐dimensional (3D) ridge defect peri‐implantitis and peri‐implant vestibuloplasty 181 virtual planning 209, 213, 216, 223, 227 mucositis 302–305, 303–304 tissue discoloration 72, 72, 81 predictability of regenerative conventional guided implant tissue phenotype 137–139, 141–144, placement 248–253, 250, 252 materials and techniques 141–144, 157–158 308–349 post‐extractive guided implant titanium mesh 336–338, predictable guidelines for placement 256–258, 256, 257 regenerative procedure 337–338 338–349 Vita ENAMIC® 6–7 titanium‐reinforced d‐PTFE identifying the nature of the V thread 279 defect 338–340, 339–340 membrane 202, 211, 223, optimal soft tissue management w 226–227, 230, 239 and closure 346, 347 tooth loss 29, 29, 38 predicting the host response wound dehiscence treatment complications and failures 340–345, 340–341, 345–346 allografts 328, 332–333 301–358 selection of regenerative alloplasts 335, 337–338, 337–338 allografts 327–333, 328–334 approach and material autografts 322, 322–323 alloplasts 334–336, 334–338 348–349, 348–349 etiology of bone grafting anatomical related treatment stability and space making for complications 309–318, 312, complications 306–308 graft material 347, 347–348 314, 316–318 autografts 318–325, 319–327, prevalence of implant‐related guided bone regeneration 206, 348–349, 348–349 treatment complications 209, 236–239 autologous bone grafts 318–325, 305–306 prevalence of implant‐related 319–327 recipient site complications treatment complications 306 bone graft fracture 323–325, 320–325, 320–327 323–327 restorative space 293–296, wound sloughing bone graft remodeling and 293–296 etiology of bone grafting resorption 321, 321 risk factors 301–302 complications 313, 316, classification and terminology rupture of the Schneiderian 320–322 302–305, 303–304 membrane 306 papillary sloughing 199 donor site complications 320 soft tissue thinning 322, 322–323 smoking 302, 309 etiology of bone grafting titanium mesh 336–338, 337–338 suture rupture 338 complications 309–318 treatment plan 21, 29 influential factors to wound tricalcium phosphate (TCP) 334, 336 x healing 314–317, 314–316 v xenogenic cortical bone barrier 233 management of mucoperiosteal xenograft flap dehiscence 317–318, VBL see vertical bone level 317–318 VCBR see vertical crestal bone guided bone regeneration soft tissue influence on 235–237 regenerative therapy outcome resorption 309–314, 309–314 vertical bone level (VBL) 57–58, peri‐implant tissue stability 162, hemorrhage 306–307 164, 174, 186 57, 58, 60 treatment complications and failures 348 z zirconia coping 63, 64 zirconia restorations 6
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