The success of a dental implant treatment requires hard and soft tissue integration and osseointegration, mechanisms that entail a direct anchorage of the implant in the bone without interposition of soft tissue. Peri-implantitis is defined as an inflammatory reaction of the tissues surrounding a functioning dental implant. During inflammation, a high incidence of autoantibodies has been reported. The hypothesis of the present study is that the occurrence of autoantibodies to self-antigens including extracellular matrix (ECM) molecules and heat shock proteins (HSPs) might affect the dental implant outcome. Therefore, we evaluated the occurrence of antibodies to ECM molecules (Collagen (C) I, III, IV, V, fibronectin, laminin) and HSPs (HSP 27, HSP 65, HSP 90) in subjects with a healthy peri-implant microenvironment (n=29) as compared to patients with peri-implantitis (n=13). We also evaluated the HSP 27 expression in gingival fibroblasts grown in an inflammatory microenvironment. Antibodies to conformational ECM epitopes of CI, CIII and laminin were observed both in subjects with healthy peri-implant conditions and peri-implantitis. Antibodies to more than one HSP linear epitope were found in patients with peri-implantitis but not with healthy peri-implant conditions (p=0.024). Gingival fibroblasts grown in an inflammatory microenvironment showed increased HSP 27 cytoplasmic and plasma membrane expression as compared to fibroblasts grown in normal conditions. Immunity to multiple linear HSPs epitopes in patients with peri-implantitis and not in patients with a healthy peri-implant microenvironment might be relevant for monitoring the implant outcome and help to understand the role of subsets of autoantibodies in implant osseointegration.

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