***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVE To monitor clinical , microbiological and host-derived alterations occurring around teeth and titanium implants during the development of experimental gingivitis/mucositis and their respective healing sequence in humans . MATERIAL AND METHODS Fifteen subjects with healthy or treated periodontal conditions and restored with dental implants underwent an experimental 3-week period of undisturbed plaque accumulation in the m and ible . Subsequently , a 3-week period with optimal plaque control was instituted . At Days 0 , 7 , 14 , 21 , 28 , 35 and 42 , the presence/absence of plaque deposits around teeth and implants was assessed , ( plaque index [ PlI ] ) and the gingival/mucosal conditions were evaluated ( gingival index[GI ] ) . Subgingival/submucosal plaque sample s and gingival/mucosal crevicular fluid ( CF ) sample s were collected from two pre-determined sites around each experimental unit . CF sample s were analyzed for matrix-metalloproteinase-8 ( MMP-8 ) and interleukin-1beta ( IL-1β ) . Microbial sample s were analyzed using DNA-DNA hybridization for 40 species . RESULTS During 3 weeks of plaque accumulation , the median PlI and GI increased significantly at implants and teeth . Implant sites yielded a greater increase in the median GI compared with tooth sites . Over the 6-week experimental period , the CF levels of MMP-8 were statistically significantly higher at implants compared with teeth ( P<0.05 ) . The CF IL-1β levels did not differ statistically significantly between teeth and implants ( P>0.05 ) . No differences in the total DNA counts between implant and tooth sites were found at any time points . No differences in the detection frequency were found for putative periodontal pathogens between implant and tooth sites . CONCLUSION Peri-implant soft tissues developed a stronger inflammatory response to experimental plaque accumulation when compared with that of their gingival counterparts . Experimental gingivitis and peri-implant mucositis were reversible at the biomarker level . Clinical ly , however , 3 weeks of resumed plaque control did not yield pre-experimental levels of gingival and peri-implant mucosal health indicating that longer healing periods are needed Background Due to the world-wide increase in treatments involving implant placement , the incidence of peri-implant disease is increasing . Late implant failure is the result of the inability to maintain osseointegration , whose most important cause is peri-implantitis . The aim of this study was to analyze the clinical , microbiological , and immunological aspects in the peri-implant sulcus fluid ( PISF ) of patients with healthy dental implants and patients with peri-implantitis . Methods PISF sample s were obtained from 24 peri-implantitis sites and 54 healthy peri-implant sites in this prospect i ve cross-sectional study . The clinical parameters recorded were : modified gingival index ( mGI ) , modified plaque index ( mPI ) and probing pocket depth ( PPD ) . The periodontopathogenic bacteria Tannerella forsythia , Treponema denticola and Porphyromonas gingivalis were evaluated , together with the total bacterial load ( TBL ) . PISF sample s were analyzed for the quantification of Interleukin (IL)-8 , IL-1β , IL-6 , IL-10 and Tumor Necrosis Factor (TNF)-α using flow cytometry ( FACS ) . Results The mGI and PPD scores in the peri-implantitis group were significantly higher than the healthy group ( p < 0.001 ) . A total of 61.5 % of the patients with peri-implantitis had both arches rehabilitated , compared with 22.7 % of patients with healthy peri-implant tissues ; there was no implant with peri-implantitis in cases that received m and ibular treatment exclusively ( p < 0.05 ) . Concentrations of Porphyromonas gingivalis ( p < 0.01 ) , association with bacteria Porphyromonas gingivalis and Treponema denticola ( p < 0.05 ) , as well as the TBL ( p < 0.05 ) are significantly higher in the peri-implantitis group . IL-1β ( p < 0.01 ) , IL-6 ( p < 0.01 ) , IL-10 ( p < 0.05 ) and TNF-α ( p < 0.01 ) are significantly higher at the sites with peri-implantitis compared to healthy peri-implant tissue , while IL-8 did not increase significantly . Conclusion The results of the present study involving a limited patient sample suggest that the peri-implant microbiota and which dental arch was rehabilitated involved could contribute to bone loss in peri-implantitis . A significant relationship is observed between the concentration of cytokines ( interleukins 1β , 6 and 10 and TNF-α ) and the inflammatory response in peri-implantitis tissue BACKGROUND While information on the prevalence of peri-implantitis is available , data describing onset and progression of the disease are limited . MATERIAL & METHODS A 9-year follow-up examination of 596 r and omly selected implant-carrying individuals identified 62 patients with moderate/severe peri-implantitis . Longitudinal assessment s of peri-implant marginal bone levels were used to construct a statistical model with bone loss as the dependent variable . A multilevel growth model estimated the pattern of bone loss for each implant/patient . Onset of peri-implantitis was determined by evaluating the cumulative percentage of implants/ patients presenting with estimated bone loss at each year following prosthesis delivery . RESULTS The analysis showed a non-linear , accelerating pattern of bone loss at the 105 affected implants . The onset of peri-implantitis occurred early , and 52 % and 66 % of implants presented with bone loss of > 0.5 mm at years 2 and 3 respectively . A total of 70 % and 81 % of subjects presented with ≥1 implants with bone loss of > 0.5 mm at years 2 and 3 respectively . CONCLUSIONS It is suggested that peri-implantitis progresses in a non-linear , accelerating pattern and that , for the majority of cases , the onset occurs within 3 years of function 
    Output:
    
Despite absence of meta- analysis , MMP-8 show to be a promising biomarker in detection of PI in literature .
Within the limitations of this study , pro-inflammatory cytokines in PICF , such as IL-1ß and IL-6 , can be used as adjunct tools to clinical parameters to differentiate H from MU and PI