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Implant related periodontal disease

Peri implant mucositis, Peri implantitis, Definition, classification, treatment modality, Comprehensive implant supportive therapy protocol

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Implant related periodontal disease

  1. 1. IMPLANT RELATED PERIODONTAL DISEASE PRESENTED BY: PRABLEEN ARORA MDS STUDENT
  2. 2. IMPLANT LOSS / FAILURE • Considered relative to the time of placement or restoration. Early implant failures • Occur before implant restoration • It probably did not achieve osseointegration, or the integration was weak or jeopardized. • Improper preparation of the recipient site which results in undue hard tissue damage such as necrosis of the bone. • Bacterial contamination and extensive inflammation of the wound that may delay healing of the soft and hard tissues • Improper mechanical stability of the implant following its insertion • Premature loading of the implant. Late implant failures • Occur after the implant has been restored. • Late implant failures occur after prosthesis installation. • Infection • Implant overload • Flemmig & Renvert (1999)
  3. 3. EXCESSIVE LOAD • “Excessive load" may be difficult to define and may vary from one subject and site to the next, factors such as occlusal force (trauma from occlusion) in relation to : 1) size of implant, 2) surface features of implant, 3) Quality of the host bone, must obviously be considered. • Clinical studies have indicated that peri-implant bone loss may be associated with load. (Lindquist et al. 1988, Sanz et al. 1991, Quirynen et al. 1992, Rangert et al. 1995)
  4. 4. INFECTION • The host response to biofilm formation on the implant includes a series of inflammatory reactions which initially occur in the soft tissue but which may subsequently progress and lead to loss of supporting bone. • The tissue destruction in the bone compartment starts in the "marginal", i.e. neck region, of the implant and crater-like bone defects develop and become visible in the radiograph.
  5. 5. • Peri-implant mucositis: Reversible inflammations of the soft tissues surrounding implants in function. • Peri-implantitis is defined as an inflammatory process affecting the tissues around an osseointegrated implant in function, resulting in loss of supporting bone. (Albrektsson & Isidor 1994)
  6. 6. Peri-implant mucositis • Clinical features of peri-implant mucositis :similar to those of in gingivitis at teeth and include classical symptoms of inflammation, such as swelling and redness. • Assessment of peri-implant mucositis must therefore always include assessment of bleeding following probing
  7. 7. HISTOPATHOLOGY • Zitzmann et al. (2001) studied the response to plaque formation in the soft tissues at implant and tooth sites in humans. • Twelve subjects with healthy periodontal and peri-implant conditions were asked to refrain from tooth/implant cleaning for a period of 3 weeks. • Clinical examinations were performed and soft tissue biopsies were harvested prior to and at the end of the plaque accumulation period. • The tissues were examined using histologic techniques. It was demonstrated that plaque buildup was associated with clinical signs of soft tissue inflammation. • Furthermore, the initially minute lesions in the gingiva and in the peri- implant mucosa markedly increased in size after 3 weeks of plaque build- up: from 0.03 mm at baseline to 0.3 mm (gingiva) and 0.2 mm2 (peri- implant mucosa). • In addition, the proportion of B cells and neutrophils increased more in the lesion in the gingiva than in its counterpart in the peri-implant mucosa.
  8. 8. • Berglundh et al. (1992) compared the reaction of the gingiva and the peri-implant mucosa to 3 weeks of de novo plaque formation. • Observed that similar amounts of plaque formed on the tooth and implant segments of the dentition. • The composition of the two developing plaques was also similar. It was therefore concluded that early microbial colonization on titanium implants followed the same pattern as that on teeth (Leonhardt et al. 1992). • Both the gingiva and the peri-implant mucosa responded to this microbial colonization with the establishment of overt inflammatory lesions, i.e. infiltrates of leukocytes in the connective tissue. • The lesions in the gingiva and in the peri-implant mucosa were matched both with respect to size and location. • Hence, both lesions were consistently found in the marginal portion of the soft tissues and between the keratinized oral epithelium and the junctional or barrier epithelium
  9. 9. Peri-implantitis Clinical features 1. An inflammatory lesion in the peri-implant mucosa . 2. Loss of periimplant bone. 3. Swelling and redness as well as bleeding on gentle probing. 4. Suppuration is also a frequent finding Diagnosis • Bleeding on probing (BoP) • Bone loss in radiographs. • Peri-implantitis initially affects the marginal part of the peri-implant tissues and the implant may remain stable and in function for varying periods of time. • Implant mobility is therefore not an essential symptom for peri-implantitis but may occur in a final stage of disease progression and indicates complete loss of integration.
  10. 10. SIGNS AND SYMPTOMS • There is radiological evidence for vertical destruction of the crestal bone. • The defect usually assumes the shape of a saucer around the implant , while the bottom part of the implant retains perfect osseointegration. • In some instances wedge-shaped defects develop along the implant. • Vertical bone destruction is associated with the formation of a peri-implant pocket. • There is bleeding after gentle probing with a blunt instrument and there may be suppuration from the pocket. • Tissues may or may not be swollen. Hyperplasia is frequently seen if implants are located in an area with nonkeratinized mucosa or if the suprastructure is an overdenture . • Pain is not a typical feature of peri-implantitis.
  11. 11. • Crater-formed defects around implants are frequently found in radiographs obtained from sites with peri-implantitis
  12. 12. • Estimation of the frequency of peri-implantitis is difficult and depends on the criteria used to separate health from disease. • A mean crestal bone loss of 0.9-1.6 mm during the first postsurgery year and bone loss in the range of 0.02 mm to 0.15 mm in the following years have been reported in numerous studies on two-stage implants with submerged initial healing phase and are considered normal for these systems. Adell R et al 1986. • A mean loss of 0.09 mm for mandibular implants and 0.01 mm for maxillary implants has been reported for one-stage nonsubmerged implants in the second year of service. Weber HP et al 1992.
  13. 13. Prevalence • Fransson et al. (2005) suggest that the prevalence of subjects with peri-implantitis within this implant population was about 28%. • Roos-Jansåker et al. (2006 b) examined 216 implant treated patients (Brånemark System®) after 9–14 years of function and reported that 16% of the subjects and 6.6% of the implants had peri-implantitis.
  14. 14. HISTOPATHOLOGY • Sanz et al. (1991) analyzed soft tissue biopsies from six patients with peri-implantitis and reported that 65% of the connective tissue portion was occupied by an inflammatory lesion. • Piattelli et al. (1998) described some pathological features of tissues harvested from 230 retrieved implants. It was reported that at sites where implants were removed due to peri- implantitis, “an inflammatory infiltrate, composed of macrophages, lymphocytes and plasma cells, was found in the connective tissue around the implants”. • Berglundh et al. (2004) found that the mucosa contained very large lesions in which numerous plasma cells, lymphocytes, and macrophages were present. • It was furthermore observed that the inflammatory cell infiltrate consistently extended to an area apical to the pocket epithelium and that the apical part of the soft tissue lesion frequently reached the bone tissue. • Berglundh et al. (2004) also reported that numerous neutrophil granulocytes (PMN cells) were present in the lesions. • Gualini and Berglundh (2003) included six subjects in a study and used immunohistochemical techniques to analyze the composition of peri-implantitis. PMN cells were found in large numbers in the central portions of the infiltrate.
  15. 15. CLASSIFICATIONS
  16. 16. • Schwarz et al. (2007) classified peri implant defect depending on the configuration of the bony defect as: Class I defect – Intraosseous Class II defect – Supra-alveolar in the crestal implant insertion area. Limitations: • This Classification informs about only two classes. • No clinical and radiological interpretation is evident.
  17. 17. Peri-implantitis is classified into Early Peri-implantitis PD4mm, Bleeding and/or suppuration on probing, Bone loss <25% of the implant length. Moderate Peri-implantitis PD6mm, Bleeding and/or suppuration on probing, Bone loss ranging from 25% to 50% of the implant length. Advanced Peri-implantitis PD8mm, Bleeding and/or suppuration on probing, Bone loss >50% of the implant length. LIMITATIONS: This classification provides a standarised method about clinical and radiographic status of implant but it does not share any information of information related to management of periimplantitis and prognosis. Atleast two aspect of implant with evidence of Bleeding and/or suppuration.  Bone loss was measured on most recently radiograph taken and compare with radiograph taken at the time of prothetic loading
  18. 18. Lang NP et al (2004) classification included treatment part in its classification. LIMITATIONS: This is a good classification which provides clinical radiological information and therapeutic part but still insufficient detail about type of bony defect and prognosis.
  19. 19. Zhang L et al (2014) demostrated classification of peri-implant bone defects (PIBDs) on the basis of their Panoramic radiographic shapes in patients with lower implant-supported overdentures. They are broadly classifieds into decreasing order of occurrence. 1. Saucer-shaped defects 2. Wedge-shaped defects 3. Flat defects 4. Undercut defects 5. Slit-like defects LIMITATIONS  This classification is given for lower implant-supported overdentures cases only and focus on different shapes and patterens of bony defects exclusively.  Lacks clinical and detailed radiographic interpretations.
  20. 20. Retrograde implantitis • Bone loss was measured on apico-coronal direction from apex of the implant to the most coronal point of extension of bone loss in millimeters. • Coronal portion of the implant sustains a normal bone to the implant interface. • Class I (Mild lesion) – Radiographic bone loss that extends < 25% of the implant length from implant apex. • Class II (Moderate lesion) – Extends 25–50% of the implant length fron implant apex. • Class III (Severe) – >50% of the implant length fron implant apex. It is a good classification of retrograde implantitis. None of the classifications described have mentioned any point about this.
  21. 21. RISK INDICATORS • A recent review by Lindhe and Meyle from the Consensus Report of the Sixth European Workshop on Periodontology concluded that risk indicators for peri- implantitis included: (1) Poor oral hygiene (2) History of periodontitis (3) Diabetes (4) Cigarette smoking (5) Alcohol consumption (6) Implant surface J Clin Periodontol 2008.
  22. 22. Dental plaque and poor oral hygiene • In a study by Ferreira et al. 2006 higher total plaque scores were statistically associated with peri-implant disease and a very poor oral hygiene status, as described by median scores of full-mouth plaque >2, was highly associated with peri-implantitis. • In another study, most patients had relatively good plaque control in their residual teeth but not at implant sites, and inadequate plaque control was detected in around 74% of the implants. Implant sites less accessible by oral hygiene measures showed more peri-implant infectious lesions (48%) than other favorable sites (4%). Strom C et al 2009. • This observation suggested that local factors such as poor oral hygiene and the presence of dental plaque play an important role in the development of peri-implantitis. Thus, the control of oral hygiene and periodontal status should be monitored before and after the implant insertion to prevent or at least to minimize the risk of developing peri-implantitis. • Furthermore, plaque retention is also influenced by the form of implant- supported prostheses, which must be determined before establishing a treatment plan as well as choosing the number and type of implants.
  23. 23. History of periodontitis • The frequency of implant failure in a partial loss of teeth was significantly higher than in a total loss. • However, study by Renvert et al. 2007 indicates that while peri- implantitis is not dependent on the partial or total loss of teeth, a history of periodontitis was a crucial risk for periimplant mucosititis and peri-implantitis. • Patients with a history of chronic periodontitis have a higher prevalence of peri-implantitis (28.6%) than healthy patients (5.8%). Lang NP et al 2003. • A recent study by Koldsland et al. 2011 also indicates that individuals with a history of periodontitis are prone to peri- implantitis if they had peri-implant bone loss >2 mm. • Likewise, a systematic review by Renvert et al. concluded that patients with treated periodontitis may be at greater risk for peri- implant infections than those without. Because the pathogenic flora in peri-implantitis are similar to that found in periodontitis, periodontal pockets are probably a reservoir of microorganisms colonizing implant surfaces.
  24. 24. Diabetes • A study by Ferreira et al. 2006 showed that patients with diabetes (diagnosed by fasting blood sugar >126 mg/dL or taking anti-diabetic medicine over the previous 2 weeks) were more prone than those without diabetes to develop peri-implantitis. • Furthermore, the presence of diabetes was statistically associated with an increased risk of peri-implantitis. It seems that poor metabolic control in diabetics made patients more susceptible to infection and implant loss. The clinician should inform diabetic patients of their possible increased risk for periimplantitis.
  25. 25. Smoking • Smoke was identified as a major risk factor of both periodontitis and peri- implantitis. • A recent study by Rodriguez-Argueta et al. 2011 showed that smokers had an increased risk of infection, implant loss, mucositis and peri-implantitis than non-smoking patients. • The pathogenic mechanisms of smoking may be explained by the toxic effects of the more than 4000 toxins present in cigarettes. • Nicotine is a potent vasoconstrictor that reduces blood flow and nutrient delivery to healing sites. • Some compounds of tobacco also act as chemotactic substances that enhance tissue destruction by enzymes released by neutrophils and macrophages. • Peri-implantitis was more frequent in smokers (9.2%) than non-smokers (5.3%).30 Smokers had more severe inflammatory signs, deeper peri- implant pockets and larger peri-implant bone loss than non-smokers. • The influence of smoking on peri-implant tissue was greater in the maxilla than the mandible. Several retrospective studies over 8 years have also shown that smokers had a high risk of developing peri-implantitis and bone loss.
  26. 26. Alcohol consumption • Individuals who use alcohol may have a vitamin K deficit disrupting the production of prothrombin, thus affecting coagulation mechanisms. • Alcohol consumption is associated with deficiencies of the complement system, alteration of the neutrophil function and modulating T lymphocyte activity. • Moreover, some substances contained in alcoholic drinks such as fusel oil, nitrosamines and ethanol, can cause bone destruction and block the stimulation of bone neoformation. • Only one study by Galindo-Moreno et al. concluded that peri-implant marginal bone loss was statistically linked to alcohol consumption >10 g per day and that alcohol induced more serious peri-implantitis than cigrarettes.
  27. 27. Implant surface characteristics • Most recent titanium implants with a rough surface showed more favorable osseointegration than those with smooth surfaces. • However, a rough surface also favored the formation and retention of dental plaque. • Roughness increased both the adhesive surface of bacteria and the difficulty in cleaning the implant. Quirynen M et al 2006. • In a study by Astrand et al. in 2004, ITI Dental Implant System implants (Straumann AG, Waldenburg, Switzerland) with a plasma-sprayed surface had a statistically higher incidence of peri-implantitis than Branemark System implants (Nobel Biocare AB, Gothenburg, Sweden) with a smooth surface. • Conversely, a systematic review by Esposito et al. showed that there was no statistically significant difference in the incidence of peri-implantitis between smooth and rough implant surfaces. • Likewise, in a recent review by Renvert et al., there was no evidence that implant surface characteristics can have a significant effect on the initiation of peri-implantitis.
  28. 28. Genetic traits • A study by Cornelini et al. showed a significant increase in the density of blood microvessels in peri-implantitis sites, but the expression of vascular endothelial growth factor (VEGF) was statistically low. • Thus, VEGF could play a protective role in peri-implantitis. • There was an correlation between the polymorphisms of the interleukin (IL)-1-specific gene and peri-implant bone loss in smokers. • Jansson et al. showed that the IL-1 genotype was a risk indicator of peri-implantitis and there was a synergistic effect between the IL-1 genotype and smoke. • However, two other studies failed to find an association between the IL-1 genotype and peri-implantitis or of implant failure or bone loss. Therefore, future prospective studies with large numbers of patients are necessary to confirm this association.
  29. 29. Lacking keratinized mucosa • A study by Block et al. suggested that the presence of keratinized gingiva around implants was correlated with the health of both soft and hard tissue as well as implant survival. • However, an analysis of multiple potential factors of peri-implant mucositis and peri-implantitis was performed, but no association between the absence of keratinized gingiva and peri-implant infection was found. • Therefore, lacking keratinized mucosa has not currently been confirmed as risk factor of peri- implantitis.
  30. 30. Other non-confirmed risks • Xerostomia could be a risk factor for peri- implantitis. • In fact, a decrease of salivary flow was often accompanied by a change in its composition and reducing bacterial clearance in the oral cavity. • More viscous saliva with a reduction of antibacterial activity promoted the formation of dental plaque and bacterial growth
  31. 31. Evidence based risk factors Substantial evidence •Poor oral Hygiene •History of periodontitis •Smoking Limited evidence •Diabetes •Alcohol consumption (> 19g / day) Controversial and limited evidence •IL-1 Polymorphism •Absence of Keratinized mucosa •Microtopography of implant surface Lindhe J, Meyle J. J Clin Periodontol 2008;35:282-285
  32. 32. DIAGNOSIS • Peri-implant diagnostic procedures can serve several functions: (i) Screening for peri-implant disease or for factors increasing the risk to develop an undesirable condition. (ii) Differential diagnosis of peri-implantitis and peri- implant mucositis. (iii) Treatment planning. (iv) Evaluation of therapy and monitoring.
  33. 33. Clinical diagnosis • A periodontal probe is an essential tool for the clinical diagnosis of peri-implantitis. Probing with a light force of 0.25 N does not cause peri-implant tissue damage and it is recommended for evaluating peri-implant disease. • Clinical signs of peri-implantitis are bleeding on probing in conjunction with peri-implant pockets >5 mm with or without suppuration. • In fact, bleeding on probing and suppuration indicate the presence of inflammation and infection. Because healthy implants generally have probing depths that are less than 4 mm, peri-implant pockets of 5 mm or more should be regarded as an indicator of bone loss and hence, a radiographic evaluation is required.
  34. 34. • A peri-implant pseudopocket could be present as soft tissues that are positioned above the implant shoulder intentionally for esthetic reasons. • Also, peri-implant hyperplasia is often found in an area of absence of keratinized gingiva or the overflow of supra-implant structures. • Contrariwise, platform-switched or abutment designs could also provoke difficult probing and the probing depth may hence underestimate the extent of the lesion • Implant mobility is not used to diagnose peri- implantitis because it indicates the complete loss of osseointegration and the failure of the implant. • Moreover, pain is not a typical sign of peri-implantitis
  35. 35. Radiographic assessment • In the First EWOP (1994) it was proposed that marginal bone loss of less than 1.5 mm during the first year in function and less than 0.2 mm per year thereafter to be one of the major criteria for success. • Baseline radiographs should be taken to determine alveolar bone levels after physiological remodeling and when clinical signs suggest peri-implantitis, a radiograph of the site is required to confirm the diagnosis. • In two recent studies by Koldsland et al (2010) it was proposed that a radiographic peri- implant bone loss >2 mm was a possible risk indicator of peri-implantitis. • In terms of dental radiographic techniques, panoramic radiography gives a complete visualization of anatomical structures around implants but its use is limited because of its low resolution and image distortion. • Periapical radiography is often used to verify marginal bone level or interproximal bone loss in peri-implantitis. However, our inability to assess facial and lingual or palate bone tables and the underestimation of intraosseous lesions are still limiting conventional radiography. • For minimizing the eventual error of a radiographic assessment of bone loss, the utilization of individual or fixed angulators could be useful to prevent image deformation. • Currently, multi-slice computer tomography and cone beam volume imaging offer implant dentistry certain advantages, such as representing infrabony lesions in three planes, true to scale and without any overlay or distortion. • Furthermore, computer-assisted image analysis, such as subtraction radiography, permits the detection of small changes in bone density.
  36. 36. Microbiological test • A microbiological test of subgingival microflora using a bacteria culture, checkerboard DNA–DNA hybridization, polymerase chain reaction (PCR), monoclonal antibody and enzyme assays have been proposed to determine an elevated risk for periodontal disease or peri-implantitis. • High levels of Porphyromonas gingivalis, P intermedia and Actinobacillus actinomycetemcomitans increased the risk for further attachment loss in maintenance patients
  37. 37. Differential Diagnosis Peri-implant mucositis • Peri-implant mucositis may be identified clinically by redness, swelling of the soft tissue without loss of supporting bone (probing depth <5 mm) and bleeding on probing are currently considered to be important indicators. • The treatment of peri-implant mucositis includes the removal of dental plaque and calculus by using appropriate instruments and oral hygiene instruction without antiseptic or combined with antiseptic. • Likewise, the literature review of Renvert et al (2008) confirmed that mechanical non-surgical therapy could be effective in the treatment of periimplant mucositis and the adjunctive use of antimicrobial mouth rinses enhanced the outcome of such therapy. • However, two later studies indicated that an adjunctive application of chlorhexidine did not enhance results in comparison with mechanical cleansing alone. • Furthermore, the treatment of peri-implant mucositis is useful for the prevention of peri-implantitis because mucositis represents an obvious precursor of peri- implantitis.
  38. 38. Occlusal overload • Occlusal overload together with peri-implantitis are the major causes of implant loss. • Factors associated with occlusal overload or occlusal trauma probably consist of an  excessive expansion of a prosthesis in the posterior region,  implant alignments,  a significant deviation of the implant axis from the function axis,  an important ratio of crown height/implant length,  a discrepancy in dimensions between the implant head and occlusal table. • An occlusal overload can cause the complete bone loss of an osteointegrated implant. • Bone destruction is accelerated if occlusal trauma is combined with peri-implant infection. • In fact, the marginal bone loss due to overload is often accompanied by attachment loss and deepening of the pockets. • After some time the newly created anaerobic environment will inevitably harbor periopathogenic flora. • Therefore, the presence of pathogenic subgingival flora after occlusal overload may reflect a secondary infection of a favorable environment which can contribute to further loss of marginal bone.
  39. 39. • Occlusal correction is necessary to stop the progress of bone destruction. Control of occlusion by progressive loading depending on bone density can reduce peri-implant bone loss in a healing phase. • A case report of occulsal overload associated with peri-implantitis used combined treatment methods including occlusal adjustment, the surgical removal of contaminated tissue and an autogenous bone graft. After 12 months, a radiograph revealed marginal bone regeneration and a normal clinical aspect was observed. Uribe R et al 2004.
  40. 40. Retrograde peri-implantitis • Retrograde peri-implantitis is defined as a clinically symptomatic periapical lesion (diagnosed as a radiolucency) that develops shortly after implant insertion while the coronal portion of the implant becomes a healthy bone at the implant interface. Quirynen M et al 2005 • Clinical symptoms include: • pain, • Tenderness • swelling or presence of a fistulous tract.
  41. 41. • The etiology of retrograde peri-implantitis may be bacterial contamination during the implant insertion or pre-existing bone inflammation (such as bacteria, a cyst or granuloma after tooth extraction). • Compared with successful implants, these periapical lesions appear on extracted tooth sites that have a history of endodontic pathology. • The lesion forms at the apex of the implant but it does not extend to the coronal, proximal or facial area. • Quirynen et al. (2005) suggested the treatment method of retrograde lesions, includes :  the complete removal of granulation tissue,  curettage of bony cavity walls  Filling substitutive bone (Bio-Oss). • The surgery was performed under the antibiotic coverage of forms of b- lactamase-resistant penicillin. • Once diagnosed, the lesion should be treated surgically rather than by observation and conservative management
  42. 42. Non-surgical treatment of peri-implantitis • Mechanical therapy alone • The formation of dental plaque was crucial to the development of the peri- implant infections (such as periimplant mucositis and peri-implantitis) that altered the biocompatibility of the implant surface. • Treatment of infected implant surface and the reduction of pathogenic bacterial flora around the implant are the main goals of peri-implantitis treatment. • The specific morphology of implant thread combined with a modified surface facilitated bacterial colonization but limited the efficiency of conventional cleaning instruments. • In addition, debridement using metal instruments harder than titanium could alter the implant surface, therefore curettes or inserts in plastic or carbon fiber were recommended. • A study by Karring et al. showed that non-surgical mechanical treatment alone was insufficient to eliminate peri-implant lesions. Although bleeding on probing had improved after 6 months, the peri-implant pocket depth was unchanged.
  43. 43. • A microbiological test of subgingival microflora using a bacteria culture, checkerboard DNA–DNA hybridization, polymerase chain reaction (PCR), monoclonal antibody and enzyme assays could suggest antibiotic therapy • In fact, peri-implantitis is associated in most cases with a mixed anaerobic flora, including Fusobacterium spp. And P. intermedia in high numbers. Antimicrobial agents such as metronidazole and ornidazole, which act specifically against strict anaerobes, seem to be an excellent choice for this type of infection. • However, a limited number of patients may have peri-implantitis lesions that are dominated by Staphylococcus spp. or metronidazole-resistant Aggregatibacter actinomycetemcomitans or enteric bacteria and yeasts. • Moreover, certain cases of peri-implantitis are characterized by periods of rapid and marked destruction compared with periodontitis. • This progression may be explained by the host response to specific infectious agents.
  44. 44. Mechanical therapy with an adjunct of an antiseptic agent • The mechanical non-surgical debridement alone was not effective in reducing bacterial flora around infected implants. • The addition of antimicrobial treatment therefore seems necessary to improve clinical results. • The antimicrobial treatment using a topical application of chlorhexidine was proposed to complete the mechanical treatment.70,71 • However, a local irrigation of 0.12% chlorhexidine combined with a local application of 0.12% chlorhexidine gel and a mouthwash containing 0.12% chlorhexidine for 10 days gave a no better result. • Peri-implantitis was treated using a plastic curette associated with an antiseptic (chlorhexidine 0.2%) and improved clinical parameters such as the reduction of bleeding on probing and of the pocket depth after 6 months, but residual defects still persisted. • These results suggested that chlorhexidine has a limited antimicrobial effect in infectious peri-implant lesions.
  45. 45. Mechanical therapy with an adjunct of antibiotic therapy • Mombelli and Lang 1992 conducted a study for the treatment of peri-implant infections by combining mechanical debridement with systemic antimicrobial therapy. • The bleeding on probing index immediately decreased after systemic antibiotic therapy and there were also quantitative and qualitative changes of pathogenic flora. • However, these parameters were reversible after the treatment period. • A local application releasing a high dose of antibiotic in infected sites for several days effectively cleared bacteria that were not eliminated by mechanical treatments. • In fact, debridement followed by an insertion of non-resorbable fibers containing tetracycline (Actisite) in peri-implant pockets for 10 days showed a significant reduction of pocket depth after 12 months. • Buchter et al. 2004 compared the efficiency of mechanical treatment alone using a plastic curette with mechanical treatment combined with a local application of bioresorbable polymer-releasing doxycycline (Atridox). The results after 4 months showed that patients treated with Atridox had a higher clinical attachment gain than those treated by debridement alone. The reduction of bleeding on probing and peri-implant pockets was statistically significant only among patients in the Atridox treatment group. • A recent study combining mechanical treatment with a repeated local application of minocycline microspheres (Arestin) after 30 and 90 days showed benefits in the therapy of peri-implantitis. This study also indicated that mechanical treatment combined with the local application of an antibiotic achieved a better result
  46. 46. Surgical treatment of peri-implantitis • The major objective for such an approach is to provide access for removal of the biofilm and calcified deposits from the implant surface in order to allow healing and reduce the risk for further disease progression. • If non-surgical treatment fails, surgical intervention with open debridement and resective or regenerative therapy is recommended. • The basic principles include the elimination of the periimplant osseous defect using ostectomy and osteoplasty as well as bacterial decontamination. • Additionally, smoothening and polishing of the supracrestal implant surface (implantoplasty) may be applied.
  47. 47. • When surgical intervention is necessary, an inverse bevel incision is recommended to facilitate flap elevation and preserve soft tissue. • Following removal of the soft-tissue collar from the infected tissue around the implant, mechanical decontamination to remove plaque and mineralized deposits from the implant surface should be performed and, for this task, instruments made of pure titanium are recommended . • The use of a titanium rotary brush makes this procedure easier than use of conventional curettes .
  48. 48. • In the presence of a crater-like fourwall bony defect or a three-wall defect, regenerative techniques are recommended and the use of autogenous bone or bone substitutes can be used to obtain bone fill.
  49. 49. • Airborne-particle abrasion devices have also been recommended for the decontamination of implant surfaces during surgery but because of the risk of developing subcutaneous emphysema, care must be taken during their use. • A number of other methods for decontamination, such as the use of lasers or abrasive devices, and implantoplasty of the exposed part of the implant, have been suggested as adjuncts to surgical resective or regenerative surgery. • Implantoplasty is an alternative option to improve the implant surface topography to reduce microbial adhesion and colonisation thus preventing re-infection of the site.This involves mechanically adjusting the exposed implant threads with rotary instruments to reduce the roughness of the surface and therefore minimise future plaque retention.
  50. 50. • Serino et al. (2011) showed that in patients with active periimplant disease surgical pocket elimination and bone recontouring in combination with plaque control before and after surgery represents an effective treatment. Two years after open reduction of inflammated peri-implant soft tissue and osseous surgery 48% of the patients had no signs of peri-implantitis and 77% of the patients had no implants with pocket depths ≥ 6 mm with bleeding and/or suppuration.
  51. 51. • In a radiographic study with 3 years follow-up, Romeo et al. (2007)showed that the marginal bone loss after resective surgery with implantoplasty was significantly lower than after resective therapy only
  52. 52. • Resective surgical therapy for peri-implantitis is a recommendable therapy option. • Ostectomy and osteoplasty combined with implantoplasty represent an effective therapy to reduce or even stop peri-implantitis progression. • Nevertheless, due to the increased postoperative recessions, this procedure is not suitable for every situation, especially in highly esthetic sensitive areas.
  53. 53. Regeneration • Resective surgical therapy may result in re- osseointegration in only minor superficial defects. • From functional, esthetic and long-time-survival point of views, full regeneration and re- osseointegration is aspired.
  54. 54. A study of autogenous bone graft on 17 patients with 25 treated implants showed a reduction of the peri-implant pocket from 6.9 to 0.7 mm (P = 0.001), corresponding to 90% bone reconstruction and improvement of marginal bone level from 6.2 to 2.3 mm after 2–3 years. Vertical bone resorption under 4.5 mm was completely regenerated. Behneke A et al (2000
  55. 55. MAINTENANCE FOR DENTAL IMPLANT PATIENTS • Patients with periodontitis-associated tooth loss are at significantly increased risk of developing periimplantitis. • The overall periodontal condition in partially edentulous implant patients can influence the clinical condition around implants. • The microflora of implants in partially edentulous patients differs from that in edentulous patients. • The implant microflora is similar to tooth microflora in the partially edentulous mouth. • Periodontal and implant maintenance are linked because maintenance of a tooth microflora consistent with periodontal health is necessary to maintain implant microflora consistent with periimplant health. • Because periimplantitis is difficult to treat,it is extremely important to treat periodontal disease before implant placement and to provide good supportive therapy with implant patients.
  56. 56. • In general, procedures for maintenance of patients with implants are similar to those for patients with natural teeth, with the following three differences: 1. Special instrumentation that will not scratch the implants are used for calculus removal on the implants. • Metal hand instruments and ultrasonic and sonic tips should be avoided because they can alter the titanium surface. • Only plastic instruments or specially designed gold plated curettes should be used for calculus removal because the implant surfaces can be easily scratched. • The rubber cup with flour of pumice, tin oxide, or special implant- polishing pastes should be used on abutment surfaces with light, intermittent pressure 2. Acidic fluoride prophylactic agents are avoided because they cause surface damage to titanium abutments 3. Nonabrasive prophy pastes are used.
  57. 57. • Known as the cumulative interceptive supportive therapy (CIST). • Depending on the clinical and eventually the radiographic diagnosis, protocols for preventive and therapeutic measures designed to intercept the development of peri-implant lesions. • This system of supportive therapy is cumulative in nature and includes four steps. • The 4 steps are Mechanical debridement, CIST • protocol A • 1. Antiseptic therapy, CIST protocol A and B • 2. Antibiotic therapy, CIST protocol A + B • 3. Antibiotic therapy, CIST protocol A + B + C • 4. Regenerative or resective therapy, CIST protocol • A+B+C+D
  58. 58. Conclusion • Successful management of peri implantitis requires a thorough understanding of the underlying medical and dental factors involved in the overall complex of the disease. The continuous development of new diagnostic and therapeutic methods has made it possible to prevent progression of the disease in most cases and to give these patients a long-term perspective for retention of their implant bone restoratio

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