Abstract
Joint distraction, the prolonged mechanical separation of the bones at a joint, has emerged as a joint-preserving treatment for end-stage osteoarthritis, with the gradually growing promise of implementation in regular clinical practice. Joint distraction of the knee has been most extensively studied, with these studies showing prolonged symptomatic improvement in combination with repair of cartilage tissue in degenerated knee joints, supporting the concept that cartilage repair can translate into real clinical benefit. The reversal of tissue degeneration observed with joint distraction could be the result of one or a combination of various proposed mechanisms, including partial unloading, synovial fluid pressure oscillation, mechanical and biochemical changes in subchondral bone, adhesion and chondrogenic commitment of joint-derived mesenchymal stem cells or a change in the molecular milieu of the joint. The overall picture that emerges from the combined evidence is relevant for future research and treatment-related improvements of joint distraction and for translation of the insights gained about tissue repair to other joint-preserving techniques. It remains to be elucidated whether optimizing the biomechanical conditions during joint distraction can actually cure osteoarthritis rather than only providing temporary symptomatic relief, but even temporary relief might be relevant for society and patients, as it will delay joint replacement with a prosthesis at an early age and thereby avert revision surgery later in life. Most importantly, improved insights into the underlying mechanisms of joint repair might provide new leads for more targeted treatment options.
Key points
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Joint distraction can induce tissue structure modifications in degenerated knee joints, accompanied by prolonged symptomatic improvement that supports the concept that cartilage repair can translate into real clinical benefit.
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It remains to be elucidated whether achieving optimal biomechanical and molecular conditions during distraction can lead to cure in osteoarthritis rather than providing only temporary symptomatic relief.
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Partial unloading, synovial fluid pressure oscillation, subchondral bone changes, adhesion and chondrogenic commitment of joint-derived mesenchymal stem cells, and an altered molecular milieu in the joint are the proposed mechanisms underlying the therapeutic effects of joint distraction.
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Greater insight into the molecular mechanisms of cartilage repair and their interplay in joint distraction might provide new leads to more targeted treatment options.
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Acknowledgements
The authors thank F.P.J.G. Lafeber for a thorough review of the manuscript and discussion on the subjects described. This work is partially supported by grants from the Dutch Arthritis Foundation (LLP9) and Nederlandse Oganizatie voor Wetenschappelijk Onderzoek (NWO) Domain Applied and Engineering Sciences (P15-23) to S.C.M.
Review criteria
To find studies involving KJD treatment in OA (summarized in Table 1), MEDLINE, EMBASE and Web of Science libraries were searched with the following terms: (distraction OR arthrodiatasis OR arthrodiastasis) AND (knee OR tibiofemoral OR tibiofibular), and were applied on title and abstract and, in Web of Science, Keywords+. Only full-text publications about clinical studies in which KJD with external fixation was applied and the primary outcomes were patient-reported outcomes and/or cartilage tissue restoration were included in Table 1. Studies that did not fully meet the criteria are discussed in the text where relevant. Ongoing unpublished studies were included based on personal communication with principal investigators.
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Glossary
- Stress
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Subject to pressure or tension.
- Strain
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Relative deformation or change in shape and size of elastic, plastic and fluid materials under applied forces.
- Shear
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A force tending to cause deformation of a material by slippage along a plane or planes parallel to the imposed stress.
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Jansen, M.P., Mastbergen, S.C. Joint distraction for osteoarthritis: clinical evidence and molecular mechanisms. Nat Rev Rheumatol 18, 35–46 (2022). https://doi.org/10.1038/s41584-021-00695-y
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