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Related Concept Videos

Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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The most apparent functions of the skeletal system are support, protection, and movement. However, bone tissue also performs several other critical metabolic functions. For one, the bone matrix acts as a reservoir for a number of minerals important to the functioning of the body, especially calcium and phosphorus. These minerals, present in the bone tissue, can be released back into the bloodstream when required. Calcium ions, for example, are essential for muscle contractions and controlling...
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Updated: Nov 29, 2025

Flow Cytometry Analysis of Immune Cell Subsets within the Murine Spleen, Bone Marrow, Lymph Nodes and Synovial Tissue in an Osteoarthritis Model
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Pathophysiological Perspective of Osteoarthritis.

Mohd Heikal Mohd Yunus1,2, Abid Nordin1, Haziq Kamal1

  • 1Department of Physiology, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur 56000, Malaysia.

Medicina (Kaunas, Lithuania)
|November 19, 2020
PubMed
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Osteoarthritis (OA) is a degenerative joint disease causing disability. This review details risk factors and mediators involved in cartilage destruction, paving the way for targeted OA treatments.

Keywords:
cytokinesosteoarthritispathogenesisproteolytic enzymes

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Area of Science:

  • Rheumatology
  • Orthopedics
  • Biochemistry

Background:

  • Osteoarthritis (OA) is a prevalent degenerative joint disease in the elderly, leading to significant disability.
  • Pathological hallmarks include cartilage erosion, synovial inflammation, and subchondral bone changes.
  • Current treatments do not halt OA progression, focusing on symptom management before surgery.

Purpose of the Study:

  • To review the significant risk factors and molecular mediators driving OA.
  • To describe the mechanisms of articular cartilage homeostasis disruption in OA.
  • To highlight the development of targeted therapies based on improved understanding of OA pathogenesis.

Main Methods:

  • Literature review of osteoarthritis risk factors and mediators.
  • Analysis of molecular pathways involved in cartilage degradation.
  • Synthesis of current understanding of catabolic and anabolic imbalances in OA.

Main Results:

  • Identified key risk factors and mediators (cytokines, proteolytic enzymes, nitric oxide) in OA progression.
  • Described how these mediators disrupt normal joint homeostasis and lead to structural changes.
  • Highlighted the imbalance between catabolic and anabolic activities in OA pathogenesis.

Conclusions:

  • Understanding OA mechanisms is crucial for developing effective treatments.
  • Targeting specific mediators offers a promising strategy to combat cartilage destruction in OA.
  • Future therapies aim to restore joint homeostasis by addressing catabolic and anabolic imbalances.