In situ demonstration of Fcγ‐receptors in human chronic marginal and periodontitis

Abstract

The distribution of receptors for the Fc portion of IgG (FcγR) in chronic marginal and apical periodontitis were studied by using a monoclonal antibody against placental FcγR and soluble immune complexes as indicators. Cryostat sections were used in indirect immunofluorescence technique. FcγR were detected on varying numbers of cells in the inflammatorry cell infiltrates, on endothelial cells of certain vessels and in fibrous tissue. In chronic marginal periodontitis FcγR were also observed on cells within the oral gingival epithelium (OGE) and the pocket epithelium (PE). There was a distinct fluorescence in stratum spinosum and occasionally in stratum basale of OGE and in the coronal portion of the PE. FcγR on Langerhans cells could not be demonstrated. In apical periodontitis FcγR were also detected on cells within the epithelium. In some cases epithelium in periapical cysts was positive. Soluble immune complexes bound to morphologically similar, but fewer cells compared to the monoclonal antibody against FcγR. The results indicate that FcγR are generally expressed on cells in inflamed tissue. Thus, this presence of FcγR on certain specialized cells such as endothelial cells and keratinocytes, may endow these cells with functions previously thought to be restricted to cells of the lymphoreticular system.

Increased levels of soluble Fcγ receptor III in gingival fluid from periodontal lesions

“…The concentration of soluble FcγRIII observed in gingival fluid is about 7 times the maximum concentration of soluble FcγRIII observed in synovial fluid of rheumatoid arthritis lesions ( 8). FcγRIII‐bearing granulocytes, lymphocytes and keratinocytes in the periodontal lesion ( 18) are exposed to enzymes, which probably contribute to release of soluble FcγR ( 2, 16, 17). Variations in inflammatory activity, activation of proteases and flow of gingival fluid may contribute to the wide range in concentration of FcγRIII observed in the gingival fluid.…”

“…FcγR can be released by apoptosis ( 14) and can also be shedded from the cell membrane by activation of phospholipase C ( 16) or proteases ( 17). FcγR were also observed in the crevicular epithelium ( 18, 24) and release of FcγR may occur by exposure to endogenous and bacterial proteases. Phospholipase activity was recently reported in oral spirochetes ( 29) and Propionibacterium acnes ( 2).…”

Fcγ‐receptor activity in the developing human placenta

“…(13) did not detect staining of endo-thelial cells in first trimester placenta, while Wuinwright & Holmes (32) detected weak staining of some vessels. As FcyR have been demonstrated on endothelium of different tissues, including full-term placenta (2,11,13,14,24,25,28), the reason for this divergence is not obvious. Functionally, FcyR on endothelial cells may serve a protective role by binding and phagocytosis of immune complexes of alloimmune or infectious origin (12).…”

Demonstration of Fey receptors in human endometrium

“…The detection of FcR on endothelial cells of the endometrium parallels observations done in other tissues. Low-affinity FcR have been demonstrated on endothelial cells in human placenta (11,12), and FcR have been detected on endothelial cells in psoriatic lesions of the skin (25), and on oral mucosal vessels (26). The functional significance of FcR on these cells is still unknown, but it has been postulated that FcR on endothelium may participate in the clearing of circulating immune complexes (27).…”