The effect of orally administered epigallocatechin-3-gallate on ligature-induced periodontitis in rats

• Published in: Journal of periodontal research 2013-12, Vol.48 (6), p.781-789
• Main Authors: Cho, A.-R., Kim, J.-H., Lee, D.-E., Lee, J.-S., Jung, U.-W., Bak, E.-J., Yoo, Y.-J., Chung, W.-G., Choi, S.-H.
• Format: Article
• Language: English
• Subjects: Acid Phosphatase - analysis; Alveolar Bone Loss - drug therapy; Alveolar Bone Loss - pathology; Alveolar Process - drug effects; Alveolar Process - pathology; Animals; Anti-Inflammatory Agents - therapeutic use; Antioxidants - therapeutic use; Biomarkers - analysis; Catechin - analogs & derivatives; Catechin - therapeutic use; Collagen - drug effects; Dentistry; Down-Regulation; epigallocatechin-3-gallate; Epithelial Attachment - drug effects; Epithelial Attachment - pathology; Immunohistochemistry; Interleukin-6; Interleukin-6 - analysis; Isoenzymes - analysis; Male; osteoclasts; Osteoclasts - drug effects; periodontitis; Periodontitis - drug therapy; Periodontitis - pathology; Random Allocation; Rats; Rats, Sprague-Dawley; Tartrate-Resistant Acid Phosphatase; Time Factors; Tooth Cervix - drug effects; Tooth Cervix - pathology; tumor necrosis factor; Tumor Necrosis Factor-alpha - drug effects
• ISSN: 0022-3484; 1600-0765
• DOI: 10.1111/jre.12071

Background and Objective Epigallocatechin‐3‐gallate (EGCG) is known for its beneficial properties, including anti‐inflammatory and anti‐oxidative activities. Recently, reports have suggested that EGCG plays a pivotal role in regulating cytokine expression and osteoclastic activity. In the present study, we investigated whether orally administered EGCG has a therapeutic effect on ligature‐induced periodontitis. Materials and Methods Forty‐eight Sprague–Dawley rats were treated with EGCG or phosphate‐buffered saline. Periodontitis was induced by tying a ligature for 7 d. After removing ligation, EGCG (200 mg/kg) or phosphate‐buffered saline was administered via oral gavage on a daily basis. Rats were killed after 1, 2 and 4 wk of administration. Histologic and histomorphometric analyses, tartrate resistant acid phosphatase staining and immunohistochemistry were carried out. Results In the control group, bone loss did not recover even after the causative factor of periodontitis was eliminated. On the other hand, distance from cemento‐enamel junction to alveolar bone crest, long junctional epithelium and collagen destruction were reduced in the EGCG group. Decreased interleukin (IL)‐6 expression was shown from the early stage of EGCG administration, followed by reduced tumor necrosis factor (TNF) expression at week 4 EGCG group. The CT area showed a higher decrease of IL‐6 expression between the control and EGCG group than alveolar bone area. Downregulation of TNF and IL‐6 expression led to a decrease in osteoclast number and activity, which resulted in reduced bone loss. Conclusions Systemic administration of EGCG could have a therapeutic effect on damaged periodontal tissue. Inhibited cytokine expression, including TNF and IL‐6 is responsible for the reduction in osteoclast formation, osteoclastic activity and collagen destruction.