Year: 2025
Type: article
Study design: Observational Study
Abstract: Background: The epiphyseal vascularization of long bones generates a particular flow pattern that is important for adequate angiogenesis to be achieved. Imaging reveals that vessel development in murine long bone involves the expansion and anastomotic fusion of endothelial buds. Impaired blood flow leads to defective angiogenesis and osteogenesis and downregulation of Notch signaling in endothelial cells. We examined whether altered blood flow and endothelial signaling via the Notch pathway—a highly conserved cell–cell communication mechanism that regulates angiogenesis and vascular remodeling—contributes to hip joint degeneration. Material and Methods: In our study, we used two groups of patients. The first is a control group of 15 patients without degenerative joint pathology. The second group consists of 51 patients diagnosed with an advanced form of degenerative joint pathology. On both study groups, we used immunohistochemical markers that highlight the endothelium of epiphyseal capillaries, the collagen matrix, and the presence of joint lubricant-secreting cells. Ultrastructural analysis was performed on hematoxylin-eosin slides that were exposed to a surface electron microscope, following a previously tested protocol. Results: The results of our study show that there are numerous anastomoses between epiphyseal vessels and that these capillaries persist even after pathological bone resorption, for a certain period of time. Discussions: Our results are complementary to recent studies on this research topic that emphasize the possibility that the main cause of joint degeneration is vascular. Revascularization of an area of bone demineralization after bone infarction has become a reality. Conclusions: This study opens new perspectives regarding the research on epiphyseal capillary vascularization and the modern concept of morpho functional rehabilitation of the hip joint.
Source: Journal of Clinical Medicine
DOI: 10.3390/jcm14165845
Language: English
Subfield: Rheumatology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,137
OpenAlex ID: W4413279829