Independent thesis Advanced level (degree of Master (Two Years)), 20 credits / 30 HE credits
Abstract
Background: Bone modeling is vital for skeletal formation and development while bone remodeling, the continuous renewal of bone tissue, plays a crucial part in maintaining overall bone strength. Cytokines, chemokines, and hormones are molecules, among others, that via receptor signaling play an active part in the modeling and remodeling processes. Recent studies show that adult and adolescent male, but not female mice, lacking the C-C chemokine receptor 3 (CCR3), have an altered cortical bone phenotype. Interestingly, neither juvenile CCR3 deficient male nor female mice show skeletal changes. However, the studies of juvenile female CCR3 deficient mice were performed using only micro-computed tomography (μCT). No static or dynamic histomorphometry analyses were conducted.
Aim: To further elucidate whether the lack of CCR3 affects bone modeling we performed detailed skeletal analyses of juvenile female mice (3-weeks of age) with CCR3 deficiency.
Method: Histomorphometric analyses were performed on a 5μm-thick sagittal section from juvenile CCR3-deficient and wild-type female mice. Static and dynamic histomorphometric parameters were analyzed.
Results: Quantification of static and dynamic histomorphometric values display no difference between genotypes in juvenile female mice.
Conclusion: In this study, we can further substantiate that the lack of CCR3 does not affectbone modeling in female juvenile mice. Additional research is necessary to clarify the importance of CCR3 in cortical bone turnover in mice and how its realation to sex
2023. , p. 15