The role of subchondral bone damage in post‐traumatic osteoarthritis

Coughlin, Thomas R.; Kennedy, Oran D.

doi:10.1111/nyas.13261

Cited by 34 publications

(27 citation statements)

References 85 publications

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“…Multipotential stromal cells (MSCs), the precursors of both osteocytes and chondrocytes, are present in the subchondral bone 9 but also in the surrounding synovium and synovial fluid (SF) 10 , with early cartilage lesions likely to be repaired by joint resident MSCs 11 . However, in OA, damage to the osteochondral junction may lead to altered molecular exchanges and activation of subchondral bone MSCs 5,12 .…”

Section: Introductionmentioning

confidence: 99%

Gene expression and functional comparison between multipotential stromal cells from lateral and medial condyles of knee osteoarthritis patients

Sanjurjo‐Rodríguez

Baboolal

Burska

et al. 2019

Sci Rep

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Osteoarthritis (OA) is the most common degenerative joint disorder. Multipotential stromal cells (MSCs) have a crucial role in joint repair, but how OA severity affects their characteristics remains unknown. Knee OA provides a good model to study this, as osteochondral damage is commonly more severe in the medial weight-bearing compartment compared to lateral side of the joint. This study utilised in vitro functional assays, cell sorting, gene expression and immunohistochemistry to compare MSCs from medial and lateral OA femoral condyles. Despite greater cartilage loss and bone sclerosis in medial condyles, there was no significant differences in MSC numbers, growth rates or surface phenotype. Culture-expanded and freshly-purified medial-condyle MSCs expressed higher levels of several ossification-related genes. Using CD271-staining to identify MSCs, their presence and co-localisation with TRAP-positive chondroclasts was noted in the vascular channels breaching the osteochondral junction in lateral condyles. In medial condyles, MSCs were additionally found in small cavities within the sclerotic plate. These data indicate subchondral MSCs may be involved in OA progression by participating in cartilage destruction, calcification and sclerotic plate formation and that they remain abundant in severe disease. Biological or biomechanical modulation of these MSCs may be a new strategy towards cartilage and bone restoration in knee OA.

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Section: Introductionmentioning

confidence: 99%

Gene expression and functional comparison between multipotential stromal cells from lateral and medial condyles of knee osteoarthritis patients

Sanjurjo‐Rodríguez

Baboolal

Burska

et al. 2019

Sci Rep

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“…20 Another possible reason for PFOA progression in the TO group is direct or thermal injury to the subchondral bone during drilling and reaming of the patellar tunnel, as subchondral bone injury affects cartilage degeneration and causes arthritic changes. 3,19 Finally, PFOA progression in the TO group might be affected by the malposition of the patellar tunnel. We tried to make 2 patellar tunnels in the proximal one-third and at the center of the medial edge of the patella.…”

Section: Discussionmentioning

confidence: 98%

Comparison of Clinical and Radiological Outcomes Between Transosseous Tunnel and Suture Anchor Patellar Fixation for Medial Patellofemoral Ligament Reconstruction: A Cohort Study With 2-Year Follow-up

Yoon

Kim

Kwon

et al. 2020

Orthopaedic Journal of Sports Medicine

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Background: Several surgical methods have been developed for medial patellofemoral ligament reconstruction (MPFLR). However, the question of which patellar fixation method, suture anchor (SA) or transosseous tunnel (TO) fixation, achieves better overall outcomes remains to be answered. Hypothesis: SA patellar fixation will present comparable clinical outcomes and a lower complication rate compared with TO patellar fixation for MPFLR. Study Design: Cohort study; Level of evidence, 3. Methods: We retrospectively reviewed the outcomes of 46 patients who underwent MPFLR with either TO fixation (n = 21; mean age, 24.4 ± 6.1 years) or SA fixation (n = 25; mean age, 24.1 ± 12.1 years) for the treatment of recurrent patellar dislocation. Clinical findings (International Knee Documentation Committee [IKDC] subjective score, Lysholm score, and Tegner activity score), radiological findings (congruence angle and patellar tilt angle), and complications (redislocation, patellar fracture, patellofemoral osteoarthritis progression, infection, and stiffness) were compared between the TO and SA groups at the 2-year follow-up visit. Results: The mean postoperative IKDC subjective and Lysholm scores did not differ significantly between groups. However, postoperative Tegner activity scores were significantly higher in the TO group than in the SA group (TO, 5.8 ± 1.4; SA, 4.9 ± 1.2; P = .012). Congruence angle did not differ significantly between the groups (TO, −3.2 ± 22.8; SA, −7.6 ± 17.8; P = .464). Patellar tilt angle was lower in the TO group than in the SA group (TO, 10.5 ± 5.4; SA, 13.7 ± 2.8; P = .015). During the follow-up period, the TO group had 1 redislocation and 2 patellar fractures, whereas the SA group had no redislocations or fractures. Patellofemoral osteoarthritis progression was significantly higher in the TO group than in the SA group at the 2-year follow-up visit (TO, 9/21; SA, 2/25; P = .006). Conclusion: Both TO and SA patellar fixation methods for MPFLR showed improved clinical outcomes. When compared with TO fixation, SA fixation presented comparable clinical outcomes and a lower complication rate.

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“…This switch, whereby chondrocytes reduce production of beneficial ECM proteins, and increase production of harmful enzymes, is thought to involve altered mitochondrial function (16). Injury also has the effect of increasing crosstalk between cartilage and surrounding joint tissues such as subchondral bone and the synovial membrane (17). The latter of which is the central source of acute inflammatory factors as it becomes quickly infiltrated by activated immune cells in response to joint injury (18).…”

Section: Joint Cells and Immune Cells Are Involved In Ptoa Developmentmentioning

confidence: 99%

Mitochondria in Injury, Inflammation and Disease of Articular Skeletal Joints

et al. 2021

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Inflammation is an important biological response to tissue damage caused by injury, with a crucial role in initiating and controlling the healing process. However, dysregulation of the process can also be a major contributor to tissue damage. Related to this, although mitochondria are typically thought of in terms of energy production, it has recently become clear that these important organelles also orchestrate the inflammatory response via multiple mechanisms. Dysregulated inflammation is a well-recognised problem in skeletal joint diseases, such as rheumatoid arthritis. Interestingly osteoarthritis (OA), despite traditionally being known as a ‘non-inflammatory arthritis’, now appears to involve an element of chronic inflammation. OA is considered an umbrella term for a family of diseases stemming from a range of aetiologies (age, obesity etc.), but all with a common presentation. One particular OA sub-set called Post-Traumatic OA (PTOA) results from acute mechanical injury to the joint. Whether the initial mechanical tissue damage, or the subsequent inflammatory response drives disease, is currently unclear. In the former case; mechanobiological properties of cells/tissues in the joint are a crucial consideration. Many such cell-types have been shown to be exquisitely sensitive to their mechanical environment, which can alter their mitochondrial and cellular function. For example, in bone and cartilage cells fluid-flow induced shear stresses can modulate cytoskeletal dynamics and gene expression profiles. More recently, immune cells were shown to be highly sensitive to hydrostatic pressure. In each of these cases mitochondria were central to these responses. In terms of acute inflammation, mitochondria may have a pivotal role in linking joint tissue injury with chronic disease. These processes could involve the immune cells recruited to the joint, native/resident joint cells that have been damaged, or both. Taken together, these observations suggest that mitochondria are likely to play an important role in linking acute joint tissue injury, inflammation, and long-term chronic joint degeneration - and that the process involves mechanobiological factors. In this review, we will explore the links between mechanobiology, mitochondrial function, inflammation/tissue-damage in joint injury and disease. We will also explore some emerging mitochondrial therapeutics and their potential for application in PTOA.

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The role of subchondral bone damage in post‐traumatic osteoarthritis

Cited by 34 publications

References 85 publications

Gene expression and functional comparison between multipotential stromal cells from lateral and medial condyles of knee osteoarthritis patients

Gene expression and functional comparison between multipotential stromal cells from lateral and medial condyles of knee osteoarthritis patients

Comparison of Clinical and Radiological Outcomes Between Transosseous Tunnel and Suture Anchor Patellar Fixation for Medial Patellofemoral Ligament Reconstruction: A Cohort Study With 2-Year Follow-up

Mitochondria in Injury, Inflammation and Disease of Articular Skeletal Joints

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