Posters
Presenting Author Academic/Professional Position
Medical Student
Academic Level (Author 1)
Medical Student
Academic Level (Author 2)
Graduate Student
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Immunology and Microbiology
Academic Level (Author 3)
Medical Student
Presentation Type
Poster
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Biomedical Science
Abstract Type
Research/Clinical
Abstract
This paper is a review based on over 50 papers from PubMed and Google Scholar that focuses on the function of osteoclasts and their role in joint degradation. Osteoclasts are specialized cells responsible for the resorption of bone tissue. They are derived from the monocyte bone lineage and play a crucial role in maintaining the balance of bone remodeling. Osteoclasts work in conjunction with osteoblasts, mesenchymal stem cells, to regulate this cycle. In healthy bone metabolism, osteoclasts use regulatory pathways that are essential for remodeling, allowing for adaptation to mechanical stress, repair of microdamage, and maintaining calcium homeostasis.
In conditions like osteoarthritis and rheumatoid arthritis, osteoclast activity can become dysregulated, contributing to joint degradation. In these diseases, osteoclasts are often implicated in excessive bone resorption, leading to the destruction of articular cartilage and bone structure. In osteoarthritis this process begins when mechanical stress on the joint leads to cartilage damage, which releases signals that recruit inflammatory cells. NF-kB activates RANK signaling, which stimulates osteoclast differentiation and activity. This leads to increased bone resorption, a process that accelerates joint degeneration by causing subchondral bone changes. This can destabilize the joint, further worsening the symptoms of joint degeneration. As osteoclasts break down the bone matrix, the inflammatory cycle stimulates additional cartilage destruction, creating a vicious feedback loop. Osteoclasts also secrete netrin 1 to induce sensory nerve axonal growth, leading to increased pain behavior. This degenerative joint disease leads to pain and loss of mobility that affects millions of people worldwide.
Osteoclasts also play a large role in rheumatoid arthritis with the help of other inflammatory mediators, such as TNFa, Il-1, and Il-6. This promotes joint degradation through mechanisms involving chronic inflammation, and osteoclasts work on the cartilage and bone leading to generalized erosion. Chronic inflammation also leads to osteoclastogenesis through RANKL signaling and aggressive bone resorption in affected joints, often resulting in severe deformities and disability.
Osteoclasts also play a key role in the development of Paget's and bone tumor formation. In Paget’s disease, there is abnormal and excessive bone resorption by osteoclasts, followed by disorganized bone formation. The increased osteoclast activity in Paget’s disease is often driven by genetic mutations and abnormal regulation of signaling pathways such as IGF1 which enhances osteocyte senescence. Similarly, in bone tumors, osteoclasts are involved in the bone remodeling process around tumors, either through direct recruitment by tumor cell or induction through the tumor microenvironment. This contributes to bone destruction and the pathological features seen in tumors like osteolytic lesions in metastatic cancers and primary bone tumors such as osteosarcoma. In both conditions, osteoclasts contribute to bone degradation, highlighting their central role in pathological bone remodeling.
The role of osteoclasts in joint degradation highlights the importance of targeting their activity for therapeutic interventions. Recent advances have led to the development of drugs that inhibit osteoclast differentiation and function. Prominent examples include bisphosphonates and monoclonal antibodies such as denosumab. These treatments aim to reduce bone resorption and mitigate the effects of joint degradation, improving patient outcomes.
Recommended Citation
Heckman, Justin Z.; Villa, Sophia M.; and Martin, Blake, "The Function of Osteoclasts and their role in Joint Degradation" (2025). Research Symposium. 85.
https://scholarworks.utrgv.edu/somrs/2025/posters/85
Included in
The Function of Osteoclasts and their role in Joint Degradation
This paper is a review based on over 50 papers from PubMed and Google Scholar that focuses on the function of osteoclasts and their role in joint degradation. Osteoclasts are specialized cells responsible for the resorption of bone tissue. They are derived from the monocyte bone lineage and play a crucial role in maintaining the balance of bone remodeling. Osteoclasts work in conjunction with osteoblasts, mesenchymal stem cells, to regulate this cycle. In healthy bone metabolism, osteoclasts use regulatory pathways that are essential for remodeling, allowing for adaptation to mechanical stress, repair of microdamage, and maintaining calcium homeostasis.
In conditions like osteoarthritis and rheumatoid arthritis, osteoclast activity can become dysregulated, contributing to joint degradation. In these diseases, osteoclasts are often implicated in excessive bone resorption, leading to the destruction of articular cartilage and bone structure. In osteoarthritis this process begins when mechanical stress on the joint leads to cartilage damage, which releases signals that recruit inflammatory cells. NF-kB activates RANK signaling, which stimulates osteoclast differentiation and activity. This leads to increased bone resorption, a process that accelerates joint degeneration by causing subchondral bone changes. This can destabilize the joint, further worsening the symptoms of joint degeneration. As osteoclasts break down the bone matrix, the inflammatory cycle stimulates additional cartilage destruction, creating a vicious feedback loop. Osteoclasts also secrete netrin 1 to induce sensory nerve axonal growth, leading to increased pain behavior. This degenerative joint disease leads to pain and loss of mobility that affects millions of people worldwide.
Osteoclasts also play a large role in rheumatoid arthritis with the help of other inflammatory mediators, such as TNFa, Il-1, and Il-6. This promotes joint degradation through mechanisms involving chronic inflammation, and osteoclasts work on the cartilage and bone leading to generalized erosion. Chronic inflammation also leads to osteoclastogenesis through RANKL signaling and aggressive bone resorption in affected joints, often resulting in severe deformities and disability.
Osteoclasts also play a key role in the development of Paget's and bone tumor formation. In Paget’s disease, there is abnormal and excessive bone resorption by osteoclasts, followed by disorganized bone formation. The increased osteoclast activity in Paget’s disease is often driven by genetic mutations and abnormal regulation of signaling pathways such as IGF1 which enhances osteocyte senescence. Similarly, in bone tumors, osteoclasts are involved in the bone remodeling process around tumors, either through direct recruitment by tumor cell or induction through the tumor microenvironment. This contributes to bone destruction and the pathological features seen in tumors like osteolytic lesions in metastatic cancers and primary bone tumors such as osteosarcoma. In both conditions, osteoclasts contribute to bone degradation, highlighting their central role in pathological bone remodeling.
The role of osteoclasts in joint degradation highlights the importance of targeting their activity for therapeutic interventions. Recent advances have led to the development of drugs that inhibit osteoclast differentiation and function. Prominent examples include bisphosphonates and monoclonal antibodies such as denosumab. These treatments aim to reduce bone resorption and mitigate the effects of joint degradation, improving patient outcomes.
