Osteoarthritis (OA) is a common joint degenerative disease that involves different anatomical structures (e.g., cartilage, synovial membrane, subchondral bone, menisci, fat pad), and the majority of patients with OA experience prolonged joint pain, which seriously compromises the quality of life. We have coined the term “neuroarthrology” to better understand the anatomical and molecular processes at play.
In OA, joint tissues are overwhelmed by a chronic cascade of cues (production of cytokines, interleukins, growth factors, and adipokines) responsible for the modification of tissues and progressively leads to pain. As there is a growing consensus that possible crosstalk between the joint structures may trigger the development and progression of the disease, a better comprehension of the regulative signal cascades underlying such mechanisms, with a focus on pain onset, may lay the foundation for future therapies that can target and control OA progression. To date, the exact pathogenesis of OA joint diseases is still unclear. Current treatment strategies mainly address symptomatic patients without a focus on limiting disease progression. A better understanding of the complex mechanisms responsible for OA development may suggest novel interpretive keys not only for explaining the peculiar OA histopathological features but also for identifying tailored clinical approaches for its management. The overall neuroanatomical and molecular pathways for joint pain will be reviewed and recent advances evaluated.
This research topic will welcome original and review articles focusing on evidence regarding the existence of nerve innervation and crosstalk between cell populations/anatomical structures of the joint tissues in patients with OA. A better comprehension of the mechanisms responsible for OA onset, from underlying molecular and cellular pathophysiology and resultant tissue modification, will, in the future, allow for more clinically effective management of the disease. Authors might consider the following:
• anatomical similarities between the joint tissues in different pathological conditions leading to OA;
• the existence of neuroanatomy and crosstalk between resident cells and anatomical features of OA mediated by molecular signaling/cues. Gender differences also may be evaluated.
• vascularization, innervation, and effective pain control will also be of interest.
Osteoarthritis (OA) is a common joint degenerative disease that involves different anatomical structures (e.g., cartilage, synovial membrane, subchondral bone, menisci, fat pad), and the majority of patients with OA experience prolonged joint pain, which seriously compromises the quality of life. We have coined the term “neuroarthrology” to better understand the anatomical and molecular processes at play.
In OA, joint tissues are overwhelmed by a chronic cascade of cues (production of cytokines, interleukins, growth factors, and adipokines) responsible for the modification of tissues and progressively leads to pain. As there is a growing consensus that possible crosstalk between the joint structures may trigger the development and progression of the disease, a better comprehension of the regulative signal cascades underlying such mechanisms, with a focus on pain onset, may lay the foundation for future therapies that can target and control OA progression. To date, the exact pathogenesis of OA joint diseases is still unclear. Current treatment strategies mainly address symptomatic patients without a focus on limiting disease progression. A better understanding of the complex mechanisms responsible for OA development may suggest novel interpretive keys not only for explaining the peculiar OA histopathological features but also for identifying tailored clinical approaches for its management. The overall neuroanatomical and molecular pathways for joint pain will be reviewed and recent advances evaluated.
This research topic will welcome original and review articles focusing on evidence regarding the existence of nerve innervation and crosstalk between cell populations/anatomical structures of the joint tissues in patients with OA. A better comprehension of the mechanisms responsible for OA onset, from underlying molecular and cellular pathophysiology and resultant tissue modification, will, in the future, allow for more clinically effective management of the disease. Authors might consider the following:
• anatomical similarities between the joint tissues in different pathological conditions leading to OA;
• the existence of neuroanatomy and crosstalk between resident cells and anatomical features of OA mediated by molecular signaling/cues. Gender differences also may be evaluated.
• vascularization, innervation, and effective pain control will also be of interest.
