Abstract
Osteoarthritis (OA) is one of the most debilitating diseases and is associated with a high personal and socioeconomic burden. So far, there is no therapy available that effectively arrests structural deterioration of cartilage and bone or is able to successfully reverse any of the existing structural defects. Efforts to identify more tailored treatment options led to the development of strategies that enabled the classification of patient subgroups from the pool of heterogeneous phenotypes that display distinct common characteristics. To this end, the classification differentiates the structural endotypes into cartilage and bone subtypes, which are predominantly driven by structure-related degenerative events. In addition, further classifications have highlighted individuals with an increased inflammatory contribution (inflammatory phenotype) and pain-driven phenotypes as well as senescence and metabolic syndrome phenotypes. Most probably, it will not be possible to classify individuals by a single definite subtype, but it might help to identify groups of patients with a predominant pathology that would more likely benefit from a specific drug or cell-based therapy. Current clinical trials addressed mainly regeneration/repair of cartilage and bone defects or targeted pro-inflammatory mediators by intra-articular injections of drugs and antibodies. Pain was treated mostly by antagonizing nerve growth factor (NGF) activity and its receptor tropomyosin-related kinase A (TrkA). Therapies targeting metabolic disorders such as diabetes mellitus and senescence/aging-related pathologies are not specifically addressing OA. However, none of these therapies has been proven to modify disease progression significantly or successfully prevent final joint replacement in the advanced disease stage. Within this review, we discuss the recent advances in phenotype-specific treatment options and evaluate their applicability for use in personalized OA therapy.
Highlights
Osteoarthritis (OA) is a multi-factorial, mostly slowly progressing, and primarily non-inflammatory degenerative disorder of the synovial joints that is often age related and/or trauma induced
The development of novel therapeutic approaches targeting the osteoarthritic degradative and inflammatory processes in cartilage, synovium, or bone requires a deep understanding of the disease status of these joint tissues at the time of the intervention
Modest improvement in functional and pain scores, safety concerns owing to increased need for joint replacement[33]
Summary
Osteoarthritis (OA) is a multi-factorial, mostly slowly progressing, and primarily non-inflammatory degenerative disorder of the synovial joints that is often age related and/or trauma induced. Felson defines criteria for characterizing OA phenotypes via an epidemiological approach[4] He discriminates between generalized arthritis and joint-specific OA, secondary and primary OA, and incident and progressive OA. The i.a. administration of 100 μg of sprifermin to participants with symptomatic radiographic knee OA every 6 or 12 months vs placebo resulted in an improvement in total femorotibial joint cartilage thickness after a follow up period of 2 years. This improvement was statistically significant, but clinical importance was not clear.
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