Extended Anterior Approach for Proximal Femur Resection and Hip Reconstruction. Technique Description and Case Report of Three Oncologic Patients.

This retrospective case report describes an extended anterior surgical approach for treating oncologic patients with proximal femur resection and hip reconstruction. Three consecutive women (mean age: 57.3; range: 33 to 81 years) with non-Hodgkins lymphoma (one case) or breast cancer (two cases) that had metastasized to the proximal femur underwent this procedure. Outcome measurements included timed-up-and-go, visual analog scale (VAS) for pain, and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores. Independent walking distance was also recorded. At a mean of 14 months postoperatively, all three patients had returned to independent flat surface and stair ambulation with minimal hip pain. Normal active hip flexion and extension range of motion were also restored. All patients had ≥ 4/5 involved hip manual muscle test strength. The surgical approach we described enabled effective return to independent flat surface and stair ambulation.

Isolated Patellofemoral Joint Arthroplasty: Can Preoperative Bone Scans Predict Survivorship?

BACKGROUND: Isolated patellofemoral joint arthritis has been identified in 10% of the population presenting with symptomatic knee osteoarthritis. Patient selection is important in order to improve survivorship following PF arthroplasty. The purpose of this study is to compare the use of a preoperative bone scan vs a magnetic resonance imaging (MRI) to identify the patient with isolated PF arthritis. METHODS: This is a retrospective review of 32 patients undergoing isolated PF arthroplasty for PF arthritis using the same implant design. Sixteen consecutive patients received a preoperative bone scan to confirm isolated PF arthritis. These patients were matched by age and gender to patients where an MRI was used to determine isolated PF arthritis. The bone scan cohort contained 13 females and three males with an average age of 48 years and average follow-up of 52 months. There was no significant difference in age, body mass index, follow-up, or preoperative range of motion between the groups. The MRI and bone scan results were reported by a radiologist specializing in orthopedic radiology. RESULTS: Survivorship was 100% in the PF arthroplasty group selected using a preoperative bone scan. Revision surgery with conversion to TKA was required in 5 of 16 patients (31%) when an MRI was used to identify isolated PF arthritis. Revision in all patients in the MRI group was due to progression of knee arthritis in the tibial-femoral joint. There were no cases of implant-related failures. CONCLUSION: Patellofemoral arthroplasty using a modern design implant demonstrated 100% survivorship when a preoperative bone scan was used for patient selection to confirm isolated PF arthritis. In the group where only an MRI was used, there was a 31% failure due to progression of the disease. Based on this study, we would recommend the use of a bone scan as a tool in the selection criteria for patients undergoing PF arthroplasty.

Unilateral heat accelerates bone elongation and lengthens extremities of growing mice.

Linear growth failure results from a broad spectrum of systemic and local disorders that can generate chronic musculoskeletal disability. Current bone lengthening protocols involve invasive surgeries or drug regimens, which are only partially effective. Exposure to warm ambient temperature during growth increases limb length, suggesting that targeted heat could noninvasively enhance bone elongation. We tested the hypothesis that daily heat exposure on one side of the body unilaterally increases femoral and tibial lengths. Mice (N = 20) were treated with 40 °C unilateral heat for 40 min/day for 14 days post-weaning. Non-treated mice (N = 6) served as controls. Unilateral increases in ear (8.8%), hindfoot (3.5%), femoral (1.3%), and tibial (1.5%) lengths were obtained. Tibial elongation rate was > 12% greater (15 µm/day) on the heat-treated side. Extremity lengthening correlated with temperature during treatment. Body mass and humeral length were unaffected. To test whether differences persisted in adults, mice were examined 7-weeks post-treatment. Ear area, hindfoot, femoral, and tibial lengths were still significantly increased ∼6%, 3.5%, 1%, and 1%, respectively, on the heat-treated side. Left-right differences were absent in non-treated controls, ruling out inherent side asymmetry. This model is important for designing noninvasive heat-based therapies to potentially combat a range of debilitating growth impediments in children.

Preventing falls with vitamin D.

Falls are the number one cause for injury-related morbidity and mortality in West Virginia's seniors. Multiple independent variables contribute to the risk of a fall: previous falls, alterations in balance and vision, impairments in gait and strength, and medications most highly correlate with the risk for a fall. Vitamin D supplementation is emerging as an easy, safe and well-tolerated fall reduction/prevention strategy due to the beneficial effects on the musculoskeletal system with improvements in strength, function and navigational abilities. From meta-analysis data, maximal fall reduction benefit in seniors is achieved when correcting vitamin D deficiency and when using adjunctive calcium supplementation. It is therefore recommended that practitioners in our state screen for fall risks and consider the addition of supplementation protocols that provide sufficient vitamin D and calcium to our seniors.

Delayed spontaneous reduction of traumatic pediatric atlantoaxial rotatory subluxation.

Pediatric atlantoaxial rotatory subluxation (AARS) is a rare finding with various etiologies and treatment recommendations. Etiologies include both traumatic and nontraumatic causes. The diagnosis is suggested by clinical presentation and confirmed with imaging. Various forms of management have been discussed in the literature. However, no overall consensus has been established. We present 2 pediatric cases showing delayed spontaneous reduction of traumatic AARS. Images from computed tomography (CT) were used for initial diagnosis and to track management progression. Although the subluxation persisted on the 1-month follow-up CT in Case 1, the final CT images in both cases showed spontaneous reduction with anatomic positioning of C1 and C2. These cases demonstrate that delayed spontaneous reduction of traumatic pediatric AARS is possible with conservative treatment. Active reduction via traction may not be necessary. In the absence of compelling surgical indications to the contrary, a conservative approach to management of traumatic pediatric AARS is warranted.

N-acetyltransferase 2 genotype modification of active cigarette smoking on breast cancer risk among hispanic and non-hispanic white women.

While it has been demonstrated that cigarette smoke contains aromatic and heterocyclic amines that initiate carcinogenesis, the association between cigarette smoking and breast cancer remains controversial. N-acetyltransferase 2 (NAT2) catalyzes arylamine carcinogen biotransformation and NAT2 genetic polymorphisms may contribute to differential susceptibility to breast cancer. We tested whether NAT2 modified the association between cigarette smoking and breast cancer risk in a population-based study of Hispanic and non-Hispanic white women in the Southwest United States. Data were available for cigarette smoking and NAT2 polymorphisms for 717 cases (Hispanic, 251 and non-Hispanic white, 466) and 735 controls (Hispanic, 245 and non-Hispanic white, 490). NAT2 genotypes were translated into rapid, intermediate, slow, or very slow acetylator phenotypes. Odds ratios (ORs) and 95% confidence intervals (95% CIs) for the joint association of NAT2 with smoking on breast cancer risk were estimated using logistic regression. Non-Hispanic white women were more likely (p < 0.001) than Hispanic women to have a slow (41.7 vs. 33.5%) or very slow (19.0 vs. 11.1%) acetylator status and less likely to have rapid/intermediate phenotypes (39.2 vs. 54.4%). Breast cancer risk was significantly increased in non-Hispanic white women with a very slow acetylator phenotype who smoked: ever versus never (OR, 2.57; 95% CI, 1.49-4.41), never versus former (OR, 2.69; 95% CI, 1.41-5.17) or current (OR, 2.46; 95% CI, 1.07-5.65), and 16 + pack-years (OR, 2.29; 95% CI, 1.16-4.51). Results for Hispanic women were not statistically significant. These findings support smoking as a risk factor for breast cancer among non-Hispanic white women with very slow NAT2 acetylator phenotype.

Subhepatotoxic exposure to arsenic enhances lipopolysaccharide-induced liver injury in mice.

Exposure to arsenic via drinking water is a serious health concern in the US. Whereas studies have identified arsenic alone as an independent risk factor for liver disease, concentrations of arsenic required to damage this organ are generally higher than found in the US water supply. The purpose of the current study was to test the hypothesis that arsenic (at subhepatotoxic doses) may also sensitize the liver to a second hepatotoxin. To test this hypothesis, the effect of chronic exposure to arsenic on liver damage caused by acute lipopolysaccharide (LPS) was determined in mice. Male C57Bl/6J mice (4-6 weeks) were exposed to arsenic (49 ppm as sodium arsenite in drinking water). After 7 months of exposure, animals were injected with LPS (10 mg/kg i.p.) and sacrificed 24 h later. Arsenic alone caused no overt hepatotoxicity, as determined by plasma enzymes and histology. In contrast, arsenic exposure dramatically enhanced liver damage caused by LPS, increasing the number and size of necroinflammatory foci. This effect of arsenic was coupled with increases in indices of oxidative stress (4-HNE adducts, depletion of GSH and methionine pools). The number of apoptotic (TUNEL) hepatocytes was similar in the LPS and arsenic/LPS groups. In contrast, arsenic pre-exposure blunted the increase in proliferating (PCNA) hepatocytes caused by LPS; this change in the balance between cell death and proliferation was coupled with a robust loss of liver weight in the arsenic/LPS compared to the LPS alone group. The impairment of proliferation after LPS caused by arsenic was also coupled with alterations in the expression of key mediators of cell cycle progression (p27, p21, CDK6 and Cyclin D1). Taken together, these results suggest that arsenic, at doses that are not overtly hepatotoxic per se, significantly enhances LPS-induced liver injury. These results further suggest that arsenic levels in the drinking water may be a risk modifier for the development of chronic liver diseases.