5.1 Introduction
Over the past few years, all aspects of dentistry have undergone inspiration a advancements in the way that clinicians are not only required to treat disease and improve function but also to cope with the ever‐ increasing esthetic demands of their patients. To date, successful restorative dentistry can be best accom- plished only when long term healthy and stable tissues surround either the natural teeth or their implant replacements.Therefore, accurate attention to both soft and hard tissue status around the natural teeth and implants before, during, and after the restorative proce- dures will not only enhance the treatment outcome but also minimize treatment complications. Implant retreated esthetics should involve a sold scientific base in its application, not only experience. All the different therapeutic modalities in the esthetic zone should be based on solid scientific research and clinical trials.
Achieving an esthetic outcome is always a new chal- lenge to the clinician. The key points controlling the esthetic outcome include: the presence of healthy proxi- mal papillae, an intact gingival form, and intact osseous architecture, while tissue phenotype influences not only the clinical result but also its longevity. Understanding the biological, microbiological, and physiological responses of the peri‐implant tissues is an absolute prerequisite, and the peri‐implant esthetic outcome is mainly determined by the patient’s presented anatomical condition and the clinician’s abilities. A thorough understanding of the anatomy of the supporting structures is essential for a correct diagnosis and treatment planning. For natural teeth, it has been estimated that over 60% of the popula- tion has at least one buccal recession defect and such defects are predominately seen in patients with good oral hygiene; in the USA, 23% of adults have one or more tooth surfaces with ≥3 mm gingival recession (Chan, Chun and MacEachern 2015) (see Figure 5.1a and b).
The biologic width around a natural tooth and a dental implant differ, in height, histology, and vascularity. Histologically, there are more collagen fibers running parallel to the implant surface, so it is similar to mucosal scar tissue with a weak adherence around dental implant collars, which can make corrective procedures unpredictable and bacterial invasion greater and rapid. Peri‐implant tissue stability in the esthetic zone helps pro- vide and sustain long-term treatment success and depends on many factors that include: tissue phenotype, labial plate of bone thickness, alveolar crest height, prosthetic mar- gins design, and other physiologic factors. Implant‐related gingival stability can be influenced by many physiologic, anatomic or technical factors (Araujo and Lindhe 2005; Gracco et al. 2009; Yu, Ji and Shen 2009).
Other technical factors might affect peri‐implant tissue stability such as the diameter of the implant used, the use of provisional restorations, the placement and timing of the final restoration delivery, and a lack of clinical experi- ence. Buser et al. (2004) indicated that the use of wide diameter implants in the anterior zone induced labial plate bone resorption. Saadoun (2007) reported that soft tissue recession around a wide‐diameter implant (≥5 mm) averaged 1.58 mm compared with 0.57 mm around a standard‐diameter implant (<5 mm). It may be prudent to use standard‐diameter implants in the esthetic zone.
Another contributing factor is implant position within the alveolar ridge and the time allowed for peri‐implant tissue maturation (Kinsel and Capoferri 2008).
Gingival recession around natural teeth is defined as present when the location of the gingival margin is apical to the cemento‐enamel junction (Peridontology AAP). A pre‐clinical study (Baker and Seymour 1976) inducing gingival recession by replacing rat incisors with acrylic resin implants suggested that gingival recession is generally associated with (1) local inflammation characterized by mononuclear cells, (2) breakdown of connective tissue, and (3) proliferation of the oral and junctional epithelium into the site of connective tissue destruction. Other precipitating fac- tors include traumatic forces (e.g. excessive brushing), habits (e.g., smoking, oral piercing), and plaque‐ induced inflammation (Chan et al. 2015).
According to various systematic reviews, single implant‐supported restoration is predictable and suc- cessful following conventional implant surgery (Berglundh et al. 2002; Creugers et al. 2000; Jung et al. 2008). However, data on clinical response and param- eters about response to trauma, prevalence implant related treatment complications, and bone remodeling rate may be considered limited. Various attempts have been made to evaluate the biologic scope of osseointe- grated implants. Kan et al. (2009) clinically evaluated the dimensions of the peri‐implant mucosa around two‐stage maxillary anterior single implants in humans after one year of function and the influence of the peri‐implant phenotype was also examined. It was concluded that the mean facial dimension of peri‐ implant mucosa of two‐stage implants is slightly greater than the average dimension of that of the dentogingival complex. The level of the interproximal papilla of the implant is independent of the proximal bone level next to the implant but is related to the interproximal bone level next to the adjacent teeth. Greater peri‐implant mucosal dimensions were noted in the presence of a thick peri‐implant phenotype com- pared with a thin phenotype.
Kan et al. (2011) evaluated 35 patients, clinically and radiographically at presurgical examination, immedi- ately after immediate implant placement, and at provi- sionalization, and recordings were made at oneyear after implant surgery and at the latest follow‐up appointment. All implants retained their function. At the follow‐up appointment, the mean mesial and distal marginal bone level changes were significantly greater than those observed at oneyear. At follow‐up, the mean mesial and distal papilla (DP) level changes were significantly smaller than those observed at oneyear, whereas the mean facial gingival level change was significantly greater than that observed at oneyear. Sites with a thick gingival phenotype exhibited significantly minor changes on the facial gingival levels than sites with a thin gingival phe- notype at both the appointments, with mean mid‐facial recession being 1.13 mm. These findings were also con- firmed from the work of Canullo and Rasperini (2007), who evaluated the soft tissue response to platform‐ switched implants after a mean of 22 months follow‐up in a case series. During the follow‐up period, the papil- lary level increased, with a mean value of 0.25 mm.
Thus, an intact facial bone wall thickness seems valu- able for any successful esthetic procedure as it has a direct relationship to mid‐facial recession (Kan et al. 2007). In a review article, Chen and Buser (2009) con- cluded that advanced mid‐facial recession is common following immediate implant treatment. Other studies showed an advanced mid‐facial recession occurred in <10% of the implants (Canullo, Iurlaro and Iannello 2009; Cosyn et al. 2012a, b; Raes et al. 2011).
Mean interproximal recession was frequently reported (11/13) and was low (<1 mm), suggesting a limited risk for advanced interproximal recession. In one study some tissue gain was observed (Canullo and Rasperini 2007). Lops et al. (2008) studied the interproximal recession with complete fill in nearly 70% of the cases; however, the changes in papilla height over time were found to be comparable for patients with a thick‐ and thin‐scalloped gingival phenotype (Kan et al. 2011). Canullo et al. (2009) demonstrated significantly less prevalent inter- proximal recession for implants with a conical connec- tion and platform switch when compared with implants with a flat‐to‐flat connection and without abutment diameter reduction.
De Rouck, Collys and Cosyn (2008) recorded on average 0.75 mm of advanced mid-facial recession and Cordaro, Torsello and Roccuzzo (2009), found advanced mid‐facial recession in 38% and 85% of the patients with a thick‐ and thin‐scalloped gingival phenotype, respectively. Tortamano et al. (2010) suggested that the need for socket grafting might limit the amount of mid‐facial recession.
Small and Tarnow (2000) evaluated 63 implants in 11 patients. Baseline measurements were recorded at stage 2 surgery in two‐stage implant systems and at stage 1 surgery in the one‐stage system. Subsequent measurements were recorded at one week, one month, three months, six months, nine months, and one year after baseline meas- urements. The majority of the recessions occurred within the first three months, with 80% of all sites. It is therefore recommended that there should be a wait of three months for the tissue to stabilize before either selecting a final abut- ment or making a final impression.
In a systematic search by Cosyn et al. (2012a) it was concluded that the average interproximal tissue reces- sion was 1 mm (less than 10% of the cases), suggesting that the risk of interproximal tissue drop and mid-facial recession is unlikely to occur, especially in patients with intact labial plate of bone, with thick overlaying soft tissues. (See Figure 5.3a and b).
The preservation or reproduction of a healthy and sta- ble mucogingival architecture surrounding dental implants placed in the anterior maxilla present estheti- cal challenges for the clinician that may arise for several reasons: the loss of soft tissue volume at the site, poor soft tissue quality at the site, and pre-existing bone loss after regular tooth extraction. While surgical recon- structive procedures have been proposed for the improvement of hard and soft tissue defects prior to implant placement, the preservation of appropriate soft tissue architecture around integrated implants remains challenging (Benic et al. 2012; Buser et al. 2004; Lang and Zitzmann 2012).
Factors that lead to implant related gingival recession can be classified as: physiological factors, which involve factors that influence recession via regular biologic pro- cesses, such as bone remodeling rate, tissue phenotype, and the influence of the thickness of the labial plate of bone; and technical factors, which deal with any techni- cal errors that occur such as the use of wide implants, poor implant position, premature delivery of the final prosthetics, failing to use provisional restoration, and excessive cement located in the gingival sulcus around dental implants (see Figure 5.4).
It is commonly agreed that areas with less than 2 mm of attached gingiva and decreased buccolingual thickness are at a higher risk of recession (Lang and Zitzmann 2012).
Peri‐implant tissue examination for mucogingival prob- lems should therefore include assessment of the presence of local inflammation, the gingival thickness and the ves- tibular depth (Hall 1984). The clinician can also use a simple “tension test” (Vincent, Machen and Levin 1984), which involves pulling the cheeks or lips away from the teeth to assess whether there is adequate attached tissue. In areas of inadequate attached tissue there will be move- ment or blanching of the gingival margin.
Facial bone thickness is considered a crucial parameter for treatment planning decisions and predicting tissue stabil- ity in the anterior esthetic area. No consensus has yet been reached regarding the amount of buccal bone thickness that is needed when placing an implant to ensure a long- term satisfactory biologic and esthetic outcome, but there are still certain guidelines that are proposed. Grunder, Gracis and Capelli (2005) emphasized the presence of an adequate facial bone thickness to ensure long‐term peri‐ implant tissue stability. The buccal bone plate, especially in the anterior region, has been described as significantly thinner compared to the lingual and palatal components in animal and human studies (Buser et al. 2008; Hämmerle, Chen and Wilson 2004), probably making them more frag- ile and more easily resorbed. A study by Fu, Lee and Wang (2011) found a mean facial bone thickness of 0.83 mm (range, 0.3–1.60 mm) at 2 mm below the bone crest. Braut et al. (2012) found a mean bone thickness of 0.5 mm (range, 0–2.1 mm) at 4 mm apical from the CEJ and 0.6 mm (range, 0–2.8 mm) at the middle of the root. A similar study by Januário, Duarte and Barriviera (2011) on 250 subjects, found a mean bone thickness for the central and lateral incisors and canines of 0.6 (60.3) mm, 0.7 (60.3) mm, and 0.6 (60.3) mm, respectively, at 1 mm apical to the bone crest and of 0.6 (60.4) mm, 0.7 (60.4) mm, and 0.6 (60.4) mm at 3 mm apical to the bone crest. The mean overall thickness varied within 0.5 (60.4) mm and 0.7 (60.4) mm. A study by Huynh‐Ba et al. (2016) in a sample of 93 sites showed a mean buccal bone thickness of 0.8 mm (range, 0.5–2 mm) for the maxillary anterior sites (canine to canine); 87.2% of the buccal bony walls had a width > 1 mm and only 2.6% of the walls were 2 mm wide. They postu- lated that a mean bone wall thickness for the anterior max- illary teeth at 4 mm apical to the CEJ of 1.19 mm (range, 0.30–3.30 mm) had a total of 43.3% with >1 mm of bone thickness and 0.82 mm (range, 0.20–1.60 mm) at the mid‐ point of the root had a total of 76.6% with <1 mm of bone thickness. For the mandibular teeth, the mean was 1.31 mm (range, 0.30–5.20 mm) with a total of 63.3% with >1 mm of bone thickness and 0.80 mm (range, 0.00–1.80 mm) with a total of 75.5% with <1 mm of bone thickness, respectively. The mean bone thickness at the apical area of the root was 1.80 mm (range, 0.20–3.60 mm) for the maxillary teeth and 3.78 mm (range, 0.00–7.90 mm) for the mandibular teeth.
Fuentes et al. (2015) have studied the anatomical dimensions of the buccal bone walls of the esthetic max- illary region for immediate implant placement, based upon cone‐beam computed tomography (CBCT) scans in a sample of adult patients. They analyzed a sample of 50 CBCT scans, and concluded that less than 10% of sites showed more than a 2‐mm thickness of the buccal bone wall, with the exception of the central incisor region, in which 14.4% of cases were≥ 2 mm.
Le and Farahani (2012), who explored the relationship between the labial bone thickness (ILBT) and crestal labial soft tissue thickness for an implant, suggest that crestal labial soft tissue thickness around implants is sig- nificantly associated with the labial bone thickness in the anterior maxillary region. In other words, they concluded a direct relationship showing that the thicker the bone, the thicker the crestal labial soft tissue thickness around implants and vice versa. Kheur et al. (2015), suggested that there is a positive correlation between the labial and pala- tal bone and soft tissue thickness; and between the labial bone thickness and the labio‐palatal socket thickness. No correlation was seen between the labial bone thickness and the labio‐palatal tooth position. They also suggested that a minimum 2 mm thickness of bone is necessary to provide support to the supracrestal soft tissue, and that an accurate analysis with CBCT imaging before extraction is necessary for immediate implant placement. Wildermanm and Wentz (1965) and Pennel et al. (1967) histologically demonstrated a relationship between bone exposure and bone resorption in thin plates. Qahash, Susuin and Poolimeni (2008) demonstrated a correlation between the width of the buccal alveolar ridge and the extent of bone resorption using incandescent and fluorescent light microscopy analysis. They suggested that the width of the buccal alveolar ridge should be at least 2 mm to maintain the alveolar bone level, and the thicker lingual bone plate provided a larger wound space that was correlated to enhanced bone regeneration, whereas implants placed closer to the buccal plate were associated with increased crestal bone loss. If after implantation the buccal site thickness is less than 2 mm, vertical bone resorption is likely to occur (see Figures 5.5a, b and 5.6a, b).
5.3.2.2 Influence of Tissue Phenotype
Tissue phenotype is considered a major influencer in the overall prediction of the fate of an immediate implant placement procedure in the esthetic zone. It predicts to a great extent the future liability for implant related tissue migration and the overall possible tissue stability, so the clinician should identify the tissue phenotype prior to the start of the treatment, and identify the potential risks involved.
In tissue phenotype; the thin tissue seems to recede more often in response to inflammation and tissue manipulation. Gingival recessions confirm the relevance of an inflammatory infiltrate in the pathogenesis (Smukler and Landsberg 1984). In thin phenotype gingi- val recessions around natural teeth, the epithelium is acanthotic and proliferative and surrounded by an inflammatory infiltrate. In addition, necrotic cells can be found. Occasionally the dentogingival epithelium penetrates into the lamina propria, thereby decreasing the width of the lamina propria and allowing the den- togingival and oral epithelia to coalesce, resulting in loss of attachment to the tooth. The inflammatory infiltrate can span the entire thickness of the width of the gingiva thus promoting a further recession. In thicker gingiva, connective tissue free of inflammatory infiltrate may be interposed between the oral and junctional epithelia, preventing a recession (Baker and Spedding 2002; Miller 1985). Baldi et al. (1999) and Hwang and Wang (2006) stated that initial gingival thickness predicts the outcome of any root coverage procedures or any restorative treatments around natural teeth.
Claffey and Shanley (1986) defined the thin pheno- type as having a gingival thickness ≤ 1.5 mm, and the thick as ≥ 2 mm or more. Clinical identification is impor- tant for better determination of the treatment outcome. Hirschfield (1923) was one of the earliest periodontists to comment on the relationships between alveolar anatomy and gingival form, noting that a thin alveolar contour was probably covered by a similar gingival form. It has been suggested that a direct correlation exists between gingival phenotype and the susceptibility to gingival recession following surgical and restorative procedures (see Figure 5.7). According to Evans and Chen (2008), the likelihood of gingival recession increases in patients with thin phenotypes present in immediate single implant‐supported restorations. It is widely accepted that some gingival/periodontal prob- lems are more likely to occur in patients with a thin phenotype. A 1991 animal study by Berglundh and colleagues concluded that thin gingival tissue can lead to marginal bone loss during formation of the peri‐ implant biologic width. Another study by Hwang and Wang (2006) reported that implant sites with thin mucosa were prone to angular bone defects, while stable crestal bone was maintained in implants surrounded by thick mucosa. According to Abrahamsson et al. (1998), thick tissues (i.e. ≥2.5 mm) can avoid significant crestal bone recession.
Fickl et al. (2008), in an interesting study that fully explained the reasons for the harmful effect of thin tissue phenotypes, stated that the thin periodontal phenotypes have an inherent osteoclastic activity that is signaled by any stimulus such as flap reflection; thus, osteoclastic activities occur at the internal and external sides and merge together, leading to a more pronounced loss of the buccal bone plate. Consequently, when the buccal bone plate is resorbed, the soft tissue complex can no longer be stabilized and will collapse into the newly formed defective space. As the buccal soft tissue occupies the place of the former buccal resorbed bone plate, the room for bone regeneration is reduced, leading to the observed major bucco-oral shrinkage, which is why serious esthetic changes in bone and mucosal anatomy may result after extraction in patients with thin‐scalloped profiles.
Patients with a thick phenotype that consists of flat soft tissue form and a thick bony architecture are often found to be prevalent in the population. This type of tissue form, according to Kao, Fagan and Conte (2008), is dense and fibrotic with a large zone of attachment, thus making it more resistant to gingival recession (see Figure 5.8a and b).
In contrast, thin gingival tissue tends to be delicate and almost translucent in appearance. The tissue appears friable with a minimal zone of attached gingiva. The soft tissue is highly accentuated and often sugges- tive of thin or minimal bone over the labial roots. Hwang and Wang (2006) documented that patients with a thin gingival phenotype were more likely to experience gingival recession following non‐surgical periodontal therapy. The thinner periodontal phenotype needs more attention when an extraction is carried out owing to its thin alveolar plate (Kao et al. 2008). The hard and soft tissue contouring is more predictable after surgery for a thick phenotype. The value of a thick phenotype is emphasized by its increased wound coverage and site protection, and implant stability created by a predictable seal around the implants’ collars. The thicker phenotype can resist mucosal recession, masks the restorative margins, and camouflages the titanium implant shadows. It also protects the biological seal around dental implants, thus reducing the tendency for crestal bone resorption. The amount of gingival thick- ness before regenerative surgery was found to be a predicting factor for the occurrence of further postop- erative recession. However, in a thin phenotype, the mucogingival corrective surgical procedures can enhance the quality of tissue, resulting in a more favorable treatment outcome. A thick phenotype is more resistant to recession and more accommodating to different implant positions (Kao et al. 2008; Siegenthaler et al. 2007; Small, Tarnow and Cho 2001) (see Figure 5.9). Dramatic alveolar bone resorption in the apical and lingual direction is possible in patients with a thin phenotype. The loss of peri‐implant tissues may result in facial plate loss, revealing a grayish color underneath; additional bone and soft tissue grafting surgeries may be necessary (see Figure 5.10a and b).
Patients with thick and flat gingival phenotypes exhibit short papillae whereas thin‐scalloped pheno- types have long papillae. This morphometric difference may be the cause of more papilla loss in the thin phenotype. Linkevicius et al. (2009) in their study con- cluded that the initial gingival tissue thickness at the crest may be considered as a significant predictor of mar- ginal bone stability around implants. If the tissue thick- ness is 2.0 mm or less, crestal bone up to 1.45 mm may occur, despite a supracrestal position of the implant– abutment interface. Nisapakultorn et al. (2010), in their study on 40 patients, documented a thin phenotype being significantly associated with an increased risk of facial mucosal recession (see Figure 5.11a and b).
The thicknesses of the crestal bone on the buccal aspect significantly influence the bone remodeling rate during the initial four‐month healing period after an immediate implant placement, while on the other hand, gingival thickness affects the treatment outcome possibly because of the difference in the amount of blood supply to the underlying bone and the susceptibility to resorption.
A delayed implant placement might be considered when there is not enough soft and hard tissue thick- ness (Buser et al. 1991, 1999, 2008, 2013). However, a thin gingival phenotype is associated with a thin alve- olar plate that makes the worst clinical outcome in the delayed immediate protocol; more ridge remodeling has been found in this phenotype when compared with a thick periodontal phenotype. Ridge preserva- tion was should be considered for most thin phenotype cases (Ahmad 2010). Atraumatic natural tooth extrac- tion is also necessary. It is the author’s recommenda- tion that a non‐staged surgical approach in thin phenotype patients or those with a high‐scalloped tis- sue profile should be undertaken whenever possible (whenever primary implant stability is achievable).
The reasons for this approach include: minimizing treatment time; decreasing the liability for scar tissue formation because multiple surgeries in the oral cavity will lead to further tissue shrinkage as well as scar tissue formation; and minimizing the likelihood of bone resorption after surgical intervention – in a staged approach, the main issue is the tendency for tissue to shrink, as happens whenever a surgical intervention is performed in thin tissue phenotype patients, which explains the preference of the non‐staged treatment approach. Treatment should involve augmenting both bone and soft tissue together in the same treatment session, be cause the risk by that of a staged approach; the resultant tissue shrinkage is a major drawback of a staged approach (see Figure 5.13a and b).
Different gingival phenotypes are found between dif- ferent age groups, with the thicker phenotype more prevalent in younger age groups. Vandana and Savitha (2005) showed thicker gingiva in a younger age group and stated that the decrease in keratinization and changes in the oral epithelium may be the contributing factors. Sanavi, Weisgold and Rose (1998) found that the inter‐radicular bone is more abundant and thicker in the thinner phenotype. This in turn can cause more recession (see Figure 5.14a and b).
In a thin gingival phenotype, a faulty prosthetic margin invading the peri‐implant tissue complex or extending beyond the implant collar might cause bone loss in this area. Thus, restoration going deeper into the sulcus will increase the risk of bone resorption as well as gingival recession via tissue displacement.
Residual cement also plays a role in the occurrence of implant related gingival recession specially in thin tissue phenotypes. It has been reported that excess luting cement can cause irritation to the gingival tissues leading to crestal bone loss and subsequent changes in the architecture of the soft tissue (Linkevicius et al. 2009). However, there is still no consensus about how excess cements cause tissue reactions and to what extent the excess cement contrib- utes to peri‐implantitis. Resin cements, with their high strength and non‐soluble characteristics, are hard to detect and will not be dissolved by oral or sulcular fluids. Excess resin cements at the restoration margin are a major cause for soft tissue recession and inflammation. The authors contended that the primary retention of cemented implant prosthesis is not dependent on the type of cement used but more on the adaptation and seating of the pros- thesis itself. Wilson (2009) demonstrated that suppuration or continued bleeding on probing around gingival mar- gins of implant restorations had an 81% correlation to the presence of excess cement. Therefore, trapped cement would cause constant irritation to the gingival sulcus, which might induce recession.
The periosteum is made up of three distinctive zones. Zone 1 has an average thickness of 10–20 μm consisting predominantly of osteoblasts representing 90% of the cell population, while collagen fibrils comprise 15% of the volume. The majority of cells in zone 2 are fibroblasts, with endothelial cells. Zone 3 has the highest volume of collagen fibrils and fibroblasts among all the three zones. Fibroblasts make up more than 90% of the cells in zone 3 (Reynders, Becker and Broos 1998; Mahajan 2012).
The structure of periosteum varies with age. In infants and children it is thicker, more vascular, active, and loosely attached as compared to adults, where it is thin- ner, less active, and firmly adherent (Tran Van, Vignery and Baron 1982). The periosteum has a rich vascular plexus of capillaries supplying blood to bone that reside within the cortex, linking the medullary and periosteal vessels which promote revascularization during wound healing. Studies have reported the existence of osteo- genic progenitors, similar to mesenchymal stem cells (MSCs), in the periosteum (Wang et al. 2013).
Studies have shown promising results with the use of periosteum to treat gingival recession defects (Mahajan 2010). Periosteum‐derived progenitor cells may serve as an optimal cell source for tissue engineer- ing based on their accessibility, ability to proliferate rapidly, and capability to differentiate into multiple mesenchymal lineages (Taba et al. 2005). A study by De Bari, Dell’Accio and Vanlaume (2006) indicates that periosteal progenitor cells are able to differentiate not only into bone and cartilage cells but also into adipo- cyte and skeletal myocyte cells.
Nobuto et al. (2005) have suggested a role for the periosteum in tissue healing and postoperative angio- genesis and concluded that after mucoperiosteal flap elevation, the periosteal vascularity exhibited potent blood vessel‐forming activity through various angio- genic mechanisms and through repair activity. Therefore, clinicians should minimize periosteal trauma and manip- ulation as much as possible during surgery to maintain the maximum tissue reparative capacity.
The higher bone loss rate with classic incision sites occurred when a papilla detached from bone, where the interdental bone in proximity to the adjacent tooth is denuded from the periosteum, the bone blood sup- ply can be affected (Evian, Corn and Rosenberg 1985). Therefore, excluding interproximal papillae from the mucoperiosteal flap (papillae preservative flaps) might help to minimize postoperative tissue recession (see Figures 5.15a, b and 5.16a–c).
Excessive periosteal stripping not only jeopardizes the soft tissue flap vascularity but may also lead to postoperative tissue necrosis, while incomplete muco- periosteal management can lead to improper soft tissue closure or a closure under tension. It is the author’s opinion that flapless implant placement intervention could be highly valuable (whenever indicated) to the overall treatment outcome for many obvious reasons. However, a strict protocol should be implemented that includes the mandatory use of CBCT along with a CAD/CAM surgical guide.
5.3.2.4 The Influence of the Immediate Implant Placement on Alveolar Bone Remodeling
Tooth extraction will be followed by marked change in the tissue volume of the alveolar ridge. In a clinical study, Schropp, Wenzel and Kostopoulos (2003) demonstrated that the loss of volume horizontally amounts to 5–7 mm within the first 12 months after tooth extraction. This corresponds to approximately 50% of the original width of the alveolar bone. Cardaropoli et al. (2005) and Araujo and Lindhe (2005) stated that the coronal thin part of the buccal bone wall of the extraction socket is often com- prised solely of bundle bone. The bundle bone loses its function after tooth extraction and is resorbed by osteo- clastic activity, which might affect the bone remodeling process. Additionally, most of the experimental studies utilized mucoperiosteal flaps exposing the buccal bone, which might have further detrimental effects on the resorption process occurring after tooth extraction (Araujo and Lindhe 2005; Cardaropoli et al. 2005). Araujo et al. (2006) studied the histological effects of sur- gical trauma on soft‐ and hard‐tissue remodeling and concluded that all test teeth demonstrated signs of attachment loss and bone loss.
Araujo and Lindhe (2005) stated that osteoclasts were indeed present in the exposed area of the alveolar ridge, which exhibited signs of surface resorption. Fickl et al. (2008) stated that when the buccal bone plate is resorbed, the soft tissue complex can no longer be stabilized and will collapse into the newly formed space. As the buccal soft tissue occupies the place of the former buccal bone plate, the room for bone regeneration is reduced, lead- ing to the observed major shrinkage, especially in thin phenotypes.
During the healing period, the buccal crestal bone undergoes variable degrees of resorptive and modeling changes characterized by a combination of bone fill within the original peri‐implant defect, resorption of the buccal plate of bone of approximately 50% of the original width, and approximately 1 mm loss of crestal bone height (Botticelli et al. 2004; Araujo and Lindhe 2005; Araujo et al. 2006; Sanz et al. 2015). This situation may be unstable and may predispose the mucosa to recession (Hermann, Schenk ad Schoolfield 2001). Araújo and Lindhe suggested that following tooth extraction, the blood vessels in the periodontium supplying the thin bone walls are severed, thereby causing facial bone plate resorption (Araujo and Lindhe 2005).
A study by Araujo et al. (2006) to evaluate tissue remodeling in fresh extraction sockets, showed that the buccal and lingual bone walls underwent marked surface resorption and the height of the thin buccal hard tissue wall was reduced at the end of fourweeks. As the process of healing continued and the buccal bone crest shifted further in the apical direction, the buccal crest was located >2 mm apical of the marginal border of the SLA surface at 12 weeks. Thus, it was concluded that the bone‐to‐implant contact established during the early phase of socket healing following implant installation was in part lost when the buccal bone wall underwent continued resorption.
Araujo et al. (2006) explained that the modeling in the marginal defect region was accompanied by marked attenuation of the dimensions of both the delicate buccal and the wider lingual bone walls. Bone loss at molar sites was more pronounced than at the premolar locations. Implant placement failed to preserve the hard tissue dimension of the ridge following tooth extraction. The buccal as well as the lingual bone walls were resorbed, although some marginal loss of osseointegration was also evident.
Araujo et al. (2006) demonstrated that the resorp- tion of the buccal/lingual walls of the extraction site occurred in two overlapping phases. During phase 1, the bundle bone was resorbed and replaced with woven bone. Since the crest of the buccal bone wall comprised solely bundle bone, this modeling resulted in substantial vertical reduction of the buccal crest. Phase 2 included resorption that occurred from the outer surfaces of both bone walls.
Schropp et al. (2003) reported a reduction of 50% of the width of the alveolar ridge at 12 months after tooth extraction. Hence, preservation of the alveolus at the time of extraction of prominent roots in the anterior maxilla is crucial. A study by Ferrus et al. (2010) confirmed that the position of the implant, the size of the horizontal buccal gap, and the buccal bone crest thickness significantly influenced the remodeling rate of the hard tissue during a four‐month period of healing after immediate implant placement into an extraction socket. Also, the sites where the buccal bone wall was thicker than 1 mm showed a better gap filling and minimal vertical resorption of the buccal crest when compared to sites with thinner bone (<1 mm). The possible relationship between gingival tis- sue form and the underlying bone was previously ana- lyzed by Fu et al. (2011), showing a moderate correlation between soft and hard tissues in the anterior region.
It seems that there is a need to preserve or increase the hard and soft tissue thickness using different types of interventions (Chen et al. 2009), which often might reduce and sometimes eliminate the need for subse- quent augmentation procedures. Wildermanm and Wentz (1965) when explaining histogenesis of repair, observed different healing patterns of buccal and lin- gual plates of the anterior mandibular region of dogs. A mean labial gingival recession of 0.5–1 mm around single implants, due the bone remodeling after implant surgery, seems to be a common finding after implant restorations. Also, at one year between single implant placement and the second‐stage surgery, a mean reduc- tion in facial bone thickness and facial bone height of 0.4 and 0.7 mm have been reported.
With a thorough understanding of the available litera- ture, it may be concluded that irrespective of the simul- taneous placement of dental implants in fresh extraction sites, there are variable degrees of bone remodeling that in turn influence the occurrence of implant related gingi- val recession, and apical migration of implant related tis- sues can occur due to many other variables. This warrants the clinician attention to take these facts into considera- tion when deciding upon any treatment plan that has a high esthetic demand.
5.3.2.5 Other Related Factors
Several regenerative techniques have been proposed to increase the alveolar volume both vertically and horizontally to prepare the alveolar ridge for correct placement of oral implants. Each of these grafting modalities has its own inherited remodeling rate that might be followed by soft tissue drop. Various authors have reported average amounts of autogenous bone block resorption varying from 20 to 50% in the absence of complications during healing. In a study by Cordaro, Amadé and Cordaro (2002), 45% resorp- tion of autogenous onlay grafts was reported (see Figure 5.17a and b).
A systematic review by Rocchietta, Fontana and Simion (2008) recorded different resorption values considering vertical bone augmentation procedures. Various recom- mendations have been made to reduce post‐regenerative bone resorption, one of which is to overbuild or over‐con- tour the defect site to compensate for future grafted bone resorption. However, excessive over‐contouring of the defect site may present challenges to an optimal soft tissue closure, risking soft tissue dehiscence. Another approach is to combine bone blocks with various bone substitutes and barrier membranes during augmentation of implant sites, which might reduce resorption of block grafts. A monocortical bone graft placed with the osseointegrated fixtures were found to provide acceptable degrees of resorption during a five year period and prevented failure of the prosthetic rehabilitation (Liu and Kerns 2014). Another study conducted by Gultekin et al. (2016), com- pared the remodeling rate and the volumetric changes after autogenous ramus block bone grafting (RBG) or guided bone regeneration (GBR) in horizontally deficient maxilla before implant placement. They concluded that both RBG and GBR hard‐tissue augmentation techniques provide adequate bone graft volume and stability for implant insertion. However, GBR causes greater resorp- tion at maxillary augmented sites than RBG, which clini- cians should consider during treatment planning.
Gingival recession occurring around dental implants could also be because of continuous muscular activity from the labial frenum attachment, which induces continuous apical pull on the gingival margin (see Figure 5.18).
A muscle pull on the gingival of the implant site will lead to continuous, steady gingival recession and action must be taken to relieve the implant from that tension. In some cases, a frenectomy few weeks before the implant surgical procedure may need to be carried out to eliminate the muscle pull, as shown in Figure 5.19a and b.
Achieving an esthetic outcome is always a new chal- lenge to the clinician. The key points controlling the esthetic outcome include: the presence of healthy proxi- mal papillae, an intact gingival form, and intact osseous architecture, while tissue phenotype influences not only the clinical result but also its longevity. Understanding the biological, microbiological, and physiological responses of the peri‐implant tissues is an absolute prerequisite, and the peri‐implant esthetic outcome is mainly determined by the patient’s presented anatomical condition and the clinician’s abilities. A thorough understanding of the anatomy of the supporting structures is essential for a correct diagnosis and treatment planning. For natural teeth, it has been estimated that over 60% of the popula- tion has at least one buccal recession defect and such defects are predominately seen in patients with good oral hygiene; in the USA, 23% of adults have one or more tooth surfaces with ≥3 mm gingival recession (Chan, Chun and MacEachern 2015) (see Figure 5.1a and b).
Other technical factors might affect peri‐implant tissue stability such as the diameter of the implant used, the use of provisional restorations, the placement and timing of the final restoration delivery, and a lack of clinical experi- ence. Buser et al. (2004) indicated that the use of wide diameter implants in the anterior zone induced labial plate bone resorption. Saadoun (2007) reported that soft tissue recession around a wide‐diameter implant (≥5 mm) averaged 1.58 mm compared with 0.57 mm around a standard‐diameter implant (<5 mm). It may be prudent to use standard‐diameter implants in the esthetic zone.
Another contributing factor is implant position within the alveolar ridge and the time allowed for peri‐implant tissue maturation (Kinsel and Capoferri 2008).
Gingival recession around natural teeth is defined as present when the location of the gingival margin is apical to the cemento‐enamel junction (Peridontology AAP). A pre‐clinical study (Baker and Seymour 1976) inducing gingival recession by replacing rat incisors with acrylic resin implants suggested that gingival recession is generally associated with (1) local inflammation characterized by mononuclear cells, (2) breakdown of connective tissue, and (3) proliferation of the oral and junctional epithelium into the site of connective tissue destruction. Other precipitating fac- tors include traumatic forces (e.g. excessive brushing), habits (e.g., smoking, oral piercing), and plaque‐ induced inflammation (Chan et al. 2015).
5.2 Prevalence of Implant Related Tissue Migration
Gingival recession represents a clinical condition in adults frequently encountered in general dental practice. Society is evolving with more patients focusing on esthetic aspects of treatment outcome, which explains the growing interest by clinicians for observing soft tis- sue dynamics, objective esthetic ratings, and patient‐ centered outcomes. The progressive shortening of the treatment time from tooth loss to implant installation, has resulted in modifications of the classic immediate implant placement procedures, which may ultimately be a reflection of the patient’s expectations (Araujo, Wennstrom and Lindhe 2006; Botticelli, Berglundh and Lindhe 2004) (see Figure 5.2a–e).According to various systematic reviews, single implant‐supported restoration is predictable and suc- cessful following conventional implant surgery (Berglundh et al. 2002; Creugers et al. 2000; Jung et al. 2008). However, data on clinical response and param- eters about response to trauma, prevalence implant related treatment complications, and bone remodeling rate may be considered limited. Various attempts have been made to evaluate the biologic scope of osseointe- grated implants. Kan et al. (2009) clinically evaluated the dimensions of the peri‐implant mucosa around two‐stage maxillary anterior single implants in humans after one year of function and the influence of the peri‐implant phenotype was also examined. It was concluded that the mean facial dimension of peri‐ implant mucosa of two‐stage implants is slightly greater than the average dimension of that of the dentogingival complex. The level of the interproximal papilla of the implant is independent of the proximal bone level next to the implant but is related to the interproximal bone level next to the adjacent teeth. Greater peri‐implant mucosal dimensions were noted in the presence of a thick peri‐implant phenotype com- pared with a thin phenotype.
Kan et al. (2011) evaluated 35 patients, clinically and radiographically at presurgical examination, immedi- ately after immediate implant placement, and at provi- sionalization, and recordings were made at oneyear after implant surgery and at the latest follow‐up appointment. All implants retained their function. At the follow‐up appointment, the mean mesial and distal marginal bone level changes were significantly greater than those observed at oneyear. At follow‐up, the mean mesial and distal papilla (DP) level changes were significantly smaller than those observed at oneyear, whereas the mean facial gingival level change was significantly greater than that observed at oneyear. Sites with a thick gingival phenotype exhibited significantly minor changes on the facial gingival levels than sites with a thin gingival phe- notype at both the appointments, with mean mid‐facial recession being 1.13 mm. These findings were also con- firmed from the work of Canullo and Rasperini (2007), who evaluated the soft tissue response to platform‐ switched implants after a mean of 22 months follow‐up in a case series. During the follow‐up period, the papil- lary level increased, with a mean value of 0.25 mm.
Thus, an intact facial bone wall thickness seems valu- able for any successful esthetic procedure as it has a direct relationship to mid‐facial recession (Kan et al. 2007). In a review article, Chen and Buser (2009) con- cluded that advanced mid‐facial recession is common following immediate implant treatment. Other studies showed an advanced mid‐facial recession occurred in <10% of the implants (Canullo, Iurlaro and Iannello 2009; Cosyn et al. 2012a, b; Raes et al. 2011).
Mean interproximal recession was frequently reported (11/13) and was low (<1 mm), suggesting a limited risk for advanced interproximal recession. In one study some tissue gain was observed (Canullo and Rasperini 2007). Lops et al. (2008) studied the interproximal recession with complete fill in nearly 70% of the cases; however, the changes in papilla height over time were found to be comparable for patients with a thick‐ and thin‐scalloped gingival phenotype (Kan et al. 2011). Canullo et al. (2009) demonstrated significantly less prevalent inter- proximal recession for implants with a conical connec- tion and platform switch when compared with implants with a flat‐to‐flat connection and without abutment diameter reduction.
De Rouck, Collys and Cosyn (2008) recorded on average 0.75 mm of advanced mid-facial recession and Cordaro, Torsello and Roccuzzo (2009), found advanced mid‐facial recession in 38% and 85% of the patients with a thick‐ and thin‐scalloped gingival phenotype, respectively. Tortamano et al. (2010) suggested that the need for socket grafting might limit the amount of mid‐facial recession.
Small and Tarnow (2000) evaluated 63 implants in 11 patients. Baseline measurements were recorded at stage 2 surgery in two‐stage implant systems and at stage 1 surgery in the one‐stage system. Subsequent measurements were recorded at one week, one month, three months, six months, nine months, and one year after baseline meas- urements. The majority of the recessions occurred within the first three months, with 80% of all sites. It is therefore recommended that there should be a wait of three months for the tissue to stabilize before either selecting a final abut- ment or making a final impression.
In a systematic search by Cosyn et al. (2012a) it was concluded that the average interproximal tissue reces- sion was 1 mm (less than 10% of the cases), suggesting that the risk of interproximal tissue drop and mid-facial recession is unlikely to occur, especially in patients with intact labial plate of bone, with thick overlaying soft tissues. (See Figure 5.3a and b).
5.3 Factors that Lead to Implant‐ related Gingival Recession
5.3.1 BackgroundThe preservation or reproduction of a healthy and sta- ble mucogingival architecture surrounding dental implants placed in the anterior maxilla present estheti- cal challenges for the clinician that may arise for several reasons: the loss of soft tissue volume at the site, poor soft tissue quality at the site, and pre-existing bone loss after regular tooth extraction. While surgical recon- structive procedures have been proposed for the improvement of hard and soft tissue defects prior to implant placement, the preservation of appropriate soft tissue architecture around integrated implants remains challenging (Benic et al. 2012; Buser et al. 2004; Lang and Zitzmann 2012).
Factors that lead to implant related gingival recession can be classified as: physiological factors, which involve factors that influence recession via regular biologic pro- cesses, such as bone remodeling rate, tissue phenotype, and the influence of the thickness of the labial plate of bone; and technical factors, which deal with any techni- cal errors that occur such as the use of wide implants, poor implant position, premature delivery of the final prosthetics, failing to use provisional restoration, and excessive cement located in the gingival sulcus around dental implants (see Figure 5.4).
It is commonly agreed that areas with less than 2 mm of attached gingiva and decreased buccolingual thickness are at a higher risk of recession (Lang and Zitzmann 2012).
Peri‐implant tissue examination for mucogingival prob- lems should therefore include assessment of the presence of local inflammation, the gingival thickness and the ves- tibular depth (Hall 1984). The clinician can also use a simple “tension test” (Vincent, Machen and Levin 1984), which involves pulling the cheeks or lips away from the teeth to assess whether there is adequate attached tissue. In areas of inadequate attached tissue there will be move- ment or blanching of the gingival margin.
5.3.2 Physiologic Factors
5.3.2.1 Influence of Thickness of the Labial Plate of BoneFacial bone thickness is considered a crucial parameter for treatment planning decisions and predicting tissue stabil- ity in the anterior esthetic area. No consensus has yet been reached regarding the amount of buccal bone thickness that is needed when placing an implant to ensure a long- term satisfactory biologic and esthetic outcome, but there are still certain guidelines that are proposed. Grunder, Gracis and Capelli (2005) emphasized the presence of an adequate facial bone thickness to ensure long‐term peri‐ implant tissue stability. The buccal bone plate, especially in the anterior region, has been described as significantly thinner compared to the lingual and palatal components in animal and human studies (Buser et al. 2008; Hämmerle, Chen and Wilson 2004), probably making them more frag- ile and more easily resorbed. A study by Fu, Lee and Wang (2011) found a mean facial bone thickness of 0.83 mm (range, 0.3–1.60 mm) at 2 mm below the bone crest. Braut et al. (2012) found a mean bone thickness of 0.5 mm (range, 0–2.1 mm) at 4 mm apical from the CEJ and 0.6 mm (range, 0–2.8 mm) at the middle of the root. A similar study by Januário, Duarte and Barriviera (2011) on 250 subjects, found a mean bone thickness for the central and lateral incisors and canines of 0.6 (60.3) mm, 0.7 (60.3) mm, and 0.6 (60.3) mm, respectively, at 1 mm apical to the bone crest and of 0.6 (60.4) mm, 0.7 (60.4) mm, and 0.6 (60.4) mm at 3 mm apical to the bone crest. The mean overall thickness varied within 0.5 (60.4) mm and 0.7 (60.4) mm. A study by Huynh‐Ba et al. (2016) in a sample of 93 sites showed a mean buccal bone thickness of 0.8 mm (range, 0.5–2 mm) for the maxillary anterior sites (canine to canine); 87.2% of the buccal bony walls had a width > 1 mm and only 2.6% of the walls were 2 mm wide. They postu- lated that a mean bone wall thickness for the anterior max- illary teeth at 4 mm apical to the CEJ of 1.19 mm (range, 0.30–3.30 mm) had a total of 43.3% with >1 mm of bone thickness and 0.82 mm (range, 0.20–1.60 mm) at the mid‐ point of the root had a total of 76.6% with <1 mm of bone thickness. For the mandibular teeth, the mean was 1.31 mm (range, 0.30–5.20 mm) with a total of 63.3% with >1 mm of bone thickness and 0.80 mm (range, 0.00–1.80 mm) with a total of 75.5% with <1 mm of bone thickness, respectively. The mean bone thickness at the apical area of the root was 1.80 mm (range, 0.20–3.60 mm) for the maxillary teeth and 3.78 mm (range, 0.00–7.90 mm) for the mandibular teeth.
Fuentes et al. (2015) have studied the anatomical dimensions of the buccal bone walls of the esthetic max- illary region for immediate implant placement, based upon cone‐beam computed tomography (CBCT) scans in a sample of adult patients. They analyzed a sample of 50 CBCT scans, and concluded that less than 10% of sites showed more than a 2‐mm thickness of the buccal bone wall, with the exception of the central incisor region, in which 14.4% of cases were≥ 2 mm.
Le and Farahani (2012), who explored the relationship between the labial bone thickness (ILBT) and crestal labial soft tissue thickness for an implant, suggest that crestal labial soft tissue thickness around implants is sig- nificantly associated with the labial bone thickness in the anterior maxillary region. In other words, they concluded a direct relationship showing that the thicker the bone, the thicker the crestal labial soft tissue thickness around implants and vice versa. Kheur et al. (2015), suggested that there is a positive correlation between the labial and pala- tal bone and soft tissue thickness; and between the labial bone thickness and the labio‐palatal socket thickness. No correlation was seen between the labial bone thickness and the labio‐palatal tooth position. They also suggested that a minimum 2 mm thickness of bone is necessary to provide support to the supracrestal soft tissue, and that an accurate analysis with CBCT imaging before extraction is necessary for immediate implant placement. Wildermanm and Wentz (1965) and Pennel et al. (1967) histologically demonstrated a relationship between bone exposure and bone resorption in thin plates. Qahash, Susuin and Poolimeni (2008) demonstrated a correlation between the width of the buccal alveolar ridge and the extent of bone resorption using incandescent and fluorescent light microscopy analysis. They suggested that the width of the buccal alveolar ridge should be at least 2 mm to maintain the alveolar bone level, and the thicker lingual bone plate provided a larger wound space that was correlated to enhanced bone regeneration, whereas implants placed closer to the buccal plate were associated with increased crestal bone loss. If after implantation the buccal site thickness is less than 2 mm, vertical bone resorption is likely to occur (see Figures 5.5a, b and 5.6a, b).
5.3.2.2 Influence of Tissue Phenotype
Tissue phenotype is considered a major influencer in the overall prediction of the fate of an immediate implant placement procedure in the esthetic zone. It predicts to a great extent the future liability for implant related tissue migration and the overall possible tissue stability, so the clinician should identify the tissue phenotype prior to the start of the treatment, and identify the potential risks involved.
In tissue phenotype; the thin tissue seems to recede more often in response to inflammation and tissue manipulation. Gingival recessions confirm the relevance of an inflammatory infiltrate in the pathogenesis (Smukler and Landsberg 1984). In thin phenotype gingi- val recessions around natural teeth, the epithelium is acanthotic and proliferative and surrounded by an inflammatory infiltrate. In addition, necrotic cells can be found. Occasionally the dentogingival epithelium penetrates into the lamina propria, thereby decreasing the width of the lamina propria and allowing the den- togingival and oral epithelia to coalesce, resulting in loss of attachment to the tooth. The inflammatory infiltrate can span the entire thickness of the width of the gingiva thus promoting a further recession. In thicker gingiva, connective tissue free of inflammatory infiltrate may be interposed between the oral and junctional epithelia, preventing a recession (Baker and Spedding 2002; Miller 1985). Baldi et al. (1999) and Hwang and Wang (2006) stated that initial gingival thickness predicts the outcome of any root coverage procedures or any restorative treatments around natural teeth.
Claffey and Shanley (1986) defined the thin pheno- type as having a gingival thickness ≤ 1.5 mm, and the thick as ≥ 2 mm or more. Clinical identification is impor- tant for better determination of the treatment outcome. Hirschfield (1923) was one of the earliest periodontists to comment on the relationships between alveolar anatomy and gingival form, noting that a thin alveolar contour was probably covered by a similar gingival form. It has been suggested that a direct correlation exists between gingival phenotype and the susceptibility to gingival recession following surgical and restorative procedures (see Figure 5.7). According to Evans and Chen (2008), the likelihood of gingival recession increases in patients with thin phenotypes present in immediate single implant‐supported restorations. It is widely accepted that some gingival/periodontal prob- lems are more likely to occur in patients with a thin phenotype. A 1991 animal study by Berglundh and colleagues concluded that thin gingival tissue can lead to marginal bone loss during formation of the peri‐ implant biologic width. Another study by Hwang and Wang (2006) reported that implant sites with thin mucosa were prone to angular bone defects, while stable crestal bone was maintained in implants surrounded by thick mucosa. According to Abrahamsson et al. (1998), thick tissues (i.e. ≥2.5 mm) can avoid significant crestal bone recession.
Fickl et al. (2008), in an interesting study that fully explained the reasons for the harmful effect of thin tissue phenotypes, stated that the thin periodontal phenotypes have an inherent osteoclastic activity that is signaled by any stimulus such as flap reflection; thus, osteoclastic activities occur at the internal and external sides and merge together, leading to a more pronounced loss of the buccal bone plate. Consequently, when the buccal bone plate is resorbed, the soft tissue complex can no longer be stabilized and will collapse into the newly formed defective space. As the buccal soft tissue occupies the place of the former buccal resorbed bone plate, the room for bone regeneration is reduced, leading to the observed major bucco-oral shrinkage, which is why serious esthetic changes in bone and mucosal anatomy may result after extraction in patients with thin‐scalloped profiles.
Patients with a thick phenotype that consists of flat soft tissue form and a thick bony architecture are often found to be prevalent in the population. This type of tissue form, according to Kao, Fagan and Conte (2008), is dense and fibrotic with a large zone of attachment, thus making it more resistant to gingival recession (see Figure 5.8a and b).
In contrast, thin gingival tissue tends to be delicate and almost translucent in appearance. The tissue appears friable with a minimal zone of attached gingiva. The soft tissue is highly accentuated and often sugges- tive of thin or minimal bone over the labial roots. Hwang and Wang (2006) documented that patients with a thin gingival phenotype were more likely to experience gingival recession following non‐surgical periodontal therapy. The thinner periodontal phenotype needs more attention when an extraction is carried out owing to its thin alveolar plate (Kao et al. 2008). The hard and soft tissue contouring is more predictable after surgery for a thick phenotype. The value of a thick phenotype is emphasized by its increased wound coverage and site protection, and implant stability created by a predictable seal around the implants’ collars. The thicker phenotype can resist mucosal recession, masks the restorative margins, and camouflages the titanium implant shadows. It also protects the biological seal around dental implants, thus reducing the tendency for crestal bone resorption. The amount of gingival thick- ness before regenerative surgery was found to be a predicting factor for the occurrence of further postop- erative recession. However, in a thin phenotype, the mucogingival corrective surgical procedures can enhance the quality of tissue, resulting in a more favorable treatment outcome. A thick phenotype is more resistant to recession and more accommodating to different implant positions (Kao et al. 2008; Siegenthaler et al. 2007; Small, Tarnow and Cho 2001) (see Figure 5.9). Dramatic alveolar bone resorption in the apical and lingual direction is possible in patients with a thin phenotype. The loss of peri‐implant tissues may result in facial plate loss, revealing a grayish color underneath; additional bone and soft tissue grafting surgeries may be necessary (see Figure 5.10a and b).
Patients with thick and flat gingival phenotypes exhibit short papillae whereas thin‐scalloped pheno- types have long papillae. This morphometric difference may be the cause of more papilla loss in the thin phenotype. Linkevicius et al. (2009) in their study con- cluded that the initial gingival tissue thickness at the crest may be considered as a significant predictor of mar- ginal bone stability around implants. If the tissue thick- ness is 2.0 mm or less, crestal bone up to 1.45 mm may occur, despite a supracrestal position of the implant– abutment interface. Nisapakultorn et al. (2010), in their study on 40 patients, documented a thin phenotype being significantly associated with an increased risk of facial mucosal recession (see Figure 5.11a and b).
The thicknesses of the crestal bone on the buccal aspect significantly influence the bone remodeling rate during the initial four‐month healing period after an immediate implant placement, while on the other hand, gingival thickness affects the treatment outcome possibly because of the difference in the amount of blood supply to the underlying bone and the susceptibility to resorption.
A delayed implant placement might be considered when there is not enough soft and hard tissue thick- ness (Buser et al. 1991, 1999, 2008, 2013). However, a thin gingival phenotype is associated with a thin alve- olar plate that makes the worst clinical outcome in the delayed immediate protocol; more ridge remodeling has been found in this phenotype when compared with a thick periodontal phenotype. Ridge preserva- tion was should be considered for most thin phenotype cases (Ahmad 2010). Atraumatic natural tooth extrac- tion is also necessary. It is the author’s recommenda- tion that a non‐staged surgical approach in thin phenotype patients or those with a high‐scalloped tis- sue profile should be undertaken whenever possible (whenever primary implant stability is achievable).
The reasons for this approach include: minimizing treatment time; decreasing the liability for scar tissue formation because multiple surgeries in the oral cavity will lead to further tissue shrinkage as well as scar tissue formation; and minimizing the likelihood of bone resorption after surgical intervention – in a staged approach, the main issue is the tendency for tissue to shrink, as happens whenever a surgical intervention is performed in thin tissue phenotype patients, which explains the preference of the non‐staged treatment approach. Treatment should involve augmenting both bone and soft tissue together in the same treatment session, be cause the risk by that of a staged approach; the resultant tissue shrinkage is a major drawback of a staged approach (see Figure 5.13a and b).
Different gingival phenotypes are found between dif- ferent age groups, with the thicker phenotype more prevalent in younger age groups. Vandana and Savitha (2005) showed thicker gingiva in a younger age group and stated that the decrease in keratinization and changes in the oral epithelium may be the contributing factors. Sanavi, Weisgold and Rose (1998) found that the inter‐radicular bone is more abundant and thicker in the thinner phenotype. This in turn can cause more recession (see Figure 5.14a and b).
In a thin gingival phenotype, a faulty prosthetic margin invading the peri‐implant tissue complex or extending beyond the implant collar might cause bone loss in this area. Thus, restoration going deeper into the sulcus will increase the risk of bone resorption as well as gingival recession via tissue displacement.
Residual cement also plays a role in the occurrence of implant related gingival recession specially in thin tissue phenotypes. It has been reported that excess luting cement can cause irritation to the gingival tissues leading to crestal bone loss and subsequent changes in the architecture of the soft tissue (Linkevicius et al. 2009). However, there is still no consensus about how excess cements cause tissue reactions and to what extent the excess cement contrib- utes to peri‐implantitis. Resin cements, with their high strength and non‐soluble characteristics, are hard to detect and will not be dissolved by oral or sulcular fluids. Excess resin cements at the restoration margin are a major cause for soft tissue recession and inflammation. The authors contended that the primary retention of cemented implant prosthesis is not dependent on the type of cement used but more on the adaptation and seating of the pros- thesis itself. Wilson (2009) demonstrated that suppuration or continued bleeding on probing around gingival mar- gins of implant restorations had an 81% correlation to the presence of excess cement. Therefore, trapped cement would cause constant irritation to the gingival sulcus, which might induce recession.
5.3.2.3 Influence of the Underlying Periosteum
Periosteum can be described as an osteoprogenitor cell containing bone envelope, capable of being activated to proliferate by trauma, tumors, and lymphocyte mito- gens. Periosteal cells secrete extracellular matrix and form a membranous structure so the periosteum offers a rich cell source for bone tissue engineering; hence, the regenerative potential of periosteum is immense (Mahajan 2012).The periosteum is made up of three distinctive zones. Zone 1 has an average thickness of 10–20 μm consisting predominantly of osteoblasts representing 90% of the cell population, while collagen fibrils comprise 15% of the volume. The majority of cells in zone 2 are fibroblasts, with endothelial cells. Zone 3 has the highest volume of collagen fibrils and fibroblasts among all the three zones. Fibroblasts make up more than 90% of the cells in zone 3 (Reynders, Becker and Broos 1998; Mahajan 2012).
The structure of periosteum varies with age. In infants and children it is thicker, more vascular, active, and loosely attached as compared to adults, where it is thin- ner, less active, and firmly adherent (Tran Van, Vignery and Baron 1982). The periosteum has a rich vascular plexus of capillaries supplying blood to bone that reside within the cortex, linking the medullary and periosteal vessels which promote revascularization during wound healing. Studies have reported the existence of osteo- genic progenitors, similar to mesenchymal stem cells (MSCs), in the periosteum (Wang et al. 2013).
Studies have shown promising results with the use of periosteum to treat gingival recession defects (Mahajan 2010). Periosteum‐derived progenitor cells may serve as an optimal cell source for tissue engineer- ing based on their accessibility, ability to proliferate rapidly, and capability to differentiate into multiple mesenchymal lineages (Taba et al. 2005). A study by De Bari, Dell’Accio and Vanlaume (2006) indicates that periosteal progenitor cells are able to differentiate not only into bone and cartilage cells but also into adipo- cyte and skeletal myocyte cells.
Nobuto et al. (2005) have suggested a role for the periosteum in tissue healing and postoperative angio- genesis and concluded that after mucoperiosteal flap elevation, the periosteal vascularity exhibited potent blood vessel‐forming activity through various angio- genic mechanisms and through repair activity. Therefore, clinicians should minimize periosteal trauma and manip- ulation as much as possible during surgery to maintain the maximum tissue reparative capacity.
The higher bone loss rate with classic incision sites occurred when a papilla detached from bone, where the interdental bone in proximity to the adjacent tooth is denuded from the periosteum, the bone blood sup- ply can be affected (Evian, Corn and Rosenberg 1985). Therefore, excluding interproximal papillae from the mucoperiosteal flap (papillae preservative flaps) might help to minimize postoperative tissue recession (see Figures 5.15a, b and 5.16a–c).
Excessive periosteal stripping not only jeopardizes the soft tissue flap vascularity but may also lead to postoperative tissue necrosis, while incomplete muco- periosteal management can lead to improper soft tissue closure or a closure under tension. It is the author’s opinion that flapless implant placement intervention could be highly valuable (whenever indicated) to the overall treatment outcome for many obvious reasons. However, a strict protocol should be implemented that includes the mandatory use of CBCT along with a CAD/CAM surgical guide.
5.3.2.4 The Influence of the Immediate Implant Placement on Alveolar Bone Remodeling
Tooth extraction will be followed by marked change in the tissue volume of the alveolar ridge. In a clinical study, Schropp, Wenzel and Kostopoulos (2003) demonstrated that the loss of volume horizontally amounts to 5–7 mm within the first 12 months after tooth extraction. This corresponds to approximately 50% of the original width of the alveolar bone. Cardaropoli et al. (2005) and Araujo and Lindhe (2005) stated that the coronal thin part of the buccal bone wall of the extraction socket is often com- prised solely of bundle bone. The bundle bone loses its function after tooth extraction and is resorbed by osteo- clastic activity, which might affect the bone remodeling process. Additionally, most of the experimental studies utilized mucoperiosteal flaps exposing the buccal bone, which might have further detrimental effects on the resorption process occurring after tooth extraction (Araujo and Lindhe 2005; Cardaropoli et al. 2005). Araujo et al. (2006) studied the histological effects of sur- gical trauma on soft‐ and hard‐tissue remodeling and concluded that all test teeth demonstrated signs of attachment loss and bone loss.
Araujo and Lindhe (2005) stated that osteoclasts were indeed present in the exposed area of the alveolar ridge, which exhibited signs of surface resorption. Fickl et al. (2008) stated that when the buccal bone plate is resorbed, the soft tissue complex can no longer be stabilized and will collapse into the newly formed space. As the buccal soft tissue occupies the place of the former buccal bone plate, the room for bone regeneration is reduced, lead- ing to the observed major shrinkage, especially in thin phenotypes.
During the healing period, the buccal crestal bone undergoes variable degrees of resorptive and modeling changes characterized by a combination of bone fill within the original peri‐implant defect, resorption of the buccal plate of bone of approximately 50% of the original width, and approximately 1 mm loss of crestal bone height (Botticelli et al. 2004; Araujo and Lindhe 2005; Araujo et al. 2006; Sanz et al. 2015). This situation may be unstable and may predispose the mucosa to recession (Hermann, Schenk ad Schoolfield 2001). Araújo and Lindhe suggested that following tooth extraction, the blood vessels in the periodontium supplying the thin bone walls are severed, thereby causing facial bone plate resorption (Araujo and Lindhe 2005).
A study by Araujo et al. (2006) to evaluate tissue remodeling in fresh extraction sockets, showed that the buccal and lingual bone walls underwent marked surface resorption and the height of the thin buccal hard tissue wall was reduced at the end of fourweeks. As the process of healing continued and the buccal bone crest shifted further in the apical direction, the buccal crest was located >2 mm apical of the marginal border of the SLA surface at 12 weeks. Thus, it was concluded that the bone‐to‐implant contact established during the early phase of socket healing following implant installation was in part lost when the buccal bone wall underwent continued resorption.
Araujo et al. (2006) explained that the modeling in the marginal defect region was accompanied by marked attenuation of the dimensions of both the delicate buccal and the wider lingual bone walls. Bone loss at molar sites was more pronounced than at the premolar locations. Implant placement failed to preserve the hard tissue dimension of the ridge following tooth extraction. The buccal as well as the lingual bone walls were resorbed, although some marginal loss of osseointegration was also evident.
Araujo et al. (2006) demonstrated that the resorp- tion of the buccal/lingual walls of the extraction site occurred in two overlapping phases. During phase 1, the bundle bone was resorbed and replaced with woven bone. Since the crest of the buccal bone wall comprised solely bundle bone, this modeling resulted in substantial vertical reduction of the buccal crest. Phase 2 included resorption that occurred from the outer surfaces of both bone walls.
Schropp et al. (2003) reported a reduction of 50% of the width of the alveolar ridge at 12 months after tooth extraction. Hence, preservation of the alveolus at the time of extraction of prominent roots in the anterior maxilla is crucial. A study by Ferrus et al. (2010) confirmed that the position of the implant, the size of the horizontal buccal gap, and the buccal bone crest thickness significantly influenced the remodeling rate of the hard tissue during a four‐month period of healing after immediate implant placement into an extraction socket. Also, the sites where the buccal bone wall was thicker than 1 mm showed a better gap filling and minimal vertical resorption of the buccal crest when compared to sites with thinner bone (<1 mm). The possible relationship between gingival tis- sue form and the underlying bone was previously ana- lyzed by Fu et al. (2011), showing a moderate correlation between soft and hard tissues in the anterior region.
It seems that there is a need to preserve or increase the hard and soft tissue thickness using different types of interventions (Chen et al. 2009), which often might reduce and sometimes eliminate the need for subse- quent augmentation procedures. Wildermanm and Wentz (1965) when explaining histogenesis of repair, observed different healing patterns of buccal and lin- gual plates of the anterior mandibular region of dogs. A mean labial gingival recession of 0.5–1 mm around single implants, due the bone remodeling after implant surgery, seems to be a common finding after implant restorations. Also, at one year between single implant placement and the second‐stage surgery, a mean reduc- tion in facial bone thickness and facial bone height of 0.4 and 0.7 mm have been reported.
With a thorough understanding of the available litera- ture, it may be concluded that irrespective of the simul- taneous placement of dental implants in fresh extraction sites, there are variable degrees of bone remodeling that in turn influence the occurrence of implant related gingi- val recession, and apical migration of implant related tis- sues can occur due to many other variables. This warrants the clinician attention to take these facts into considera- tion when deciding upon any treatment plan that has a high esthetic demand.
5.3.2.5 Other Related Factors
Several regenerative techniques have been proposed to increase the alveolar volume both vertically and horizontally to prepare the alveolar ridge for correct placement of oral implants. Each of these grafting modalities has its own inherited remodeling rate that might be followed by soft tissue drop. Various authors have reported average amounts of autogenous bone block resorption varying from 20 to 50% in the absence of complications during healing. In a study by Cordaro, Amadé and Cordaro (2002), 45% resorp- tion of autogenous onlay grafts was reported (see Figure 5.17a and b).
A systematic review by Rocchietta, Fontana and Simion (2008) recorded different resorption values considering vertical bone augmentation procedures. Various recom- mendations have been made to reduce post‐regenerative bone resorption, one of which is to overbuild or over‐con- tour the defect site to compensate for future grafted bone resorption. However, excessive over‐contouring of the defect site may present challenges to an optimal soft tissue closure, risking soft tissue dehiscence. Another approach is to combine bone blocks with various bone substitutes and barrier membranes during augmentation of implant sites, which might reduce resorption of block grafts. A monocortical bone graft placed with the osseointegrated fixtures were found to provide acceptable degrees of resorption during a five year period and prevented failure of the prosthetic rehabilitation (Liu and Kerns 2014). Another study conducted by Gultekin et al. (2016), com- pared the remodeling rate and the volumetric changes after autogenous ramus block bone grafting (RBG) or guided bone regeneration (GBR) in horizontally deficient maxilla before implant placement. They concluded that both RBG and GBR hard‐tissue augmentation techniques provide adequate bone graft volume and stability for implant insertion. However, GBR causes greater resorp- tion at maxillary augmented sites than RBG, which clini- cians should consider during treatment planning.
Gingival recession occurring around dental implants could also be because of continuous muscular activity from the labial frenum attachment, which induces continuous apical pull on the gingival margin (see Figure 5.18).
A muscle pull on the gingival of the implant site will lead to continuous, steady gingival recession and action must be taken to relieve the implant from that tension. In some cases, a frenectomy few weeks before the implant surgical procedure may need to be carried out to eliminate the muscle pull, as shown in Figure 5.19a and b.
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