Clinical, imaging and histopathological correlations of gingival overgrowth: a retrospective analysis in northeastern Romanian population.

BACKGROUND: Gingival overgrowth refers to an increase in the size of the gingival tissue. The etiology varies, and is often a multi-factor issue; what may contribute to gingival enlargement are aspects, such as disease, local and systemic conditions and idiopathic factors. The aim of the present study is to analyze and to correlate the clinical, epidemiological, imaging and histopathological (HP) features of gingival overgrowth in northeastern Romanian population. PATIENTS, MATERIALS AND METHODS: We conducted a clinical, imaging, and pathological study on 98 patients with gingival overgrowth, who underwent a surgical intervention for a gingival biopsy in the Office of Oral and Maxillofacial Surgery, "Prof. Dr. Nicolae Oblu" Emergency Clinical Hospital, Iasi, Romania, during a 14-month period (January 1, 2018 to February 28, 2019). All patients with localized gingival overgrowth had clinical and imaging investigations done and then were referred to an oral and maxillofacial facility. A surgeon performed the excision of the gingival overgrowth and then sent the surgical specimens to the Laboratory of Pathology for HP examination. RESULTS: Local inflammation was found responsible for the gingival overgrowth in most of the cases, with the number of females outnumbering that of the males. A very good correlation was found between clinical and HP diagnosis when epithelial hyperplasia, peripheral giant cell granuloma and pyogenic granuloma were involved and a moderate one when fibrous hyperplasia was involved. CONCLUSIONS: These findings suggest that the occurrence of gingival overgrowth can have many causes, which highlights the importance of clinical pathology in assisting practitioners with making a better diagnosis.

Gingival leukemic infiltration as the first manifestation of acute myeloid leukemia.

Leukemic infiltration of the gingival tissue associated or not with gingival enlargement may be the first manifestation of acute leukemia, despite being rarely reported in the literature. A 10-year-old female patient presented with a 1-month history of an asymptomatic, firm, and pinkish-red generalized gingival overgrowth. There was no bone resorption. Incisional biopsy of the gingival tissue was performed, with histopathological examination revealing a diffuse and hypercellular infiltration of monocytoid cells. The patient was referred to a hematologist and underwent a bone marrow biopsy, which led to a conclusive diagnosis of acute myeloid leukemia. The patient was treated with chemotherapy and we observed regression of gingival enlargement after 4 weeks from the initial therapy.

Arthropathy, osteolysis, keloids, relapsing conjunctival pannus and gingival overgrowth: a variant of polyfibromatosis?

Polyfibromatosis is a rare fibrosing condition characterized by fibromatosis in different body areas and by keloid formation, and which can be associated with arthropathy and osteolysis. Familial occurrence has been described, but the cause remains unknown. Here, we describe a patient with characteristics of polyfibromatosis with arthropathy who had in addition severe conjunctival fibrosis, distinctive face, gingival overgrowth, and pigmented keloids. We discuss the resemblances and differences with polyfibromatosis and descriptions of other, similar patients. We conclude that at present it remains uncertain whether the patient has a variant of polyfibromatosis or a separate entity.

Gingival crevicular fluid and serum matrix metalloproteinase-8 and tissue inhibitor of matrix metalloproteinase-1 levels in renal transplant patients undergoing different immunosuppressive therapy.

AIM: We investigated gingival crevicular fluid (GCF) and serum matrix metalloproteinase-8 (MMP-8) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) levels from renal transplant patients receiving cyclosporine-A (CsA) and having gingival overgrowth (GO), from patients receiving CsA therapy and having no GO and patients receiving tacrolimus therapy. MATERIAL AND METHODS: GCF samples were collected from sites with GO (GO+) and without GO (GO-) in CsA patients having GO; and GO- sites in CsA patients having no GO; sites from tacrolimus, gingivitis and healthy subjects. GCF and serum MMP-8 and TIMP-1 levels were determined by a time-resolved immunofluorometric assay (IFMA) and enzyme-linked immunosorbent assay. RESULTS: GO+ sites in CsA patients having GO had elevated GCF MMP-8 levels compared with those of CsA patients having no GO, tacrolimus and healthy subjects (p<0.005), but these levels were similar to those of gingivitis. The GCF MMP-8 level was higher in GO+ compared with GO- sites in CsA patients having GO (p<0.05). GCF TIMP-1 levels were similar between groups. Tacrolimus patients had lower GCF MMP-8 levels than gingivitis (p<0.005), but levels similar to the healthy group. CONCLUSION: These results show that CsA and tacrolimus therapy has no significant effect on GCF MMP-8 levels, and gingival inflammation seems to be the main reason for their elevations.