Objectives: Osteoarthritis (OA) is one of the harmful disorders affecting the body joint including the temporomandibular joint (TMJ). Simvastatin is presumed to possess antiosteoarthritic effect beside its antilipidemic influences, so that the present study tried to estimate its effect on the monoiodoacetate (MIA)-induced TMJOA. Subjects and Methods: thirty young adult female Sprague-Dawley rats were randomly categorized into; control, osteoarthritis and osteoarthritis with simvastatin groups. Both MIA for OA induction and simvastatin for therapy were delivered unilaterally via the intra-articular route at the right side as a single dose for each. Results: the simvastatin administration has relatively reduced the MIA-induced osteoarthritic manifestations, and/or inhibited the progress of some osteoarthritic degenerative features but it failed to control others. Conclusion: temporomandibular joint osteoarthritis (TMJOA) treatment by simvastatin showed relative antiosteoarthritic effect and modulated the structure of some joint components to compensate the damaged induced structures with MIA administration.
Tramadol is a centrally acting analgesic with weak opioid agonist properties, which also has monoaminergic activity, exerted via inhibition of neuronal uptake of serotonin and norepinephrine. Tramadol is generally well tolerated and the most common adverse events are nausea, dizziness, drowsiness, sweating, vomiting and dry mouth. The effect of intraperitoneal injection of tramadol and pilocarpine were studied in rats on the flow of saliva, histological and histochemical change in the parotid salivary gland. The rats were divided into three groups, first group, rats received saline and used as control. The second group treated with 10 mg tramadol hydrochloride for three days. The third group treated with tramadol hydrochloride for three days followed with 1 mg pilocarpine. The rats were sacrificed at the fourth day after the end of experimental procedure. The administration of tramadol caused decreased in salivary flow rate by approximately 60 %. The parotid histopathological changes include vacuolation and atrophy of acini and excessive widening of the interstitial tissue area which are replaced by extensive fibrosis fibrosis mostly associated with the degenerated ducts and acini and their replaced by inflammatory cells.
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