Peri--implant diseases are defined as inflammatory lesions of the surrounding peri--implant tissues, and they include peri--implant mucositis (inflammatory lesion limited to the surrounding mucosa of an implant) and peri--implantitis (inflammatory lesion of the mucosa, affecting the supporting bone with resulting loss of osseointegration). This review aims to describe the different approaches to manage both entities and to critically evaluate the available evidence on their efficacy.Therapy of peri--implant mucositis and non--surgical therapy of peri--implantitis usually involve the mechanical debridement of the implant surface by means of curettes, ultrasonic devices, air--abrasive devices or lasers, with or without the adjunctive use of local antibiotics or antiseptics. The efficacy of these therapies has been demonstrated for mucositis. Controlled clinical trials show an improvement in clinical parameters, especially in bleeding on probing.For peri--implantitis, the results are limited, especially in terms of probing pocket depth reduction.Surgical therapy of peri--implantitis is indicated when non--surgical therapy fails to control the inflammatory changes. The selection of the surgical technique should be based on the characteristics of the peri--implant lesion. In presence of deep circumferential and intrabony defects surgical interventions should be aimed for thorough debridement, implant surface decontamination and defect reconstruction. In presence of defects without clear bony walls or with a predominant suprabony component, the aim of the surgical intervention should be the thorough debridement and the repositioning of the marginal mucosa that enables the patient for effective oral hygiene practices, although this aim may compromise the aesthetic result of the implant supported restoration.3

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These data suggest that not only IL1beta, IFNgamma, and TNFalpha but also IL10, IL12, and IL17 are involved in the OA-TMJ pathogenesis. Furthermore, an inflammatory response characterised by the predominant expression of IL12 mRNA and down-regulated expression of IL10 mRNA is associated with the degenerative changes observed in OA-TMJ.

These results demonstrate a differential potential of P. gingivalis capsular serotypes to induce DC responses and a higher capacity of strains K1 W83 and K2 HG184 than other K serotypes to trigger cytokine expression.