Conventional diagnostic criteria for periodontal diseases (plaque-induced gingivitis and periodontitis).

This narrative review addresses conventional diagnostic criteria used in clinical practice to discriminate between periodontal health, gingivitis, and periodontitis. Visual examination of the color and texture of the periodontal tissues, assessment of plaque deposits, periodontal probing assessments, and diagnostic imaging enable the collation of information to make a periodontal diagnosis, followed by an appropriate treatment plan. The periodontal probe is an essential diagnostic tool to assess probing pocket depth, clinical attachment level, bleeding on probing, and the degree of furcation involvement at multirooted teeth. When clinical signs and symptoms of periodontitis are identified, diagnostic imaging enables evaluation of the level and extent of bone destruction and bone defect morphology. The diagnostic process requires clinicians who are trained to evaluate, record, and interpret these measures. This narrative review focuses on conventional clinical diagnostic parameters which, despite their limitations, are considered the current standard of care.

Peri-implant mucositis and peri-implantitis: key features and differences.

Peri-implant diseases are frequent complications that occur around osseointegrated endosseous implants and are the result of an imbalance between the bacterial challenge and host response. Peri-implant diseases may affect the peri-implant mucosa only (peri-implant mucositis) or also involve the supporting bone (peri-implantitis). Early detection of peri-implant diseases and timely treatment is important for the success of dental implant treatment. Peri-implant probing is essential to assess the peri-implant health status and should be done at each recall visit. Dental practitioners should be familiar with the clinical and radiological features of both conditions in order to make an accurate diagnosis and determine the appropriate treatment required. This article aims to provide clinicians with an understanding of the key differences between peri-implant health, peri-implant mucositis and peri-implantitis.

Surgical peri-implantitis treatment with and without guided bone regeneration. A randomized controlled trial.

OBJECTIVE: To evaluate the efficacy of reconstructive peri-implantitis treatment. MATERIALS AND METHODS: Forty participants, with peri-implantitis and a contained intraosseous defect, were randomized to access flap (control) or access flap with xenograft and collagen membrane (test). All received systemic antimicrobials. Blinded examiners recorded probing depths (PD), bleeding and suppuration on probing (BOP & SOP), soft tissue levels, and marginal bone levels (MBL) at baseline and 12 months. Patient reported outcomes were recorded. The primary outcome was PD change. RESULTS: All 40 participants (40 implants) completed the 12-month study. The mean (standard deviation) PD reduction (deepest site) was 4.2 (1.8) mm in the control and 3.7 (1.9) mm in the test group. MBL gain (deepest site) was 1.7 (1.6) mm in the control and 2.4 (1.4) mm in the test group. Absence of BOP & SOP was observed at 60% of both control and test implants. Buccal recession was 0.9 (1.6) mm in the control and 0.4 (1.1) mm in the test group. A successful outcome (absence of PD ≥ 5 mm with BOP, absence of SOP and absence of progressive bone loss) was achieved for 90% of the control and 85% of test group implants. No statistically significant differences in clinical or radiographic parameters were found between treatment groups. 30% of participants experienced mild gastro-intestinal disturbances. Reporting followed CONSORT guidelines. CONCLUSION: Similar clinical and radiographic improvements at 12 months were observed with high levels of patient satisfaction for both the access flap and xenograft covered by collagen membrane groups. Registered clinical trials.gov. ID:NCT03163602 (23/05/2017).

Supportive care for the prevention of disease recurrence/progression following peri-implantitis treatment: A systematic review.

OBJECTIVES: This systematic review aimed to evaluate the efficacy of supportive care provision, frequency and protocol in patients treated for peri-implantitis, as reported in prospective and retrospective studies of at least 3-years duration. MATERIALS AND METHODS: A systematic search of three electronic databases was undertaken up to 21 July 2022 and supplemented by hand-search to identify studies that included participants treated for peri-implantitis and followed for at least 3 years. Owing to high heterogeneity, a meta-analysis was not appropriate, and therefore, data and risk of bias were explored qualitatively. PRISMA guidelines for reporting were followed. RESULTS: The search identified 2596 studies. Of 270 records selected during screening, 255 were excluded through independent review and 15 studies (10 prospective and 5 retrospective, with at least 20 patients) were retained for qualitative assessments. Study designs, population characteristics, supportive care protocols and reported outcomes varied markedly. Thirteen of the 15 studies had low risk of bias. Supportive peri-implant care (SPIC) following different surgical peri-implantitis treatment protocols and with recall intervals varying between 2 months and annually resulted in peri-implant tissue stability (no disease recurrence or progression) ranging from 24.4% to 100% at patient level and from 28.3% to 100% at implant level. Sevenhundred and eighty-five patients with 790 implants were included in this review. CONCLUSIONS: Provision of SPIC following peri-implantitis therapy may prevent disease recurrence or progression. Insufficient evidence is available to identify (i) a specific supportive care protocol for secondary prevention of peri-implantitis, (ii) the effect of adjunctive local antiseptic agents in the secondary prevention of peri-implantitis and (iii) the impact of frequency of supportive care measures. Prospective, randomised, controlled studies designed to evaluate supportive care protocols are needed in future.

Occurrence, associated factors and soft tissue reconstructive therapy for buccal soft tissue dehiscence at dental implants: Consensus report of group 3 of the DGI/SEPA/Osteology Workshop.

OBJECTIVES: To systematically assess the literature and report on (1) the frequency of occurrence of buccal soft tissue dehiscence (BSTD) at implants, (2) factors associated with the occurrence of BSTD and (3) treatment outcomes of reconstructive therapy for the coverage of BSTD. MATERIALS AND METHODS: Two systematic reviews addressing focused questions related to implant BSTD occurrence, associated factors and the treatment outcomes of BSTD coverage served as the basis for group discussions and the consensus statements. The main findings of the systematic reviews, consensus statements and implications for clinical practice and for future research were formulated within group 3 and were further discussed and reached final approval within the plenary session. RESULTS: Buccally positioned implants were the factor most strongly associated with the risk of occurrence of BSTD, followed by thin tissue phenotype. At immediate implants, it was identified that the use of a connective tissue graft (CTG) may act as a protective factor for BSTD. Coverage of BSTD may be achieved with a combination of a coronally advanced flap (CAF) and a connective tissue graft, with or without prosthesis modification/removal, although feasibility of the procedure depends upon multiple local and patient-related factors. Soft tissue substitutes showed limited BSTD coverage. CONCLUSION: Correct three-dimensional (3D) positioning of the implant is of utmost relevance to prevent the occurrence of BSTD. If present, BSTD may be covered by CAF +CTG, however the evidence comes from a low number of observational studies. Therefore, future research is needed for the development of further evidence-based clinical recommendations.

Implant Disease Risk Assessment IDRA-a tool for preventing peri-implant disease.

OBJECTIVE: This treatment concept paper introduces a risk assessment tool, the Implant Disease Risk Assessment, (IDRA) which estimates the risk for a patient to develop peri-implantitis. MATERIALS AND METHODS: The functional risk assessment diagram was constructed incorporating eight parameters, each with documented evidence for an association with peri-implantitis. RESULTS: The eight vectors of the diagram include (1) assessment of a history of periodontitis (2) percentage of sites with bleeding on probing (BOP) (3) number of teeth/implants with probing depths (PD) ≥5 mm (4) the ratio of periodontal bone loss (evaluated from a radiograph) divided by the patient's age (5) periodontitis susceptibility as described by the staging and grading categories from the 2017 World Workshop on the Classification of Periodontal and Peri-implant Diseases (Journal of Periodontology, 89 Suppl 1, S159-S172, 2018) (6) the frequency/compliance with supportive periodontal therapy (7) the distance in mm from the restorative margin of the implant-supported prosthesis to the marginal bone crest and (8) prosthesis-related factors including cleanability and fit of the implant-supported prosthesis. CONCLUSION: The combination of these factors in a risk assessment tool, IDRA, may be useful in identifying individuals at risk for development of peri-implantitis.

Peri-implant mucositis.

OBJECTIVES: This narrative review was prepared for the 2017 World Workshop of the American Academy of Periodontology and European Federation of Periodontology to address key questions related to the clinical condition of peri-implant mucositis, including: 1) the definition of peri-implant mucositis, 2) conversion of peri-implant health to the biofilm-induced peri-implant mucositis lesion, 3) reversibility of peri-implant mucositis, 4) the long-standing peri-implant mucositis lesion, 5) similarities and differences between peri-implant mucositis at implants and gingivitis at teeth, and 6) risk indicators/factors for peri-implant mucositis. METHODS: A literature search of MEDLINE (PubMed) and The Cochrane Library up to and including July 31, 2016, was carried out using the search strategy (peri-implant[All Fields] AND ("mucositis"[MeSH Terms] OR "mucositis"[All Fields])) OR (periimplant[All Fields] AND mucosits[All Fields]). Prospective, retrospective, and cross-sectional studies and review papers that focused on risk factors/indicators for peri-implant mucositis as well as experimental peri-implant mucositis studies in animals and humans were included. FINDINGS: Peri-implant mucositis is an inflammatory lesion of the soft tissues surrounding an endosseous implant in the absence of loss of supporting bone or continuing marginal bone loss. A cause-and-effect relationship between experimental accumulation of bacterial biofilms around titanium dental implants and the development of an inflammatory response has been demonstrated. The experimental peri-implant mucositis lesion is characterized by an inflammatory cell infiltrate present within the connective tissue lateral to the barrier epithelium. In long-standing peri-implant mucositis, the inflammatory cell infiltrate is larger in size than in the early (3-week) experimental peri-implant mucositis lesion. Biofilm-induced peri-implant mucositis is reversible at the host biomarker level once biofilm control is reinstituted. Reversal of the clinical signs of inflammation may take longer than 3 weeks. Factors identified as risk indicators for peri-implant mucositis include biofilm accumulation, smoking, and radiation. Further evidence is required for potential risk factors, including diabetes, lack of keratinized mucosa, and presence of excess luting cement. CONCLUSIONS: Peri-implant mucositis is caused by biofilm accumulation which disrupts the host-microbe homeostasis at the implant-mucosa interface, resulting in an inflammatory lesion. Peri-implant mucositis is a reversible condition at the host biomarker level. Therefore, the clinical implication is that optimal biofilm removal is a prerequisite for the prevention and management of peri-implant mucositis. An understanding of peri-implant mucositis is important because it is considered a precursor for peri-implantitis.

Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions.

A classification for peri-implant diseases and conditions was presented. Focused questions on the characteristics of peri-implant health, peri-implant mucositis, peri-implantitis, and soft- and hard-tissue deficiencies were addressed. Peri-implant health is characterized by the absence of erythema, bleeding on probing, swelling, and suppuration. It is not possible to define a range of probing depths compatible with health; Peri-implant health can exist around implants with reduced bone support. The main clinical characteristic of peri-implant mucositis is bleeding on gentle 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 due to swelling or decrease in probing resistance. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri-implant mucositis. Peri-implantitis is a plaque-associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri-implant mucosa and subsequent progressive loss of supporting bone. Peri-implantitis sites exhibit clinical signs of inflammation, bleeding on probing, and/or suppuration, increased probing depths and/or recession of the mucosal margin in addition to radiographic bone loss. The evidence is equivocal regarding the effect of keratinized mucosa on the long-term health of the peri-implant tissue. It appears, however, that keratinized mucosa may have advantages regarding patient comfort and ease of plaque removal. Case definitions in day-to-day clinical practice and in epidemiological or disease-surveillance studies for peri-implant health, peri-implant mucositis, and peri-implantitis were introduced. The proposed case definitions should be viewed within the context that there is no generic implant and that there are numerous implant designs with different surface characteristics, surgical and loading protocols. It is recommended that the clinician obtain baseline radiographic and probing measurements following the completion of the implant-supported prosthesis.

Peri-implant mucositis.

OBJECTIVES: This narrative review was prepared for the 2017 World Workshop of the American Academy of Periodontology and European Federation of Periodontology to address key questions related to the clinical condition of peri-implant mucositis, including: 1) the definition of peri-implant mucositis, 2) conversion of peri-implant health to the biofilm-induced peri-implant mucositis lesion, 3) reversibility of peri-implant mucositis, 4) the long-standing peri-implant mucositis lesion, 5) similarities and differences between peri-implant mucositis at implants and gingivitis at teeth, and 6) risk indicators/factors for peri-implant mucositis. METHODS: A literature search of MEDLINE (PubMed) and The Cochrane Library up to and including July 31, 2016, was carried out using the search strategy (peri-implant[All Fields] AND ("mucositis"[MeSH Terms] OR "mucositis"[All Fields])) OR (periimplant[All Fields] AND mucosits[All Fields]). Prospective, retrospective, and cross-sectional studies and review papers that focused on risk factors/indicators for peri-implant mucositis as well as experimental peri-implant mucositis studies in animals and humans were included. FINDINGS: Peri-implant mucositis is an inflammatory lesion of the soft tissues surrounding an endosseous implant in the absence of loss of supporting bone or continuing marginal bone loss. A cause-and-effect relationship between experimental accumulation of bacterial biofilms around titanium dental implants and the development of an inflammatory response has been demonstrated. The experimental peri-implant mucositis lesion is characterized by an inflammatory cell infiltrate present within the connective tissue lateral to the barrier epithelium. In long-standing peri-implant mucositis, the inflammatory cell infiltrate is larger in size than in the early (3-week) experimental peri-implant mucositis lesion. Biofilm-induced peri-implant mucositis is reversible at the host biomarker level once biofilm control is reinstituted. Reversal of the clinical signs of inflammation may take longer than 3 weeks. Factors identified as risk indicators for peri-implant mucositis include biofilm accumulation, smoking, and radiation. Further evidence is required for potential risk factors, including diabetes, lack of keratinized mucosa, and presence of excess luting cement. CONCLUSIONS: Peri-implant mucositis is caused by biofilm accumulation which disrupts the host-microbe homeostasis at the implant-mucosa interface, resulting in an inflammatory lesion. Peri-implant mucositis is a reversible condition at the host biomarker level. Therefore, the clinical implication is that optimal biofilm removal is a prerequisite for the prevention and management of peri-implant mucositis. An understanding of peri-implant mucositis is important because it is considered a precursor for peri-implantitis.

Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions.

A classification for peri-implant diseases and conditions was presented. Focused questions on the characteristics of peri-implant health, peri-implant mucositis, peri-implantitis, and soft- and hard-tissue deficiencies were addressed. Peri-implant health is characterized by the absence of erythema, bleeding on probing, swelling, and suppuration. It is not possible to define a range of probing depths compatible with health; Peri-implant health can exist around implants with reduced bone support. The main clinical characteristic of peri-implant mucositis is bleeding on gentle 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 due to swelling or decrease in probing resistance. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri-implant mucositis. Peri-implantitis is a plaque-associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri-implant mucosa and subsequent progressive loss of supporting bone. Peri-implantitis sites exhibit clinical signs of inflammation, bleeding on probing, and/or suppuration, increased probing depths and/or recession of the mucosal margin in addition to radiographic bone loss. The evidence is equivocal regarding the effect of keratinized mucosa on the long-term health of the peri-implant tissue. It appears, however, that keratinized mucosa may have advantages regarding patient comfort and ease of plaque removal. Case definitions in day-to-day clinical practice and in epidemiological or disease-surveillance studies for peri-implant health, peri-implant mucositis, and peri-implantitis were introduced. The proposed case definitions should be viewed within the context that there is no generic implant and that there are numerous implant designs with different surface characteristics, surgical and loading protocols. It is recommended that the clinician obtain baseline radiographic and probing measurements following the completion of the implant-supported prosthesis.

Supportive peri-implant therapy following anti-infective surgical peri-implantitis treatment: 5-year survival and success.

OBJECTIVES: To evaluate clinical outcomes of supportive peri-implant therapy (SPIT) following surgical treatment of peri-implantitis. MATERIALS AND METHODS: Twenty-four partially dentate patients with 36 dental implants diagnosed with peri-implantitis were treated by an anti-infective surgical protocol followed by regular supportive therapy. SPIT included removal of supra- and submucosal biofilm at the treated implants using titanium or carbon fibre curettes, or ultrasonic devices. In addition, professional prophylaxis (calculus/biofilm removal) at other implants/teeth and oral hygiene reinforcement was provided. Clinical measurements and radiographs were obtained at 1, 3 and 5 years. A successful treatment outcome was defined as implant survival with the absence of peri-implant probing depths (PD) ≥ 5 mm with concomitant bleeding/suppuration and absence of progression of peri-implant bone loss. RESULTS: Twelve months after treatment, there was 100% survival of the treated implants and 79% of patients (19 of 24) had a successful treatment outcome according to the defined success criteria. At 3 years, 75% of the patients (18 of 24) had a successful treatment outcome, two patients (8%) were lost to follow-up (LTF), while 8% lost an implant, and two patients had recurrence of peri-implantitis. Between 3 and 5 years, an additional two patients were LTF, and an additional two patients each lost one implant. Thus, at 5 years 63% of patients (15 of 24) had a successful treatment outcome. Complete resolution of peri-implantitis, defined as absence of bleeding at all sites, was achieved in 42% of implants (N = 15) at 5 years. CONCLUSION: Five years following regular supportive therapy, the peri-implant conditions established following peri-implantitis surgery were maintained in the majority of patients and implants. Some patients had recurrence of peri-implantitis and some lost implants over the 5-year period.

The therapy of peri-implantitis: a systematic review.

PURPOSE: To evaluate the success of treatments aimed at the resolution of peri-implantitis in patients with osseointegrated implants. MATERIALS AND METHODS: The potentially relevant literature was assessed independently by two reviewers to identify case series and comparative studies describing the treatment of peri-implantitis with a follow-up of at least 3 months. Medline, Embase, and The Cochrane Library were searched. For the purposes of this review, a composite criterion for successful treatment outcome was used which comprised implant survival with mean probing depth < 5 mm and no further bone loss. RESULTS: A total of 43 publications were included: 4 papers describing 3 nonsurgical case series, 13 papers describing 10 comparative studies of nonsurgical interventions, 15 papers describing 14 surgical case series, and 11 papers describing 6 comparative studies of surgical interventions. No trials comparing nonsurgical with surgical interventions were found. The length of follow-up varied from 3 months to 7.5 years. Due to the heterogeneity of study designs, peri-implantitis case definitions, outcome variables, and reporting, no meta-analysis was performed. Eleven studies could be evaluated according to a composite success criterion. Successful treatment outcomes at 12 months were reported in 0% to 100% of patients treated in 9 studies and in 75% to 93% of implants treated in 2 studies. Commonalities in treatment approaches between studies included (1) a pretreatment phase, (2) cause-related therapy, and (3) a maintenance care phase. CONCLUSIONS: While the available evidence does not allow any specific recommendations for the therapy of peri-implantitis, successful treatment outcomes at 12 months were reported in a majority of patients in 7 studies. Although favorable short-term outcomes were reported in many studies, lack of disease resolution as well as progression or recurrence of disease and implant loss despite treatment were also reported. The reported outcomes must be viewed in the context of the varied peri-implantitis case definitions and severity of disease included as well as the heterogeneity in study design, length of follow-up, and exclusion/inclusion criteria.

Surgical and nonsurgical periodontal therapy. Learned and unlearned concepts.

This review aims to highlight concepts relating to nonsurgical and surgical periodontal therapy, which have been learned and unlearned over the past few decades. A number of treatment procedures, such as gingival curettage and aggressive removal of contaminated root cementum, have been unlearned. Advances in technology have resulted in the introduction of a range of new methods for use in nonsurgical periodontal therapy, including machine-driven instruments, lasers, antimicrobial photodynamic therapy and local antimicrobial-delivery devices. However, these methods have not been shown to offer significant benefits over and above nonsurgical debridement using hand instruments. The method of debridement is therefore largely dependent on the preferences of the operator and the patient. Recent evidence indicates that specific systemic antimicrobials may be indicated for use as adjuncts to nonsurgical debridement in patients with advanced disease. Full-mouth disinfection protocols have been proven to be a relevant treatment option. We have learned that while nonsurgical and surgical methods result in similar long-term treatment outcomes, surgical therapy results in greater probing-depth reduction and clinical attachment gain in initially deep pockets. The surgical technique chosen seems to have limited influence upon changes in clinical attachment gain. What has not changed is the importance of thorough mechanical debridement and optimal plaque control for successful nonsurgical and surgical periodontal therapy.

Anti-infective treatment of peri-implant mucositis: a randomised controlled clinical trial.

AIM: To compare the effectiveness of two anti-infective protocols for the treatment of peri-implant mucositis. MATERIALS AND METHODS: Twenty-nine patients with one implant diagnosed with peri-implant mucositis (bleeding on probing [BOP] with no loss of supporting bone) were randomly assigned to a control or test group. Following an assessment of baseline parameters (probing depth, BOP, suppuration, presence of plaque), all patients received non-surgical mechanical debridement at the implant sites and were instructed to brush around the implant twice daily using a gel provided for a period of 4 weeks. The test group (15 patients) received a chlorhexidine gel (0.5%), and the control group (14 patients) received a placebo gel. The study was performed double blind. After 4 weeks, patients were instructed to discontinue using the gel and to continue with routine oral hygiene at the implant sites. Baseline parameters were repeated at 1 and 3 months. RESULTS: At 1 month, there was a statistically significant reduction in the mean number of sites with BOP and mean probing depth measurements at implants in both groups. There were also some statistically significant changes in these parameters from 1 to 3 months. However, there were no statistically significant differences between test and control groups. One month following treatment, 76% of implants had a reduction in BOP. Complete resolution of BOP at 3 months was achieved in 38% of the treated implants. The presence of a submucosal restoration margin resulted in significantly lower reductions in probing depth following treatment. CONCLUSIONS: Non-surgical debridement and oral hygiene were effective in reducing peri-implant mucositis, but did not always result in complete resolution of inflammation. Adjunctive chlorhexidine gel application did not enhance the results compared with mechanical cleansing alone. Implants with supramucosal restoration margins showed greater therapeutic improvement compared with those with submucosal restoration margins.

Geographic modelling of jaw fracture rates in Australia: a methodological model for healthcare planning.

BACKGROUND/AIM: While Australians are one of the healthiest populations in the world, inequalities in access to health care and health outcomes exist for Indigenous Australians and Australians living in rural or urban areas of the country. Hence, the purpose of this study was to develop an innovative methodological approach for predicting the incidence rates of jaw fractures and estimating the demand for oral health services within Australia. MATERIALS AND METHODS: Population data were obtained from the Australian Bureau of Statistics and was divided across Australia by statistical local area and related to a validated remoteness index. Every episode of discharge from all hospitals in Western Australia for the financial years 1999/2000 to 2004/2005 indicating a jaw fracture as the principle oral condition, as classified by the International Classification of Disease (ICD-10AM), was the inclusion criterion for the study. Hospitalization data were obtained from the Western Australian Hospital Morbidity Data System. RESULTS: The model estimated almost 10 times higher jaw fracture rates for Indigenous populations than their non-Indigenous counterparts. Moreover, incidence of jaw fractures was higher among Indigenous people living in rural and remote areas compared with their urban and semi-urban counterparts. In contrast, in the non-Indigenous population, higher rates of jaw fractures were estimated for urban and semi-urban inhabitants compared with their rural and remote counterparts. CONCLUSIONS: This geographic modelling technique could be improved by methodological refinements and further research. It will be useful in developing strategies for health management and reducing the burden of jaw fractures and the cost of treatment within Australia. This model will also have direct implications for strategic planning for prevention and management policies in Australia aimed at reducing the inequalities gap both in terms of geography as well as Aboriginality.

Comparative biology of chronic and aggressive periodontitis vs. peri-implantitis.

This review was undertaken to address the similarities and dissimilarities between the two disease entities of periodontitis and peri-implantitis. The overall analysis of the literature on the etiology and pathogenesis of periodontitis and peri-implantitis provided an impression that these two diseases have more similarities than differences. First, the initiation of the two diseases is dependent on the presence of a biofilm containing pathogens. While the microbiota associated with periodontitis is rich in gram-negative bacteria, a similar composition has been identified in peri-implant diseases. However, increasing evidence suggests that S. aureus may be an important pathogen in the initiation of some cases of peri-implantitis. Further research into the role of this gram-positive facultative coccus, and other putative pathogens, in the development of peri-implantitis is indicated. While the initial host response to the bacterial challenge in peri-implant mucositis appears to be identical to that encountered in gingivitis, persistent biofilm accumulation may elicit a more pronounced inflammatory response in peri-implant mucosal tissues than in the dentogingival unit. This may be a result of structural differences (such as vascularity and fibroblast-to-collagen ratios). When periodontitis and peri-implantitis were produced experimentally by applying plaque-retaining ligatures, the progression of mucositis to peri-implantitis followed a very similar sequence of events as the development of gingivitis to periodontitis. However, some of the peri-implantitis lesions appeared to have periods of rapid progression, in which the infective lesion reached the alveolar bone marrow. It is therefore reasonable to assume that peri-implantitis in humans may also display periods of accelerated destruction that are more pronounced than that observed in cases of chronic periodontitis. From a clinical point of view the identified and confirmed risk factors for periodontitis may be considered as identical to those for peri-implantitis. In addition, patients susceptible to periodontitis appear to be more susceptible to peri-implantitis than patients without a history of periodontitis. As both periodontitis and peri-implantitis are opportunistic infections, their therapy must be antiinfective in nature. The same clinical principles apply to debridement of the lesions and the maintenance of an infection-free oral cavity. However, in daily practice, such principles may occasionally be difficult to apply in peri-implantitis treatment. Owing to implant surface characteristics and limited access to the microbial habitats, surgical access may be required more frequently, and at an earlier stage, in periimplantitis treatment than in periodontal therapy. In conclusion, it is evident that periodontitis and peri-implantitis are not fundamentally different from the perspectives of etiology, pathogenesis, risk assessment, diagnosis and therapy. Nevertheless, some difference in the host response to these two infections may explain the occasional rapid progression of peri-implantitis lesions. Consequently, a diagnosed peri-implantitis should be treated without delay.

Nd:YAG (1064 nm) laser for the treatment of chronic periodontitis: a pilot study.

AIM: To evaluate the clinical and microbiological effects of neodymium: yttrium-aluminum-garnet laser therapy as an adjunct to scaling and root planing during the hygienic phase. METHODS: In eight patients, sites with a mean probing pocket depth (PPD) of ≥5 mm were treated by either scaling and root planing (n=28) (control) or by scaling and root planing and adjunctive laser therapy (n=28) (power: 5W). Re-evaluation was at 4-6 weeks. Thereafter, remaining pockets (mean PPD ≥5 mm) were eliminated by either laser surgery (power: 7 W) or gingivectomy (control). RESULTS: At baseline, the mean PPD of sites originally presenting with a mean PPD ≥4 mm were 4.69 and 4.73 mm in the test and control sites, respectively. Six months following surgery, there was a similar average mean PPD reduction in the test (1.18 mm, P<0.01) and control sites (1.35 mm, P<0.01). Also, the reduction in bleeding on probing in both groups was statistically significant (P<0.01, paired t-tests). No statistically-significant differences between the test and control sites were found for any clinical or microbiological parameters at baseline, after initial, and 3 or 6 months' post-surgical therapy. CONCLUSION: During the hygienic phase, neodymium: yttrium-aluminum-garnet (1064 nm) laser treatment yielded no superiority in clinical efficacy compared to conventional debridement. Laser gingivectomy resulted in similar treatment outcomes (mean PPD and bleeding on probing reduction), as did conventional gingivectomy.