Mefenamic acid decreases inflammation but not joint lesions in experimental osteoarthritis

Abstract

Mefenamic acid is a non-steroidal anti-inflammatory drug able to control the symptoms of osteoarthritis (OA), but its effects on protection of cartilage and bone are still unclear. This study aimed to investigate whether the control of inflammation by mefenamic acid translates into decreased joint lesions in experimental OA in rats. OA was induced by injecting 1 mg of monosodium iodoacetate (MIA) into the joints of rats. The animals were treated with mefenamic acid (50 mg/kg, daily, oral gavage) either pre-MIA injection (preventive) or post-MIA injection (therapeutic). Joint swelling and hyperalgesia were evaluated at baseline and 1, 3, 14 and 28 days after induction of OA. Intra-articular lavage and kinetics of cell migration into the synovium were measured 3 and 28 days after OA induction. Histopathological analysis, Osteoarthritis Research Society International (OARSI) score, total synovium cells count, cartilage area and levels of proteoglycans in joints were also evaluated. Mefenamic acid prevented joint oedema and hyperalgesia induced by MIA in the acute phase (3 days) of the disease. In the chronic phase (28 days), preventive and therapeutic regimens decreased the number of mononuclear cells in the joint cavity. In contrast, thickening of the synovium, bone resorption, loss of cartilage and levels of proteoglycans were unaffected by mefenamic acid when it was administered either preventively or therapeutically. Thus, mefenamic acid had anti-inflammatory effects but did not reduce the progression of OA lesions, thereby indicating that it is only effective for symptomatic control of OA.

Expression profiling of LncRNA and miRNA in SDF-1-induced articular chondrocyte degeneration

“…Osteoarthritis (OA) is a kind of chronic and progressive multifactorial disease characterized by subchondral bone destruction, reduced chondrocytes, and degradation of cartilage matrix (1)(2)(3). With the further study of the pathogenesis of OA at the gene level, the regulation pathway mediated by non-coding ribonucleic acid (RNA) has been nding to play an important role in the gene regulating process (4,5).…”

Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1

“…Osteoarthritis is a chronic and progressive multifactorial disease characterized by subchondral bone destruction, reduced numbers of chondrocytes, and degradation of the cartilaginous matrix [ 1 , 2 , 3 ]. Long noncoding ribonucleic acids (lncRNAs) and microRNAs (miRNAs) play important roles in mediating gene regulatory pathways in the pathogenesis of osteoarthritis and other diseases, including acute early phase spinal cord injury [ 4 , 5 , 6 ].…”

Chronic pain and gait analysis in dogs with degenerative hip joint disease treated with repeated intra-articular injections of platelet-rich plasma or allogeneic adipose-derived stem cells

“…Non-steroidal anti-inflammatory drugs alone or combined with other analgesics have been widely used for pain and inflammation relief associated with canine OA [ 6 , 24 , 28 ]. However, these medications are not adequately effective to prevent the deterioration of articular cartilage [ 1 , 25 ] and when used for prolonged periods may induce potential adverse effects [ 24 , 28 ].…”