The term “inflammatory hyperplasia” is used to describe a large range of commonly occurring nodular growths of the oral mucosa that histologically represent inflamed fibrous and granulation tissuse. The size of these reactive hyperplastic masses may be greater or lesser, depending on the degree to which one or more of the components of the inflammatory reaction and healing response are exaggerated in the particular lesion. Some are predominantly epithelial overgrowths with only scanty connective-
tissue stroma; others are fibromatous with a thin epithelial covering and may exhibit either angiomatous, desmoplastic (collagenous), or fibroblastic features. In many lesions, different sections may reveal examples of each of these histologic patterns. Like scar tissue, some inflammatory hyperplasias appear to mature and become less vascular (paler and less friable) and more collagenous (firmer and smaller) with time. Others appear to have a high proliferative ability for exophytic growth until they are excised.This variability of histologic appearance is reflected in the wide range of clinical characteristics that inflammatory hyperplasias show and in the clinical names many of them have acquired that suggest a specific etiology or natural history. Names such as “fibroma” and “papilloma” are therefore often used to describe these lesions even though there is no evidence to suggest a neoplastic etiology. The major etiologic factor for these lesions is generally assumed to be chronic trauma (such as that produced by ill-fitting dentures, calculus, overhanging dental restorations, acute or chronic tissue injury from biting, and fractured teeth), and chronic irritants can be convincingly demonstrated in many cases (eg, palatal papillary hyper-
plasia associated with aged maxillary dentures). With some of these lesions, (eg, pregnancy epulis and the central giant cell tumor associated with hyperparathyroidism), the levels of circulating hormones also undoubtedly play a role. The majority of lesions occur on the surface of the oral mucous membrane, where irritants are quite common. Two deeper lesions (pseudosarcomatous fasciitis and giant cell reparative granuloma of bone) are also classified as inflammatory hyperplasias, on the basis of their histologic structure and clinical behavior.
As surface outgrowths of the oral mucous membrane, most inflammatory hyperplasias are subject to continual masticatory trauma and frequently are ulcerated and hemorrhagic. Dilated blood vessels, acute and chronic inflammatory exudates, and localized abscesses are additional reasons for the swollen, distended, and red to purple inflamed appearance of some inflammatory hyperplasias. Epithelial hyperplasia frequently produces a lesion with a textured surface or an area of mucosa resembling carpet pile. Erosion of the underlying cortical bone rarely occurs with inflammatory hyperplasia of the oral mucosa; when it is noted, there should be a strong suspicion that an aggressive process or even malignancy is involved, and a section of the affected bone should be included with the biopsy specimen.
Unless otherwise specified in the following description of lesions of this type, excisional biopsy is indicated except when the procedure would produce marked deformity; in such acase, incisional biopsy is mandatory. If the chronic irritant is eliminated when the lesion is excised, the majority of inflammatory hyperplasias will not recur. This confirms the benign nature of these lesions (as would be expected from their histologic structure).
The following are examples of inflammatory hyperplasias: fibrous inflammatory hyperplasias (clinical fibroma, epulis fissuratum, and pulp polyp); palatal papillary hyperplasia; pyogenic granuloma; pregnancy epulis; giant cell granuloma (giant cell epulis and central giant cell tumor of the jaw); pseudosarcomatous fasciitis; proliferative myositis; and pseudoepitheliomatous hyperplasia.
As surface outgrowths of the oral mucous membrane, most inflammatory hyperplasias are subject to continual masticatory trauma and frequently are ulcerated and hemorrhagic. Dilated blood vessels, acute and chronic inflammatory exudates, and localized abscesses are additional reasons for the swollen, distended, and red to purple inflamed appearance of some inflammatory hyperplasias. Epithelial hyperplasia frequently produces a lesion with a textured surface or an area of mucosa resembling carpet pile. Erosion of the underlying cortical bone rarely occurs with inflammatory hyperplasia of the oral mucosa; when it is noted, there should be a strong suspicion that an aggressive process or even malignancy is involved, and a section of the affected bone should be included with the biopsy specimen.
Unless otherwise specified in the following description of lesions of this type, excisional biopsy is indicated except when the procedure would produce marked deformity; in such acase, incisional biopsy is mandatory. If the chronic irritant is eliminated when the lesion is excised, the majority of inflammatory hyperplasias will not recur. This confirms the benign nature of these lesions (as would be expected from their histologic structure).
The following are examples of inflammatory hyperplasias: fibrous inflammatory hyperplasias (clinical fibroma, epulis fissuratum, and pulp polyp); palatal papillary hyperplasia; pyogenic granuloma; pregnancy epulis; giant cell granuloma (giant cell epulis and central giant cell tumor of the jaw); pseudosarcomatous fasciitis; proliferative myositis; and pseudoepitheliomatous hyperplasia.