The prevalence of osteoarthritis (OA) is rising for reasons that are not fully understood. In this Opinion article, we review the possibility that OA is an evolutionary mismatch disease, which is a disease more common today than in the past because genes inherited from previous generations are inadequately or imperfectly adapted to modern environmental conditions. We focus on four major environmental factors in OA pathogenesis that have become ubiquitous within the past half-century: obesity, metabolic syndrome, dietary changes and physical inactivity. Because a cure for OA does not yet exist, prevention strategies that target these modifiable environmental factors are needed to curb further increases in OA prevalence.

/pdf/modern-day-environmental-factors-in-the-pathogenesis-of-51nikrrcms.pdf

Modern-day environmental factors in the pathogenesis of osteoarthritis.

Cartilage homeostasis is governed by articular chondrocytes via their ability to modulate extracellular matrix production and degradation. In turn, chondrocyte activity is regulated by growth factors such as those of the transforming growth factor β (TGFβ) family. Members of this family include the TGFβs, bone morphogenetic proteins (BMPs), and growth and differentiation factors (GDFs). Signaling by this protein family uniquely activates SMAD-dependent signaling and transcription but also activates SMAD-independent signaling via MAPKs such as ERK and TAK1. This review will address the pivotal role of the TGFβ family in cartilage biology by listing several TGFβ family members and describing their signaling and importance for cartilage maintenance. In addition, it is discussed how (pathological) processes such as aging, mechanical stress, and inflammation contribute to altered TGFβ family signaling, leading to disturbed cartilage metabolism and disease.

TGFβ/BMP Signaling Pathway in Cartilage Homeostasis

The articular cartilage is exquisitely sensitive to mechanical load. Its structure is largely defined by the mechanical environment and destruction in osteoarthritis is the pathophysiological consequence of abnormal mechanics. It is often overlooked that disuse of joints causes profound loss of volume in the articular cartilage, a clinical observation first described in polio patients and stroke victims. Through the 1980s, the results of studies exploiting experimental joint immobilisation supported this. Importantly, this substantial body of work was also the first to describe metabolic changes that resulted in decreased synthesis of matrix molecules, especially sulfated proteoglycans. The molecular mechanisms that underlie disuse atrophy are poorly understood despite the identification of multiple mechanosensing mechanisms in cartilage. Moreover, there has been a tendency to equate cartilage loss with osteoarthritic degeneration. Here, we review the historic literature and clarify the structural, metabolic and clinical features that clearly distinguish cartilage loss due to disuse atrophy and those due to osteoarthritis. We speculate on the molecular sensing pathways in cartilage that may be responsible for cartilage mechanoadaptation.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/JP275451

Mechanoadaptation: articular cartilage through thick and thin.

Type III collagen is a key regulator of the collagen fibrillar structure and biomechanics of articular cartilage and meniscus.

Osteoarthritis (OA) is a chronic joint disease that generally occurs worldwide with pain and disability. The progression is slow, and it is mostly diagnosed midlife and often disturbs the knees, hips, feet, hands, and spine. Sex, age, obesity, occupation, and hereditary factors are risk factors that increase the opportunity for OA. Physical examinations involving X-rays and MRI, joint fluid analysis and blood tests are common tools for the diagnosis of OA. Interventions including exercise, manual therapy, lifestyle modification, and medication can help relieve pain and maintain mobility in the affected joints, yet none of the therapies enables the promotion of regeneration of degenerated tissues. Mesenchymal stem cells (MSCs) are a promising source for the treatment of OA due to their multipotency for differentiation into chondrocytes and their ability to modulate the immune system. Herein, we review the pathogenesis and treatment of OA and address the current status of MSCs as a novel potential therapeutic agent in OA treatment.

Mesenchymal stem cells in osteoarthritis therapy: a review.

Thinning of articular cartilage after joint unloading or immobilization. An experimental investigation of the pathogenesis in mice.

Background and Objective: Chondrocytes in the growth plate are a major player in the process of endochondral ossification through from proliferation to hypertrophy, leading to the longitudinal growth of the skeleton. Exercise promotes the longitudinal growth, whereas excessive exercise inhibits bone growth. The exercise condition is defined as a combination of intensity, frequency, and duration; and what these combinations leading to the best for the bone growth remain unclear. Our objective was to determine what combination of different exercise conditions lead to the best for a favorable response in the growth plate.
Methods: A total of 27 male young mice were divided into control group and 8 treadmill exercise groups; high-intensity (running), high-frequency (every day), and long-duration (60 min); high-intensity, high-frequency, and short-duration (15 min); high-intensity, low-frequency (Once in 3 d), and longduration; high-intensity, low-frequency, and short-duration; low-intensity (walking), high-frequency, and long-duration; low-intensity, high-frequency, and short-duration; low-intensity, low-frequency, and long-duration; low-intensity, low-frequency, and short-duration. We quantified histologic characteristics in the growth plate after exercise.
Results: The thickness of the growth plate, cell proliferation, and the number of hypertrophic chondrocytes in the growth plate increased in the high-intensity exercise compared with the lowintensity; further, osteoclasts in the primary spongiosa increased by high-intensity and low-frequency and long-duration exercise.
Conclusion: Our results suggest that chondrocyte activity and bone metabolism promote in highintensity and low-frequency and long-duration in young mice. These findings may shed light on the underlying of the promotion of the longitudinal bone growth by exercise.

/pdf/effects-of-different-exercises-on-the-growth-plate-in-young-4dkwtvkl5i.pdf

Effects of different exercises on the growth plate in young growing mice

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Thinning of articular cartilage after joint unloading or immobilization. An experimental investigation of the pathogenesis in mice.

Effects of different exercises on the growth plate in young growing mice