Prevalence and predictive factors for peri-implant disease and implant failure: a cross-sectional analysis.

Background: Long-term studies worldwide indicate that peri-implant inflammation is a frequent finding and that the prevalence of peri-implantitis correlates with loading time. Implant loss, although less frequent, has serious oral health and economic consequences. An understanding of predictive factors for peri-implant disease and implant loss would help providers and patients make informed decisions.

Role of fibroblast populations in peri-implantitis.

Purpose: To understand the contribution of stromal cells, such as granulation tissue fibroblasts, to peri-implantitis with regard to (1) the secretion of constitutive factors promoting migration/survival of infiltrates into osseointegrated sites; and (2) the effect of exogenous infiltrate cytokines on the cells' secretion.

Materials And Methods: Fibroblasts were cultured from eight peri-implantitis sites. Multiplexed enzyme-linked immunosorbent assay was used to quantify factors secreted by the cells either unstimulated or stimulated with gamma interferon (IFN gamma), interleukin 4 (IL4), or tumor necrosis factor alpha (TNF alpha).

Cutting edge: proliferating fibroblasts respond to collagenous C1q with phosphorylation of p38 mitogen-activated protein kinase and apoptotic features.

Interactions of C1q collagen tails with human fibroblasts induce G(1) mitotic arrest. The hypothesis tested in this study is that the antiproliferative effect of C1q tails is mediated through activation of stress responsive pathway(s). Upon C1q treatment, proliferating fibroblasts were examined by immunoblotting with a panel of Abs to the mitogen-activated protein kinase (MAPK) superfamily.