Article

An unusual case of generalized severe gingival enlargement during pregnancy

Department of Periodontology, Howard University of Dentistry, Washington, DC, USA.
General dentistry 11/2010; 58(6):e272-8.
Source: PubMed

ABSTRACT

Increased hormone levels that are present during puberty and pregnancy are associated with localized or generalized gingival enlargement. This article reviews the gingival alterations that can occur during pregnancy and describes a case of generalized severe gingival enlargement associated with pregnancy and its management. A 36-year-old woman had severe bilateral gingival enlargement of short duration. The patient denied taking any medications. The laboratory report revealed no systemic abnormalities; however, the report disclosed that she was pregnant. Surgical therapy for the gingival enlargement included gingivectomy and gingivoplasty of all quadrants, which reduced the size of the enlarged gingiva. Postoperative visits demonstrated uneventful healing, with no recurrence seen at the one-year follow-up appointment. It appears that the English literature includes only one other case report that discusses generalized gingival enlargement during pregnancy. Pregnancy-related gingival enlargement should be included as a differential diagnosis in women who have non-drug-induced generalized gingival enlargement.

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    • "Renal phenotype: bilateral medullary nephrocalcinosis , focal clusters of sclerosed glomeruli , marked periglomerular fibrosis with lymphocytic and plasma cell infiltration of the renal interstitium199200201202. Amelogenesis imperfecta/ gingival fibromatosis syndrome (AIGFS), ORPHA 171836, MIM 614253**[11]MIM, Mendelian Inheritance in Man; *SOS-1, Son-of-Sevenless-1; *CAMK, calcium/calmodulin-dependent protein kinase IV; *ABCA5, ATP-binding cassette, subfamily A, member 5; *KCNH1, potassium channel, voltagegated , subfamily H, member-1; *ANTXR2, anthrax toxin receptor 2; *FAM20A, family with sequence similarity 20, member A. **Considering the significant overlap in the oral phenotype between cases with amelogenesis imperfecta (AI) with hamartomas and unerupted teeth, amelogenesis imperfecta/gingival fibromatosis syndrome (AIGFS), and enamel-renal syndrome (ERS) in the published literature as well as the pathognomonic character of the oral phenotype in the absence of other developmental health problems, the two OMIM entries for ERS and AIGFS (ERS:MIM#204690 and AIGFS:MIM#614253) have been combined[198]Diseases associated with " gingival enlargement " Gingival enlargement covers broad etiological entities classified into five general groups: 1. Enlargement associated with non-genetic diseases GF can be directly or indirectly linked to poor nutrition (vitamin C deficiency)[42], systemic hormonal stimulation (pregnancy or puberty)[43], blood dyscrasias (leukemia)44454647, Wegener's granulomatosis[48], orofacial granulomatosis[49], pyogenic granuloma[50]and sarcoidosis[51]. It may also be associated with pseudotumors[52,53], benign neoplasms, e.g. "
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    ABSTRACT: Gingival fibromatosis is a rare and heterogeneous group of disorders that develop as slowly progressive, local or diffuse enlargements within marginal and attached gingiva or interdental papilla. In severe cases, the excess tissue may cover the crowns of the teeth, thus causing functional, esthetic, and periodontal problems, such as bone loss and bleeding, due to the presence of pseudopockets and plaque accumulation. It affects both genders equally. Hereditary, drug-induced, and idiopathic gingival overgrowth have been reported. Hereditary gingival fibromatosis can occur as an isolated condition or as part of a genetic syndrome. The pathologic manifestation of gingival fibromatosis comprises excessive accumulation of extracellular matrix proteins, of which collagen type I is the most prominent example. Mutation in the Son-of-Sevenless-1 gene has been suggested as one possible etiological cause of isolated (non-syndromic) hereditary gingival fibromatosis, but mutations in other genes are also likely to be involved, given the heterogeneity of this condition. The most attractive concept of mechanism for drug-induced gingival overgrowth is epithelial-to-mesenchymal transition, a process in which interactions between gingival cells and the extracellular matrix are weakened as epithelial cells transdifferentiate into fibrogenic fibroblast-like cells. The diagnosis is mainly made on the basis of the patient’s history and clinical features, and on histopathological evaluation of affected gingiva. Early diagnosis is important, mostly to exclude oral malignancy. Differential diagnosis comprises all pathologies in the mouth with excessive gingival overgrowth. Hereditary gingival fibromatosis may present as an autosomal-dominant or less commonly autosomal-recessive mode of inheritance. If a systemic disease or syndrome is suspected, the patient is directed to a geneticist for additional clinical examination and specialized diagnostic tests. Treatments vary according to the type of overgrowth and the extent of disease progression, thus, scaling of teeth is sufficient in mild cases, while in severe cases surgical intervention is required. Prognosis is precarious and the risk of recurrence exists.
    Full-text · Article · Jan 2016 · Orphanet Journal of Rare Diseases