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Lymphotoxin‐alpha Concentrations at Sites of Periodontitis and Gingival Overgrowth
Author(s) -
Johnson Roger B,
Lester S. Reid,
Bain Jennifer L,
Serio Francis G
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.651.1
Subject(s) - gingival sulcus , gingival margin , gingivectomy , medicine , bleeding on probing , periodontitis , dentistry
Objective There are no studies available comparing lymphotoxin‐alpha (LT‐alpha) gingival concentrations between sites of periodontal disease and gingival overgrowth (OG). Methods Gingiva was obtained from human donors prior to extraction of the adjacent teeth. The tissue was grouped based on adjacent pocket depth and bleeding on probing (BOP). Gingiva adjacent to a = 3 mm sulcus without BOP were classified as "normal" (N; n=26); Gingiva adjacent to a 4‐6 mm sulcus featuring BOP were classified as "diseased, moderate" (DM; n=23) and gingiva adjacent to > 6 mm sulci were classified as "diseased, severe" (DSev; n=28). OG gingiva was obtained following gingivectomy from patients receiving nifedipine/cyclosporine treatment (n=24). Tissues were solubilized and IL‐6, IL‐1‐β and LT‐alpha concentrations were assessed by ELISA. Data were compared by factorial ANOVA and a post‐hoc Tukey test. Groups were defined as significantly different when p<0.05. Results Gingival concentrations of IL‐6 were significantly greater at DSev than at N sites (p<0.001) and significantly greater within OG than within gingiva adjacent to N, DM, and DSev sites (p<0.001). In contrast, IL‐1‐β concentrations within OG tissues were significantly lower than within gingiva adjacent to N, DM, and DSev sites (p<0.001). LT‐alpha concentrations were significantly greater within OG than within gingiva adjacent to N, DM, and DSev sites (p<0.001) and at DM compared to N and DSev sites (p<0.05). Conclusion Our data suggest that LT‐alpha may have an important role in the etiology of OG gingival inflammation and could be a target for therapeutic intervention for OG.