The histopathology of inflammatory gingival enlargement

Abstract

Meso- and ectodermal inflammatory gingival hyperplasia have been illustrated and discussed. The relation between the various types of hyperplastic gingival lesions has been stressed, and it has been shown that lesions such as puberty gingivitis, pregnancy gingivitis, granuloma gravidarum, granuloma pyogenicum, and giant cell epulis are inflammatory in nature and they all have a similar tendency to undergo fibrosis, scarring, and partial ossification resulting in a so-called “fibroepithelial papilloma,” fibroid or ossifying fibroid epulis. Peripheral zones of irritation and inflammation, found mainly in the crevicular areas and at the base of protruding lesions, seem to act as a stimulus for continuous growth of the lesions. The fibrotic hyperplastic gingival tissues will, to a large extent, persist even following elimination of the initial source of irritation, and those anatomical changes may predispose to future irritation. Traumatization or other circulatory disturbance will initiate mucoid degencration of collagenous lesions. The possibility for one type of inflammatory reaction becoming or coexisting with other types of proliferative responses has been shown. The alteration in character and inflammatory response of the gingival tissues following previous episodes of injury has been emphasized. The complex of local and systemic factors which determines the variations in gingival inflammatory response to injury is only partially known. It is of basic importance in the management of these lesions that an exact differential histologic diagnosis be made of the different types of gingival enlargements. An understanding of the inflammatory nature of the lesions which have been discussed in this paper should encourage a different and more conservative management than would be utilized for neoplastic disease.