Reduction of bone turnover with bisphosphonate treatment alters bone mineral and matrix properties. Our objective was to investigate the effect of bisphosphonate treatment on bone tissue properties near fragility fracture sites in the proximal femur in postmenopausal women with osteoporosis. The mineral and collagen properties of cortico-cancellous biopsies from the proximal femur were compared in bisphosphonate-naive (-BIS, n=20) and bisphosphonate-treated (+BIS, n=20, duration 7 ± 5 y) patients with intertrochanteric (IT) and subtrochanteric (ST) fractures using Fourier transform infrared imaging (FTIRI). The mean values of the FTIRI parameter distributions were similar across groups, but the widths of the parameter distributions tended to be reduced in the +BIS group relative to the -BIS group. Specifically, the distribution widths of the cortical collagen maturity and crystallinity were reduced in the +BIS group relative to those of the -BIS group by 28% (+BIS 0.45 ± 0.18 vs. -BIS 0.63 ± 0.28, p=0.03) and 17% (+BIS 0.087 ± 0.012 vs. -BIS 0.104 ± 0.036, p=0.05), respectively. When the tissue properties were examined as a function of fracture morphology within the +BIS group, the FTIR parameters were generally similar regardless of fracture morphology. However, the cortical mineral:matrix ratio was 8% greater in tissue from patients with atypical ST fractures (n =6) than that of patients with typical (IT or spiral ST) fractures (n=14) (Atypical 5.6 ± 0.3 vs. Typical 5.2 ± 0.5, p=0.03). Thus, although the mean values of the FTIR properties were similar in both groups, the tissue in bisphosphonate-treated patients had a more uniform composition than that of bisphosphonate-naïve patients. The observed reductions in mineral and matrix heterogeneity may diminish tissue-level toughening mechanisms.

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Object Lateral transpsoas interbody fusion (LTIF) permits anterior column lumbar interbody fusion via a direct lateral approach. The authors sought to answer 3 questions. First, what is the effect of LTIF on lumbar foraminal area? Second, how does interbody cage placement affect intervertebral height? And third, how does the change in foraminal area and cage position correlate with changes in Oswestry Disability Index (ODI) and 12-Item Short Form Health Survey (SF-12) scores? Methods Included patients underwent LTIF with or without posterior instrumentation and received preoperative and postoperative CT scans. Disc heights, neural foraminal area between adjacent-level pedicles, and anteroposterior cage position were measured from sagittal CT images. Preoperative and postoperative ODI and SF-12 scores were matched with the change in foraminal area from the clinically most severely affected side for analysis of the relationship between outcomes instruments and change in foraminal area. Results Average foraminal area increased by 36.2 mm2, or 35% of the preoperative area (p < 0.01), without statistically significant differences by side, level, or anteroposterior cage position. Preoperative anterior and posterior disc heights measured 6.2 mm and 3.7 mm, respectively, compared with postoperative measurements of 9.8 mm (p < 0.01) and 6.3 mm (p < 0.01), respectively, without significant differences by level or cage position. Despite significant overall improvement in ODI and SF-12 scores, there was no correlation with foraminal area increase. Conclusions Average foraminal area increased approximately 35% after cage placement without variation based on cage position. While ODI and SF-12 scores increased significantly, there was no significant association with cage position or foraminal area change, likely attributable to the multifactorial nature of preoperative pain.

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Postoperative surgical site infection (SSI) is a common complication after posterior lumbar spine surgery. This review details an approach to the prevention, diagnosis and treatment of SSIs. Factors contributing to the development of a SSI can be split into three categories: (1) microbiological factors; (2) factors related to the patient and their spinal pathology; and (3) factors relating to the surgical procedure. SSI is most commonly caused by Staphylococcus aureus. The virulence of the organism causing the SSI can affect its presentation. SSI can be prevented by careful adherence to aseptic technique, prophylactic antibiotics, avoiding myonecrosis by frequently releasing retractors and preoperatively optimizing modifiable patient factors. Increasing pain is commonly the only symptom of a SSI and can lead to a delay in diagnosis. C-reactive protein and magnetic resonance imaging can help establish the diagnosis. Treatment requires acquiring intra-operative cultures to guide future antibiotic therapy and surgical debridement of all necrotic tissue. A SSI can usually be adequately treated without removing spinal instrumentation. A multidisciplinary approach to SSIs is important. It is useful to involve an infectious disease specialist and use minimum serial bactericidal titers to enhance the effectiveness of antibiotic therapy. A plastic surgeon should also be involved in those cases of severe infection that require repeat debridement and delayed closure.