6.1 Introduction
In 1965, an orthopedic surgeon, Branemark, installed the first titanium tooth implant on a human volunteer . Then, the first immediate implant placement was accredited to Professor Wilfried Schulte in 1978. Since 1990, the placement of dental implants in the post-extraction site has been a subject of considerable concern in the field of implant density. The option of implant placement as a replacement for tooth loss became very common in the 1990s, motivated by the development of guided bone regeneration.
In 1965, an orthopedic surgeon, Branemark, installed the first titanium tooth implant on a human volunteer . Then, the first immediate implant placement was accredited to Professor Wilfried Schulte in 1978. Since 1990, the placement of dental implants in the post-extraction site has been a subject of considerable concern in the field of implant density. The option of implant placement as a replacement for tooth loss became very common in the 1990s, motivated by the development of guided bone regeneration.
The dental specialist has, however, started to concentrate steadily on the esthetic outcome of the post-extraction implant placement over the past years, and some reports have highlighted a substantial risk of experiencing mucosal recessions, soft and hard tissue pathology with dental implants. The aim of this chapter is to discuss the common soft tissue pathology around dental implants and its management. It is worth starting this chapter with the anatomical difference between peri-implant soft tissue and soft tissue around the tooth and common soft tissue pathology around dental implant etiology and elements considered for diagnosis and management to get the decision tree in determination of management protocol.
6.2 Peri-Implant Soft Tissue
The scientists explored the anatomical difference between peri-implant soft tissue and tooth soft tissue to better clarify the anatomical variations between the inter- face of tooth-soft tissue and implant-soft tissue. The soft tissue profile and care around implants is significantly more complicated than around teeth for three primary factors:
1. Marginal mucosal area.
2. Attachment of connective tissues.
3. The vascular supply gaps.
The measurements of the supracrustal gingival tissue (SGT) (initially called biological width) are close to those present on the natural tooth and vary from 3 to 4 mm. The junctional epithelium is around 2 mm in length, and the connective tis- sue is nearly 1–1.5 mm. It binds to the implant and contains collagen fiber bundles, some of which invest in the periosteum of the bone crest and run a course parallel with the surface of the implant with more collagen and fewer fibroblasts. The three main sources of blood supply around the natural tooth are the following:
(a) The supraperiosteal vessels which supply the free and attached gingiva.
(b) Blood vessels from the periodontal ligament.
(c) Blood vessels from the alveolar bone.
The essential blood vessels from the periodontal ligament are absent in the case of implants. The single source of blood was from the supraperiosteal vessel at the alveolar bone periosteum. There is also a hypovascular–hypocellular connective tis- sue zone around the implant that is not found around natural tooth and more vulner- able to the inflammatory response (Fig. 6.1).
6.3 Peri-Implant Soft Tissue Importance
The mucosa surrounding the dental implant forms tight gingival cuff consisting of epithelium and connective tissues established during healing after the surgery. Multiple findings have evidence on comparisons and variations at the dent–gingival junction between peri-implant soft tissue and gingiva around natural tooth (Table 6.1).
6.4 Etiology of the Common Soft Tissue Pathology Around Dental Implants
Three main categories cause the soft tissue pathology around dental implants, broadly classified as inflammatory, reactive, and autoimmune. The inflammatory group is characterized by two major conditions of the inflamed peri-implant tissues and its underlying supporting bone: peri-implant mucositis and peri-implantitis. Reactive lesions in the oral cavity primarily include pyogenic granuloma (PG), peripheral giant cell granuloma (PGCG), and fibrous hyperplasia. Lastly, oral lichens planus, an autoimmune mucocutaneous inflammatory disease, should be considered.
6.5 Inflammatory Conditions That Cause Soft Tissue Pathology Around Dental Implants and Bone Loss
6.5.1 Peri-Implant Mucositis and Peri-Implantitis
Peri-implant mucositis is defined as a reversible inflammation in the soft tissues surrounding the implant, which constitute the main common soft tissue pathology around the dental implant (Fig. 6.2). The advanced/progressive form of it is peri- implantitis, which involves the soft and hard tissue component and defined as inflammation associated with loss of supporting bone around an implant (Fig. 6.3). This section of the chapter will focus on these common two conditions affecting soft and hard tissue around the dental implant in terms of etiology, diagnosis, and management.
6.5.2 Etiological and Risk Factors
The main etiology of both conditions is bacterial biofilm on the implant and restora- tions. However, many other multifactorial risk factors have been documented in the literature and attributed to the following: smoking, residual cement, trauma from occlusion, width and thickness of keratinized mucosa, foreign body reaction, untreated periodontal diseases, type of implant surface, genetic trait, lack of compli- ance, psychological reasons, and systematic diseases.
There is also evidence for radiation therapy as a risk indicator for peri-implant mucositis. There is some evidence for diabetes mellitus as a risk indicator for peri-implant mucositis. Poorly controlled diabetes mellitus (HbA1c levels > 10.1) was shown to be associated with increased bleeding on probing at implants. Ferreira et al. also reported an association with peri-implant mucositis and systemic disease. However, the systemic diseases described included “diabetes mellitus, hormonal changes, menopause, chemotherapy, thyroid alterations, cardiac problems, and alcohol use,” and thus the results of the study are difficult to interpret.
6.5.3 Diagnosis Criteria
The main clinical characteristics of peri-implant mucositis include bleeding on gen- tle probing; erythema, swelling, and/or suppuration may also be present. An increase in probing depth is often observed in the presence of peri-implant mucositis because of swelling or a decrease in probing resistance, which needs to be considered to avoid misdiagnosis. The absence of bone loss beyond crestal-bone-level changes, confirmed by radiographs, indicates alterations resulting from initial bone remodel- ing. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri-implant mucositis and can be resolved by nonsurgical periodontal therapy.
The diagnosis of peri-implantitis requires the presence of bleeding and/or sup- puration on gentle probing, an increase in probing depth compared to previous examinations, and the presence of bone loss beyond the crestal bone levels. In the absence of previous examination data, diagnosis of peri-implantitis can be based on the combination of the following: the presence of bleeding and/or suppuration on gentle probing, probing depths of ≥6 mm, and bone levels ≥3 mm apical to the most coronal portion of the intra-osseous part of the implant.
6.5.4 Treatment of Peri-Implant Mucositis and Peri-Implantitis
Peri-implant mucositis is primarily caused by a disruption of the host–microbe homeostasis at the implant–mucosa interface and is a reversible condition at the host biomarker level. Regular supportive peri-implant therapy with biofilm removal is an important first preventive strategy against the conversion of health to peri- implant mucositis and also against the progression of peri-implant mucositis to peri-implantitis.
In addition to the biofilm removal, it is very substantial to determine the goal of therapy for both peri-implant mucositis and peri-implantitis, which is usually con- fined to control of the bacterial etiology, elimination of soft tissue inflammation, implant surface decontamination, regenerative approach, resective approach, implant surface modification (implantoplasty), and re-osseointegration.
Furthermore, it is important to take into consideration the limitations of the therapy, ranging from accessibility, implant configuration, implant surface structure, soft tissue conditions, defect configuration, and grafting materials to the amount of bone loss .
As mentioned earlier, biofilm removal by nonsurgical mechanical debridement (MD) is the first treatment procedure for the treatment of peri-implant mucositis along with local chemotherapeutic antiseptic agents. There are numerous therapies, such as antibiotic and probiotic therapy, laminin coatings on implant surfaces, low- level laser therapy, and photodynamic therapy (PDT), that have been assessed as adjuncts to MD for the treatment of peri-implant diseases.
Photodynamic therapy (PDT) is another form of local therapy that has been used as an adjunct to MD for peri-implant diseases in several studies. In this form of adjunct therapy, a dye (photosensitizer) is locally delivered to the peri- implant sulci of infected sites and is then exposed to a laser with a wavelength usu- ally ranging between 660 to 800 nm. The resultant reaction produces reactive oxygen species (ROS), which possibly reduce inflammation and counts of pathogenic microbes at the treatment sites, thereby facilitating the overall healing process. Studies have explored the contribution of PDT as an aide treatment to routine oral hygiene maintenance instructions for the treatment of periodontal and peri-implant diseases. It has also been proposed that MD with adjunct PDT is more effective in reducing peri-implant soft tissue inflammation (peri-implant mucositis) than MD alone.
In cases of peri-implant mucositis, the etiology attributed to the lack of keratinized tissue (KT) surgical periodontal treatment, including gingival graft after the phase of MD, is considered. Although there was debate in the dental literature about the prevalence of peri-implant soft tissue diseases and lack of KT, an increase in the width of KT may be considered in order to improve and simplify the patient’s oral hygiene and to preserve the level of mucosal tissue. For dental implants and natural teeth alike, the value of having an acceptable width and density of KT tends to be important, comparably to teeth without KT, which were observed to be more vulnerable to more impairment of attachment. Tissue breakdown has also been found to develop more rapidly with dental implants than with teeth (Figs. 6.4 and 6.5).
Peri-implant mucositis, the most common soft tissue pathology around dental implants, seems to be a precursor to subsequent peri-implantitis. The treatment dur- ing the transitional stage typically involves antibacterial therapy, combined with MD before attempting surgical regeneration of peri-implant alveolar bone lost due to infection. Lang et al. in 1997 published a review of clinical trials on thera- pies for peri-implant infections, revealing that the inflammatory process in soft and mineralized peri-implant tissues can be controlled. This renders the site susceptible to regenerative procedures aimed at re-establishing osseointegration after nonsurgi- cal therapy and the administration of local and systematic antibiotics. However, as of today, no controlled studies have been performed to document the possibility of true osseointegration. A previous cited study proposed a well- documented system for the management of peri-implant diseases called cumulative interceptive supportive therapy (CIST). This approach is very helpful for the devel- opment of a joint effort for the management of soft and hard tissue conditions (Fig. 6.6).
Surgical treatment therapy for peri-implantitis, as it is the progressive disease of the common soft tissue pathology around dental implants, is mainly a regenerative approach. The treatment consisted of flap reflection, surface decontamination, use of enamel matrix derivative (EMD) or platelet-derived growth factor (PDGF), and guided bone regeneration with mineralized freeze-dried bone and/or anorganic bovine bone combined with PDGF or EMD and covered with an absorbable mem- brane and/or subepithelial connective tissue graft (Fig. 6.7).
However, the destructive soft tissue pathological inflammatory process affects both soft and hard tissues, leading to pocket formation and progressive bone resorption around osseointegrated oral implants. Explanation may be indicated in advanced stages with severe bone loss when soft tissue pathology cannot be eradicated with re-augmentation of the site for new implant placement and restoration (Fig. 6.8).
According to published studies, peri-implant diseases are very common. Therefore, it is imperative for the clinician to examine and evaluate patients who have been provided with implant-supported restorations on a regular basis.
The following aspects are recommended for the clinical routine:
When implant treatment is considered, patients should be informed of the risks for biological complications (peri-implant diseases) and the need for preventive care. An individual risk assessment, including systemic and local risk indicators, should be performed, and modifiable risk factors, such as residual increased probing pocket depth in the remaining dentition or smoking, should be eliminated. Hence, treatment of periodontal disease aiming for elimination of residual pockets with bleeding on probing and smoking cessation should precede implant placement.
The correct fit of implant components and the superstructures has to be ensured to avoid additional niches for biofilm adherence. If cemented implant restorations have been selected, the restoration margins should be located at the mucosal margin in order to allow meticulous removal of excess cement.
To facilitate personal oral hygiene, clinicians should consider having keratinized attached surrounding the transmucosal implant portion already during implant placement (for one-stage implant placement) or during abutment connection (for two-stage implant placement).
Professional supportive care should be established according to the individual needs of the patient (e.g., 3, 6, or 12-month recall intervals), and their compliance has to be confirmed. Particularly in patients with a history of aggressive periodontitis indicating an increased susceptibility for periodontal and peri-implant diseases, shorter recall intervals should be considered. During recall, peri-implant tissues must be regularly examined, including probing assessments with special emphasis on bleeding on probing.
6.6 Reactive Condition That Causes Soft Tissue Pathology Around Dental Implants and Bone Loss
6.6.1 Pyogenic Granuloma
Pyogenic granuloma is a common, reactive inflammatory hyperplasia of the oral cavity. Although the term “pyogenic” is used, PG is not an infectious lesion. PG usually occurs as a response to different stimulating factors such as local trauma or irritation and iatrogenic and hormonal factors. Because of the female hor- mone factor, it has a very high incidence in young females, principally in the second decade of life. Clinically, PG presents as a painless, smooth, or lobulated shape. It is classed as a hemorrhagic lesion because of its vascular structure, and its color ranges from pink to dark red. It is presented clinically as sessile with an average size of 1 cm and has a smooth, shiny surface. In addition, it bleeds very easily when touched. Sometimes, its surface may be covered by a pseudo-membrane due to secondary ulcerations.
It was reported that oral PG was found in 18% of patients who had benign oral masses. It was also noted that PG can be observed in individuals as young as 10 years old up to the age of 70. It is the second most common soft tissue pathology around dental implants after peri-implant mucositis, soft tissue fistula, and peri- implantitis. As mentioned previously, local trauma is the main etiological factor, with 30–50% of patients with PG having a history of local trauma. The occurrence of implant-related PG was associated with inappropriate healing caps of implants (Fig. 6.9).
Biopsy as a diagnostic approach is warranted because peripheral odontogenic lesions, benign and malignant neoplasms, metastatic lesions, and a variety of other lesions may clinically resemble this reactive nodular lesion of the gingiva. The his- topathologic analysis of PG usually reveals an intense vascular proliferation with extensive areas of ulceration, mixed inflammatory infiltrate, numerous granulation tissue, and abundant macrophages (multinucleated giant cells) (Fig. 6.9c). There are several treatment options for PG, such as surgical excision, cryother- apy, electro-cauterization, laser applications, and steroid injections . However providing adequate keratinized soft tissue should be the first step to prevent such lesions for reactive lesions related to dental implants. In addition, management should involve the detection and elimination of the possible local irritant factors, such as abnormal superstructure and healing cap implant relationships or unfavor- able implant–bone relationships. Soft tissue site preparation with gingival graft augmentation before implant placement is necessary to enhance the thickness and width of the keratinized gingiva when there is inadequate gingiva thickness and a lack of keratinization (Fig. 6.10).
6.7 Autoimmune Conditions That Cause Soft Tissue Pathology Around Dental Implants and Bone Loss
6.7.1 Oral Lichen Planus
Oral lichen planus (OLP) is a chronic mucocutaneous inflammatory disease. It affects the skin, nails, hair, and mucous membranes (oral and genital). It most commonly affects middle-aged individuals, predominantly females. Its preva- lence is between 0.1% and 2.2%. OLP is a T cell-mediated autoimmune disor- der of uncertain etiology. Besides immune dysregulation, many etiological factors may also be involved, including traumatic insults, medication, dental materi- als, and stress. It commonly affects buccal mucosa, tongue, and gingiva.
Due to the adverse effects of implant placement on LP and vice versa, implant placement should be done with caution. LP patients treated with dental implants are at a risk of implant failure due to the inability of the epithelium to attach to the implant surface, which allows the bacteria to access the preimplant tissue, leading to the failure of osseointegration. It has also been recommended that lichen planus patients be handled with care during the remission phase when the cases are stabilized. It should not be placed during the active phase of the LP, which will cause implant failure (Fig. 6.11).
Corticosteroids are the main treatment for symptomatically OLP. Topical steroids are considered first-line treatment because they are more effective in treating superficial inflammation, especially in EOLP. Other treatment modalities are being tried to increase the efficacy and decrease the complications of corticosteroids. The therapeutic potential of photodynamic therapy and lasers has been investigated. Ozone therapy is also being used to treat OLP due to its strong antimicrobial activity. Oral corticosteroid dose of 4 mg/daily after insertion of dental implants in patients with suppressed OLP to ensure suppression of the activated immune system is required as an element of the supportive implant therapy (SIT) [Fig. 6.12].
6.8 Conclusion
An adequate treatment plan and supportive periodontal and implant therapy, along with proper oral hygiene care, are the keys to the success of dental implant treat- ment. However, just like its natural predecessor, a dental implant may be subject to destructive soft and hard tissue pathology. Soft tissue pathology is the first sign of peri-implant diseases. Therefore, in the case of peri-implant soft tissue pathology, the knowledge of the accurate etiology as inflammatory, reactive, or autoimmune is essential to formulating the treatment goals of each clinical case situation. Following the decision trees at the end of this chapter will facilitate the platform form in the field of dental implant practice (Fig. 6.13).
6.2 Peri-Implant Soft Tissue
The scientists explored the anatomical difference between peri-implant soft tissue and tooth soft tissue to better clarify the anatomical variations between the inter- face of tooth-soft tissue and implant-soft tissue. The soft tissue profile and care around implants is significantly more complicated than around teeth for three primary factors:
1. Marginal mucosal area.
2. Attachment of connective tissues.
3. The vascular supply gaps.
The measurements of the supracrustal gingival tissue (SGT) (initially called biological width) are close to those present on the natural tooth and vary from 3 to 4 mm. The junctional epithelium is around 2 mm in length, and the connective tis- sue is nearly 1–1.5 mm. It binds to the implant and contains collagen fiber bundles, some of which invest in the periosteum of the bone crest and run a course parallel with the surface of the implant with more collagen and fewer fibroblasts. The three main sources of blood supply around the natural tooth are the following:
(a) The supraperiosteal vessels which supply the free and attached gingiva.
(b) Blood vessels from the periodontal ligament.
(c) Blood vessels from the alveolar bone.
The essential blood vessels from the periodontal ligament are absent in the case of implants. The single source of blood was from the supraperiosteal vessel at the alveolar bone periosteum. There is also a hypovascular–hypocellular connective tis- sue zone around the implant that is not found around natural tooth and more vulner- able to the inflammatory response (Fig. 6.1).
6.3 Peri-Implant Soft Tissue Importance
The mucosa surrounding the dental implant forms tight gingival cuff consisting of epithelium and connective tissues established during healing after the surgery. Multiple findings have evidence on comparisons and variations at the dent–gingival junction between peri-implant soft tissue and gingiva around natural tooth (Table 6.1).
6.4 Etiology of the Common Soft Tissue Pathology Around Dental Implants
Three main categories cause the soft tissue pathology around dental implants, broadly classified as inflammatory, reactive, and autoimmune. The inflammatory group is characterized by two major conditions of the inflamed peri-implant tissues and its underlying supporting bone: peri-implant mucositis and peri-implantitis. Reactive lesions in the oral cavity primarily include pyogenic granuloma (PG), peripheral giant cell granuloma (PGCG), and fibrous hyperplasia. Lastly, oral lichens planus, an autoimmune mucocutaneous inflammatory disease, should be considered.
6.5 Inflammatory Conditions That Cause Soft Tissue Pathology Around Dental Implants and Bone Loss
6.5.1 Peri-Implant Mucositis and Peri-Implantitis
Peri-implant mucositis is defined as a reversible inflammation in the soft tissues surrounding the implant, which constitute the main common soft tissue pathology around the dental implant (Fig. 6.2). The advanced/progressive form of it is peri- implantitis, which involves the soft and hard tissue component and defined as inflammation associated with loss of supporting bone around an implant (Fig. 6.3). This section of the chapter will focus on these common two conditions affecting soft and hard tissue around the dental implant in terms of etiology, diagnosis, and management.
6.5.2 Etiological and Risk Factors
The main etiology of both conditions is bacterial biofilm on the implant and restora- tions. However, many other multifactorial risk factors have been documented in the literature and attributed to the following: smoking, residual cement, trauma from occlusion, width and thickness of keratinized mucosa, foreign body reaction, untreated periodontal diseases, type of implant surface, genetic trait, lack of compli- ance, psychological reasons, and systematic diseases.
There is also evidence for radiation therapy as a risk indicator for peri-implant mucositis. There is some evidence for diabetes mellitus as a risk indicator for peri-implant mucositis. Poorly controlled diabetes mellitus (HbA1c levels > 10.1) was shown to be associated with increased bleeding on probing at implants. Ferreira et al. also reported an association with peri-implant mucositis and systemic disease. However, the systemic diseases described included “diabetes mellitus, hormonal changes, menopause, chemotherapy, thyroid alterations, cardiac problems, and alcohol use,” and thus the results of the study are difficult to interpret.
6.5.3 Diagnosis Criteria
The main clinical characteristics of peri-implant mucositis include bleeding on gen- tle probing; erythema, swelling, and/or suppuration may also be present. An increase in probing depth is often observed in the presence of peri-implant mucositis because of swelling or a decrease in probing resistance, which needs to be considered to avoid misdiagnosis. The absence of bone loss beyond crestal-bone-level changes, confirmed by radiographs, indicates alterations resulting from initial bone remodel- ing. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri-implant mucositis and can be resolved by nonsurgical periodontal therapy.
The diagnosis of peri-implantitis requires the presence of bleeding and/or sup- puration on gentle probing, an increase in probing depth compared to previous examinations, and the presence of bone loss beyond the crestal bone levels. In the absence of previous examination data, diagnosis of peri-implantitis can be based on the combination of the following: the presence of bleeding and/or suppuration on gentle probing, probing depths of ≥6 mm, and bone levels ≥3 mm apical to the most coronal portion of the intra-osseous part of the implant.
6.5.4 Treatment of Peri-Implant Mucositis and Peri-Implantitis
Peri-implant mucositis is primarily caused by a disruption of the host–microbe homeostasis at the implant–mucosa interface and is a reversible condition at the host biomarker level. Regular supportive peri-implant therapy with biofilm removal is an important first preventive strategy against the conversion of health to peri- implant mucositis and also against the progression of peri-implant mucositis to peri-implantitis.
In addition to the biofilm removal, it is very substantial to determine the goal of therapy for both peri-implant mucositis and peri-implantitis, which is usually con- fined to control of the bacterial etiology, elimination of soft tissue inflammation, implant surface decontamination, regenerative approach, resective approach, implant surface modification (implantoplasty), and re-osseointegration.
Furthermore, it is important to take into consideration the limitations of the therapy, ranging from accessibility, implant configuration, implant surface structure, soft tissue conditions, defect configuration, and grafting materials to the amount of bone loss .
As mentioned earlier, biofilm removal by nonsurgical mechanical debridement (MD) is the first treatment procedure for the treatment of peri-implant mucositis along with local chemotherapeutic antiseptic agents. There are numerous therapies, such as antibiotic and probiotic therapy, laminin coatings on implant surfaces, low- level laser therapy, and photodynamic therapy (PDT), that have been assessed as adjuncts to MD for the treatment of peri-implant diseases.
Photodynamic therapy (PDT) is another form of local therapy that has been used as an adjunct to MD for peri-implant diseases in several studies. In this form of adjunct therapy, a dye (photosensitizer) is locally delivered to the peri- implant sulci of infected sites and is then exposed to a laser with a wavelength usu- ally ranging between 660 to 800 nm. The resultant reaction produces reactive oxygen species (ROS), which possibly reduce inflammation and counts of pathogenic microbes at the treatment sites, thereby facilitating the overall healing process. Studies have explored the contribution of PDT as an aide treatment to routine oral hygiene maintenance instructions for the treatment of periodontal and peri-implant diseases. It has also been proposed that MD with adjunct PDT is more effective in reducing peri-implant soft tissue inflammation (peri-implant mucositis) than MD alone.
In cases of peri-implant mucositis, the etiology attributed to the lack of keratinized tissue (KT) surgical periodontal treatment, including gingival graft after the phase of MD, is considered. Although there was debate in the dental literature about the prevalence of peri-implant soft tissue diseases and lack of KT, an increase in the width of KT may be considered in order to improve and simplify the patient’s oral hygiene and to preserve the level of mucosal tissue. For dental implants and natural teeth alike, the value of having an acceptable width and density of KT tends to be important, comparably to teeth without KT, which were observed to be more vulnerable to more impairment of attachment. Tissue breakdown has also been found to develop more rapidly with dental implants than with teeth (Figs. 6.4 and 6.5).
Peri-implant mucositis, the most common soft tissue pathology around dental implants, seems to be a precursor to subsequent peri-implantitis. The treatment dur- ing the transitional stage typically involves antibacterial therapy, combined with MD before attempting surgical regeneration of peri-implant alveolar bone lost due to infection. Lang et al. in 1997 published a review of clinical trials on thera- pies for peri-implant infections, revealing that the inflammatory process in soft and mineralized peri-implant tissues can be controlled. This renders the site susceptible to regenerative procedures aimed at re-establishing osseointegration after nonsurgi- cal therapy and the administration of local and systematic antibiotics. However, as of today, no controlled studies have been performed to document the possibility of true osseointegration. A previous cited study proposed a well- documented system for the management of peri-implant diseases called cumulative interceptive supportive therapy (CIST). This approach is very helpful for the devel- opment of a joint effort for the management of soft and hard tissue conditions (Fig. 6.6).
Surgical treatment therapy for peri-implantitis, as it is the progressive disease of the common soft tissue pathology around dental implants, is mainly a regenerative approach. The treatment consisted of flap reflection, surface decontamination, use of enamel matrix derivative (EMD) or platelet-derived growth factor (PDGF), and guided bone regeneration with mineralized freeze-dried bone and/or anorganic bovine bone combined with PDGF or EMD and covered with an absorbable mem- brane and/or subepithelial connective tissue graft (Fig. 6.7).
However, the destructive soft tissue pathological inflammatory process affects both soft and hard tissues, leading to pocket formation and progressive bone resorption around osseointegrated oral implants. Explanation may be indicated in advanced stages with severe bone loss when soft tissue pathology cannot be eradicated with re-augmentation of the site for new implant placement and restoration (Fig. 6.8).
According to published studies, peri-implant diseases are very common. Therefore, it is imperative for the clinician to examine and evaluate patients who have been provided with implant-supported restorations on a regular basis.
The following aspects are recommended for the clinical routine:
When implant treatment is considered, patients should be informed of the risks for biological complications (peri-implant diseases) and the need for preventive care. An individual risk assessment, including systemic and local risk indicators, should be performed, and modifiable risk factors, such as residual increased probing pocket depth in the remaining dentition or smoking, should be eliminated. Hence, treatment of periodontal disease aiming for elimination of residual pockets with bleeding on probing and smoking cessation should precede implant placement.
The correct fit of implant components and the superstructures has to be ensured to avoid additional niches for biofilm adherence. If cemented implant restorations have been selected, the restoration margins should be located at the mucosal margin in order to allow meticulous removal of excess cement.
To facilitate personal oral hygiene, clinicians should consider having keratinized attached surrounding the transmucosal implant portion already during implant placement (for one-stage implant placement) or during abutment connection (for two-stage implant placement).
Professional supportive care should be established according to the individual needs of the patient (e.g., 3, 6, or 12-month recall intervals), and their compliance has to be confirmed. Particularly in patients with a history of aggressive periodontitis indicating an increased susceptibility for periodontal and peri-implant diseases, shorter recall intervals should be considered. During recall, peri-implant tissues must be regularly examined, including probing assessments with special emphasis on bleeding on probing.
6.6 Reactive Condition That Causes Soft Tissue Pathology Around Dental Implants and Bone Loss
6.6.1 Pyogenic Granuloma
Pyogenic granuloma is a common, reactive inflammatory hyperplasia of the oral cavity. Although the term “pyogenic” is used, PG is not an infectious lesion. PG usually occurs as a response to different stimulating factors such as local trauma or irritation and iatrogenic and hormonal factors. Because of the female hor- mone factor, it has a very high incidence in young females, principally in the second decade of life. Clinically, PG presents as a painless, smooth, or lobulated shape. It is classed as a hemorrhagic lesion because of its vascular structure, and its color ranges from pink to dark red. It is presented clinically as sessile with an average size of 1 cm and has a smooth, shiny surface. In addition, it bleeds very easily when touched. Sometimes, its surface may be covered by a pseudo-membrane due to secondary ulcerations.
It was reported that oral PG was found in 18% of patients who had benign oral masses. It was also noted that PG can be observed in individuals as young as 10 years old up to the age of 70. It is the second most common soft tissue pathology around dental implants after peri-implant mucositis, soft tissue fistula, and peri- implantitis. As mentioned previously, local trauma is the main etiological factor, with 30–50% of patients with PG having a history of local trauma. The occurrence of implant-related PG was associated with inappropriate healing caps of implants (Fig. 6.9).
Biopsy as a diagnostic approach is warranted because peripheral odontogenic lesions, benign and malignant neoplasms, metastatic lesions, and a variety of other lesions may clinically resemble this reactive nodular lesion of the gingiva. The his- topathologic analysis of PG usually reveals an intense vascular proliferation with extensive areas of ulceration, mixed inflammatory infiltrate, numerous granulation tissue, and abundant macrophages (multinucleated giant cells) (Fig. 6.9c). There are several treatment options for PG, such as surgical excision, cryother- apy, electro-cauterization, laser applications, and steroid injections . However providing adequate keratinized soft tissue should be the first step to prevent such lesions for reactive lesions related to dental implants. In addition, management should involve the detection and elimination of the possible local irritant factors, such as abnormal superstructure and healing cap implant relationships or unfavor- able implant–bone relationships. Soft tissue site preparation with gingival graft augmentation before implant placement is necessary to enhance the thickness and width of the keratinized gingiva when there is inadequate gingiva thickness and a lack of keratinization (Fig. 6.10).
6.7 Autoimmune Conditions That Cause Soft Tissue Pathology Around Dental Implants and Bone Loss
6.7.1 Oral Lichen Planus
Oral lichen planus (OLP) is a chronic mucocutaneous inflammatory disease. It affects the skin, nails, hair, and mucous membranes (oral and genital). It most commonly affects middle-aged individuals, predominantly females. Its preva- lence is between 0.1% and 2.2%. OLP is a T cell-mediated autoimmune disor- der of uncertain etiology. Besides immune dysregulation, many etiological factors may also be involved, including traumatic insults, medication, dental materi- als, and stress. It commonly affects buccal mucosa, tongue, and gingiva.
Due to the adverse effects of implant placement on LP and vice versa, implant placement should be done with caution. LP patients treated with dental implants are at a risk of implant failure due to the inability of the epithelium to attach to the implant surface, which allows the bacteria to access the preimplant tissue, leading to the failure of osseointegration. It has also been recommended that lichen planus patients be handled with care during the remission phase when the cases are stabilized. It should not be placed during the active phase of the LP, which will cause implant failure (Fig. 6.11).
Corticosteroids are the main treatment for symptomatically OLP. Topical steroids are considered first-line treatment because they are more effective in treating superficial inflammation, especially in EOLP. Other treatment modalities are being tried to increase the efficacy and decrease the complications of corticosteroids. The therapeutic potential of photodynamic therapy and lasers has been investigated. Ozone therapy is also being used to treat OLP due to its strong antimicrobial activity. Oral corticosteroid dose of 4 mg/daily after insertion of dental implants in patients with suppressed OLP to ensure suppression of the activated immune system is required as an element of the supportive implant therapy (SIT) [Fig. 6.12].
6.8 Conclusion
An adequate treatment plan and supportive periodontal and implant therapy, along with proper oral hygiene care, are the keys to the success of dental implant treat- ment. However, just like its natural predecessor, a dental implant may be subject to destructive soft and hard tissue pathology. Soft tissue pathology is the first sign of peri-implant diseases. Therefore, in the case of peri-implant soft tissue pathology, the knowledge of the accurate etiology as inflammatory, reactive, or autoimmune is essential to formulating the treatment goals of each clinical case situation. Following the decision trees at the end of this chapter will facilitate the platform form in the field of dental implant practice (Fig. 6.13).
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