Osteoarthritis (OA) is one of the most burdensome and prevalent diseases for individuals and societies amidst the global aging trend, being amongst the leading causes of disability worldwide. OA is characterized by chronic degeneration and irreversible destruction of the entire synovial joint as the key pathological feature. In this regard, OA has traditionally been accepted as a degenerative disease caused by the accumulation of biomechanical stress.
Recent studies on the pathogenic signaling targets and therapeutic targets of OA have shown that it is an inflammatory disease triggered by multifaceted pathological factors.
Due to the complexity of OA pathology, there are no clear therapeutic interventions for this disease. However, progression of the disease results in pain sensitization, irreversible destruction of joint structures and skeletal fragility fractures. Therefore, there is an urgent need to understand the interventions, biomarkers and therapeutic targets that can cure OA or at least inhibit and prevent its progression; to a more advanced understanding of the disease pathology. With respect to endocrinology, there are emerging reports that obesity and various metabolic syndromes in particular play a significant role in the pathogenesis of OA. These metabolic disorders may significantly contribute to the risk of OA by triggering metabolism and low-grade inflammation in the body. Therefore, from an endocrinological perspective, a deeper understanding of the signaling pathways and biomarkers underlying this pathology and the exploration of interventions to modulate it is expected to serve as an important basis for the development of novel therapeutic interventions for some OA phenotypes.
In this context, this Research Topic aims to gather the latest knowledge on the relationship between metabolic syndrome, including obesity and type 2 diabetes, and OA. In particular, this relationship includes triggering the progression of osteoarthritis and skeletal fragility pathologies by "low-grade inflammation" and the triggering of metabolic disorders by gut microbiome dysbiosis. This topic, therefore, aims to explore the common links in the pathogenesis of osteoarthritis by pathological mechanisms generated in metabolic syndrome conditions, based on a variety of methodologies ranging from molecular level laboratory studies to clinical evidence and therapeutic interventions.
We welcome, but are not limited to, original research, clinical trials, case reports, reviews, systematic reviews, hypothesis & theory and general commentary articles that focus on the following subtopics:
- Role and mechanisms of metabolic disorders or metabolic syndrome in the pathogenesis and exacerbation of osteoarthritis;
- Potential candidate molecules to prevent osteoarthritis by modulating metabolic syndrome or metabolic disorders;
- Bioinformatic and experimental biological analysis of the underlying mechanisms of low-intensity inflammation that bridge metabolic syndrome and metabolic disorders to osteoarthritis;
- Therapeutic interventions or observational clinical studies that have implications for the prevention and treatment of osteoarthritis through modulation of metabolic disorders or metabolic syndrome, including molecular pathways, cellular effects, and effects on disease.
Osteoarthritis (OA) is one of the most burdensome and prevalent diseases for individuals and societies amidst the global aging trend, being amongst the leading causes of disability worldwide. OA is characterized by chronic degeneration and irreversible destruction of the entire synovial joint as the key pathological feature. In this regard, OA has traditionally been accepted as a degenerative disease caused by the accumulation of biomechanical stress.
Recent studies on the pathogenic signaling targets and therapeutic targets of OA have shown that it is an inflammatory disease triggered by multifaceted pathological factors.
Due to the complexity of OA pathology, there are no clear therapeutic interventions for this disease. However, progression of the disease results in pain sensitization, irreversible destruction of joint structures and skeletal fragility fractures. Therefore, there is an urgent need to understand the interventions, biomarkers and therapeutic targets that can cure OA or at least inhibit and prevent its progression; to a more advanced understanding of the disease pathology. With respect to endocrinology, there are emerging reports that obesity and various metabolic syndromes in particular play a significant role in the pathogenesis of OA. These metabolic disorders may significantly contribute to the risk of OA by triggering metabolism and low-grade inflammation in the body. Therefore, from an endocrinological perspective, a deeper understanding of the signaling pathways and biomarkers underlying this pathology and the exploration of interventions to modulate it is expected to serve as an important basis for the development of novel therapeutic interventions for some OA phenotypes.
In this context, this Research Topic aims to gather the latest knowledge on the relationship between metabolic syndrome, including obesity and type 2 diabetes, and OA. In particular, this relationship includes triggering the progression of osteoarthritis and skeletal fragility pathologies by "low-grade inflammation" and the triggering of metabolic disorders by gut microbiome dysbiosis. This topic, therefore, aims to explore the common links in the pathogenesis of osteoarthritis by pathological mechanisms generated in metabolic syndrome conditions, based on a variety of methodologies ranging from molecular level laboratory studies to clinical evidence and therapeutic interventions.
We welcome, but are not limited to, original research, clinical trials, case reports, reviews, systematic reviews, hypothesis & theory and general commentary articles that focus on the following subtopics:
- Role and mechanisms of metabolic disorders or metabolic syndrome in the pathogenesis and exacerbation of osteoarthritis;
- Potential candidate molecules to prevent osteoarthritis by modulating metabolic syndrome or metabolic disorders;
- Bioinformatic and experimental biological analysis of the underlying mechanisms of low-intensity inflammation that bridge metabolic syndrome and metabolic disorders to osteoarthritis;
- Therapeutic interventions or observational clinical studies that have implications for the prevention and treatment of osteoarthritis through modulation of metabolic disorders or metabolic syndrome, including molecular pathways, cellular effects, and effects on disease.
