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.

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.

The purpose of this study was to evaluate the recolonization patterns of the subgingival microflora of adult Periodontitis patients after a single session of scaling and root planing. In each of eight patients, three clinically diseased sites were investigated microbiologically by darkfield microscopy and cultural analysis. After initial clinical and microbiological parameters were determined, each subject received a single session of scaling and root planing but no oral hygiene instructions. Clinical indices were measured and microbial parameters were reassessed 7, 21, and 60 days after treatment in a manner such that each of the test sites was sampled only once after treatment. Recolonization was evaluated by matching any single site with its own preoperative site. A significant improvement in probing depth was noted for up to 60 days after treatment, while the gingival index did not change markedly during the course of the study. The microbial composition of treated sites 7 days after scaling and root planing, as determined by both cultural and darkfield data, was similar to that of periodontally healthy sites. Differences between cultural and darkfield data became apparent at the 21 day sampling point. The darkfield data showed that the sites consisted of cocci with few spirochetes. Cultural data demonstrated that the majority of the cocci were anaerobic, namely Streptococcus intermedius, Veillonella párvula, and Peptostreptococcus micros. At 60 days, there was no significant variation in any of the parameters from pretreatment levels. The most prevalent anaerobic rods prior to and 60 days after therapy were Fusobacterium nucleatum, Bacteroides gingivalis, and B. intermedius. These results indicate that a single session of scaling and root planing is clearly insufficient to maintain a healthy subgingival microflora. The conflicting findings between darkfield microscopy and cultural microbiology and between darkfield microscopy and clinical gingival inflammation suggest that darkfield microscopy is inadequate to identify a pathogenic microflora.

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A single episode of non-surgical mechanical therapy did not significantly reduce biochemical markers associated with bone resorption in patients exhibiting chronic periodontitis. Future longitudinal studies are warranted to specifically evaluate the relationship between C-telopeptide pyridinoline cross-links and periodontal disease progression.

Human parotid saliva histidine-rich polypeptides exerted antifungal activity against Candida albicans at concentrations similar to the known antifungal activity of the imidazole antibiotics. Inhibition of both growth and viability could be demonstrated by optical density monitoring and plating assays. Inhibition of growth was observed to be greatest when the histidine-rich polypeptides were added to the inoculum before addition to the growth media. However, complete inhibition by these polypeptides was still noted during active growth at turbidities of C. albicans corresponding to 106 CFU/ml. At higher cell densities, growth was delayed but not halted under the experimental conditions investigated. Candidacidal activity was observed with both growing and nongrowing cells. With respect to the latter, reaction of cells in buffer with the histidine-rich polypeptides for a period of 30 min resulted in killing of >90% of two different strains of C. albicans, whereas a third strain was found to be less susceptible. Moreover, the kinetics of loss of cell viability correlated with the loss of potassium from the cells. In addition to the histidine-rich polypeptides, hen egg white lysozyme, poly-L-lysine, and poly-L-histidine affected C. albicans. Both of the polyamino acids completely inhibited the growth of the yeast whereas lysozyme was not as potent. Where delays in growth were observed for all of these agents, including the histidine-rich polypeptides, turbidities reached those of untreated controls after a 24-h period. Enhanced effects were noted if C. albicans was preincubated with these agents in 0.025 2-(N-morpholino)-ethanesulfonic acid buffer, pH 5.2, before growth in the yeast synthetic medium.

In conclusion, implants were colonized by the indigenous periodontal microbiota and were well maintained in patients with a history of periodontitis. No significant association between progressing or non-progressing periodontal or peri-implant sampled sites in terms of loss of attachment and infection with at least one of the searched periodontal pathogens was found, suggesting that the presence of putative periodontopathogens at peri-implant and periodontal sites may not be associated with future attachment loss or implant failure.

The present study demonstrated enhanced clinical outcomes when using novel MPMs compared to OMs in guided tissue regeneration procedures. These results may be affected by the penetration of gingival CT contained stem cells and periosteal cells and their differentiation into components of the attachment apparatus.