Publications

OBJECTIVE

To analyze whether rectal testing among women increased chlamydia and gonorrhea case-finding and whether reported receptive anal intercourse was a risk factor for rectal infection.

METHODS

From March 2007 to August 2008, women receiving pelvic examinations at the San Francisco sexually transmitted disease clinic were tested for rectal gonorrhea and chlamydia by using a transcription-mediated amplification assay. Results of testing and clinical and demographic data were analyzed using a cross-sectional study design.

RESULTS

Of 1,308 women with both rectal and vaginal tests, test results were positive for 79 patients (6.0%) for rectal chlamydia or gonorrhea and 88 patients (6.7%) for genital chlamydia or gonorrhea. Test results were positive for 13 patients (1.0%) at the rectum only, increasing detection from 88 to 101 patients (14.8%; 95% confidence interval 8.1-23.9). No correlation existed between reported anal sex and rectal chlamydia (P=.74); however, 50% of women with rectal gonorrhea reported anal sex compared with 21% of women without rectal gonorrhea (P=.002).

CONCLUSION

Sexually transmitted disease clinics might improve chlamydia and gonorrhea case-finding through rectal testing of women, but more study is needed to determine the effects of finding and treating such infections. Reporting anal intercourse did not predict rectal chlamydial infection among women tested at both the rectum and the vagina.

LEVEL OF EVIDENCE

II.

Bone injury induces an inflammatory response that involves neutrophils, macrophages and other inflammatory cells. The recruitment of inflammatory cells to sites of injury occurs in response to specific signaling pathways. The CC chemokine receptor type 2 (CCR2) is crucial for recruiting macrophages, as well as regulating osteoclast function. In this study, we examined fracture healing in Ccr2-/- mice. We first demonstrated that the expression of Ccr2 transcripts and the filtration of macrophages into fracture calluses were most robust during the early phases of fracture healing. We then determined that the number of macrophages at the fracture site was significantly lower in Ccr2-/- mice compared with wild-type controls at 3 days after injury. As a result, impaired vascularization, decreased formation of callus, and delayed maturation of cartilage were observed at 7 days after injury in mutant mice. At day 14, Ccr2-/- mice had less bone in their calluses. At day 21, Ccr2-/- mice had larger calluses and more bone compared with wild-type mice, suggesting a delayed remodeling. In addition, we examined the effect of Ccr2 mutation on osteoclasts. We found that a lack of Ccr2 did not affect the number of osteoclasts within fracture calluses at 21 days after injury. However, Ccr2-/- osteoclasts exhibited a decreased ability to resorb bone compared with wild-type cells, which could contribute to the delayed remodeling of fracture calluses observed in Ccr2-/- mice. Collectively, these results indicate that a deficiency of Ccr2 reduces the infiltration of macrophages and impairs the function of osteoclasts, leading to delayed fracture healing.