Green Tea Modulates Cytokine Expression in the Periodontium and Attenuates Alveolar Bone Resorption in Type 1 Diabetic Rats.
Diabetes mellitus comprises a heterogeneous group of disorders with the main feature of hyperglycemia. Chronic hyperglycemia increases the severity of periodontal disease via an exacerbated inflammatory response, activated by advanced glycation end products and their receptor, RAGE. Therefore, anti-inflammatory agents represent potential inhibitors of this pathological interaction. In particular, green tea has been shown to possess anti-inflammatory properties mediated by its polyphenol content.


OBJECTIVE
This study investigated the mechanisms by which green tea attenuates the spontaneous onset of diabetes-induced periodontitis.


METHODS
Diabetes was induced in rats via a single intraperitoneal injection of streptozotocin (STZ). Diabetic and control animals were divided into water-treated and green tea-treated subgroups and were analyzed at 15, 30, 60 and 90 days after diabetes induction. Immunohistochemistry was performed to quantitatively evaluate tumor necrosis factor-α (TNF-α), receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG), interleukin-10 (IL-10) and runt-related transcription factor 2 (RUNX-2) expression in serial sections of each hemimaxilla. Morphometric measurements of the distance from the cementum-enamel junction (CEJ) of the superior distal root of the first molar to the alveolar bone crest (ABC) were performed to assess bone loss.


RESULTS
Diabetes resulted in significant bone loss and alterations in the number of cells that stained positive for inflammatory mediators. In the diabetic rats treated with green tea, we observed a decreased number of cells expressing RANKL and TNF-α compared with that observed in the diabetic rats treated with water. Additionally, green tea increased the numbers of cells that stained positive for OPG, RUNX-2 and IL-10 in the diabetic rats.


CONCLUSIONS
Green tea intake reduces expression of the pro-inflammatory cytokine TNF-α and the osteoclastogenic mediator RANKL to normal levels while increasing expression of the anti-inflammatory cytokine IL-10, the osteogenesis-related factor RUNX-2 and the anti-osteoclastogenic factor OPG. Therefore, green tea represents a potential therapeutic agent for the treatment of diabetes-related periodontal disease.
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, Bauru, São Paulo, Brazil.
Gabriela
G
Gennaro
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, Bauru, São Paulo, Brazil.
Marcela
M
Claudino
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, Bauru, São Paulo, Brazil.
Tania Mary
TM
Cestari
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, Bauru, São Paulo, Brazil.
Daniele
D
Ceolin
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, Bauru, São Paulo, Brazil.
Patrícia
P
Germino
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, Bauru, São Paulo, Brazil.
Gustavo Pompermaier
GP
Garlet
Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University, Bauru, São Paulo, Brazil.
Gerson Francisco
GF
de Assis
D000818:Animals; D050659:Core Binding Factor Alpha 1 Subunit / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis*; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects*; D008297:Male; D053244:Osteoprotegerin / Q000378:metabolism; D010519:Periodontium / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013662:Tea
D050659:Core Binding Factor Alpha 1 Subunit; D016207:Cytokines; D053244:Osteoprotegerin; C493717:Runx2 protein, rat; D013662:Tea; C506032:Tnfrsf11b protein, rat