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Glucosamine oral administration as an adjunct to hyaluronic acid injection in treating temporomandibular joint osteoarthritis
Author(s) -
Cen Xiao,
Liu Yan,
Wang Shasha,
Yang Xianrui,
Shi Zongdao,
Liang Xinhua
Publication year - 2018
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12760
Subject(s) - medicine , osteoarthritis , placebo , temporomandibular joint , hyaluronic acid , glucosamine , randomized controlled trial , oral administration , arthropathy , gastroenterology , adjunct , anesthesia , dentistry , pathology , linguistics , chemistry , philosophy , alternative medicine , organic chemistry , anatomy
Objective To investigate the therapeutic effect of oral glucosamine ( GS ) as an adjunct to hyaluronic acid ( HA ) injection on patients with temporomandibular joint osteoarthritis ( TMJ OA ). Methods In this clinical trial, 136 participants, diagnosed as TMJ OA clinically and radiographically, were enrolled and randomized into two groups (group GS + HA : oral GS + HA injection; group placebo + HA : oral placebo + HA injection). Pain, maximum interincisal mouth opening ( MMO ), the levels of IL ‐1β, IL ‐6, and TGF ‐β in TMJ synovial were defined as the outcome measurements and conducted before operation, and at 1‐month and 1‐year follow‐up. Results In both groups, pain scores were decreased and MMO s were increased at 1‐month and 1‐year follow‐up, the changes at 1‐year follow‐up showed statistically significant intergroup differences. At 1‐month follow‐up, only IL ‐6 concentration was lower in group GS + HA than that in group placebo + HA . One year later, TGF ‐β concentration was higher and IL ‐6 and IL ‐1β concentrations were lower in group GS + HA than those in group placebo + HA . Conclusions Both strategies alleviated symptoms in short term, but the patients treated with GS benefited more than those with placebo in long term, which may be due to the suppression of IL ‐1β and IL ‐6 and the stimulation of TGF ‐β.