The Current Role of Disease-modifying Osteoarthritis Drugs

Contemporary treatments for osteoarthritis (OA) pursue only to alleviate the pain caused by the illness. Discovering 
disease-modifying osteoarthritis drugs (DMOADs) that can induce the repair and regeneration of articular tissues 
would be of substantial usefulness. The purpose of this manuscript is to review the contemporary role of DMOADs 
in managing OA. A narrative literature review on the subject, exploring the Cochrane Library and PubMed 
(MEDLINE) was performed. It was encountered that many publications have analyzed the impact of several 
DMOAD methods, including anti-cytokine therapy (tanezumab, AMG 108, adalimumab, etanercept, anakinra), 
enzyme inhibitors (M6495, doxycycline, cindunistat, PG-116800), growth factors (bone morphogenetic protein-7, 
sprifermin), gene therapy (micro ribonucleic acids, antisense oligonucleotides), peptides (calcitonin) and others 
(SM04690, senolitic, transient receptor potential vanilloid 4, neural EGFL-like 1, TPCA-1, tofacitinib, lorecivivint and 
quercitrin). Tanezumab has been demonstrated to alleviate hip and knee pain in individuals with OA but can cause 
major adverse events (osteonecrosis of the knee, rapid illness progression, augmented prevalence of total joint 
arthroplasty of involved joints, particularly when tanezumab is combined with nonsteroidal anti-inflammatory drugs. 
SM04690 (a Wnt inhibitor) has been demonstrated to be safe and efficacious in alleviating pain and ameliorating 
function as measured by the Western Ontario and McMaster Universities Arthritis Index. The intraarticular injection 
of lorecivivint is deemed safe and well tolerated, with no important reported systemic complications. In conclusion, 
even though DMOADs seem promising, their clinical effectiveness has not yet been demonstrated for managing 
OA. Until forthcoming studies can proved the medications’ capacity to repair and regenerate tissues affected by OA, 
physicians should keep using treatments that only intend to alleviate pain. 
Level of evidence: III