Lack of CCR3 leads to a skeletal phenotype only in male mice.

We recently showed that adult male mice that lacked the C-C-chemokine receptor 3 (CCR3) exhibited disturbed bone remodeling, which resulted in a cortical bone phenotype of thin femoral cortical bone. However, it remains unknown whether this phenotype would be present during bone modeling, or it affects female mice. Here, we analyzed juvenile and adolescent CCR3-deficient mice to determine when bone modeling was affected in the absence of CCR3 signaling. To investigate whether the CCR3 bone phenotype was sex-related, we analyzed both young female and male mice, and adult females. Micro-computed tomography (µCT) and histomorphometric analyses in adolescent CCR3-deficient male mice revealed reduced cortical bone volume and thickness, and an increase in periosteal mineralization. Interestingly, no skeletal phenotype was observed in adolescent or adult female CCR3-deficient mice. Among juvenile CCR3-deficient mice, neither males nor females showed a skeletal phenotype, which indicated that bone modeling was not affected by the CCR3 deficiency. In summary, adolescent and adult male mice that lacked CCR3 receptors exhibited a cortical phenotype that was not present in female mice, probably due to an estrogen protective mechanism. Based on these and our previous results, we suggest that the importance of CCR3 in cortical bone turnover is related to sex hormones. Because only a few molecules are known to control cortical bone turnover, our novel finding that CCR3 regulated cortical bone thickness only in males suggested that CCR3 is a novel target for controlling cortical bone morphology in male individuals, and perhaps, in post-menopausal women.

Dizziness and the Acute Vestibular Syndrome at the Emergency Department: A Population-Based Descriptive Study.

BACKGROUND: Dizziness is a common occurrence witnessed at emergency departments (EDs). This study aims to describe the epidemiology and management of dizzy patients with and without an acute vestibular syndrome (AVS) in the ED at Umeå University Hospital. METHODS: A total of n = 2,126 ED dizziness visits during 3 years were identified. Data were obtained through retrospective review of medical records. Cases were stratified based on presentation, including AVS and neurological deficits. The outcomes analyzed included cerebrovascular causes of dizziness. A Poisson distribution was assumed when calculating incidence CIs. RESULTS: Dizziness accounted for 2.1% of all ED visits, incidence 477/100,000 inhabitants (95% CI 457-498). Among dizzy patients, 19.2% had an AVS, incidence 92/100,000 inhabitants (95% CI 74-113). Top medical diagnostic groups were otovestibular (15.1%), cardiovascular (8.7%) and neurological diseases (7.7%), including stroke and transitory ischemic attack (4.8%). Cerebrovascular causes of dizziness were more common among those with an AVS (10.0%) vs. those without (3.6%), p < 0.01. CONCLUSION: The risk for cerebrovascular causes of dizziness, although low in an unselected cohort, increases with the presence of neurological signs and an AVS. These population-based data may be useful when planning and implementing dizziness and AVS management algorithms at EDs.