Margareta Hultin | PubMed Health

PubMed2005

Peri-implantitis.

The risk of developing peri-implantitis seems to be more pronounced in patients with a history of periodontitis. Pretreatment to eliminate periodontal pathogens from the patient's oral cavity before dental implant treatment therefore is important to reduce the risk of peri-implantitis. Smoking has been shown to be a negative risk factor for treatment success. Several protocols have been used in the treatment of peri-implantitis. Mechanical infection control following surgical flap procedures, particularly in conjunction with antimicrobial therapy, is the most successful concept. There is no reliable evidence that suggests which intervention is the most effective for treating peri-implantitis. This article includes background information on the biology of tissue-destructive periodontitis and peri-implantitis to help clinicians interpret the clinical manifestation of the risk for peri-implantitis.

Anti-Bacterial Agents↗

PubMed2002

Microbiological findings and host response in patients with peri-implantitis.

The aim of the present study was to characterise microbiota and inflammatory host response around implants and teeth in patients with peri-implantitis. We included 17 partly edentulous patients with a total of 98 implants, of which 45 showed marginal bone loss of more than three fixture threads after the first year of loading. Nineteen subjects with stable marginal tissue conditions served as controls. Oral hygiene, gingival inflammation, and probing pocket depth were evaluated clinically at teeth and implants. Microbiological and crevicular fluid samples were collected from five categories of sites: 1) implants with peri-implantitis (PI), 2) stable implants (SI) in patients with both stable and peri-implantitis implants, 3) control implants (CI) in patients with stable implants alone, 4) teeth in patients (TP) and 5) controls (TC). Crevicular fluid from teeth and implants was analysed for elastase activity, lactoferrin and IL-1 beta concentrations. Elastase activity was higher at PI than at CI in controls. Lactoferrin concentration was higher at PI than at SI in patients with peri-implantitis. Higher levels of both lactoferrin and elastase activity were found at PI than at teeth in patients. The concentrations of IL-1 beta were about the same in the various sites. Microbiological DNA-probe analysis revealed a putative periodontal microflora at teeth and implants in patients and controls. Patients with peri-implantitis harboured high levels of periodontal pathogens, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus and Treponema denticola. These findings indicate a site-specific inflammation rather than a patient-associated specific host response.

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