Variations in the diagnosis and treatment of somatic dysfunction between 4 osteopathic residency programs.

CONTEXT: The American Osteopathic Association requires the integration of osteo-pathic principles and practice in all specialty residency training programs that it accredits, but the 4 residencies with the most integration of osteopathic manipulative medicine (OMM) have differences in training and emphasis on OMM as a primary treatment modality. OBJECTIVE: To study differences in OMM use for spinal pain between the neuro-musculoskeletal medicine/OMM (NMM/OMM), the family practice/osteopath-ic manipulative treatment (FP/OMT), the integrated FP/OMT and NMM/OMM (FP/NMM), and the internal medicine and NMM/OMM (IM/NMM) specialty residency training programs. METHODS: Medical records were reviewed for patient encounters from September 2011 through October 2013 at NMM/OMM, FP/OMT, FP/NMM, and IM/NMM residencies in a family medicine and OMM specialty clinic. Records were screened for a diagnosis of cervicalgia, thoracalgia, lumbago, or backache. The identifed encounters were compared to determine between-specialty differences in the number of chief complaints, non-somatic dysfunction assessments, body regions with diagnosed somatic dysfunction, body regions managed with OMT, and number and type of OMT techniques used. RESULTS: Eighteen residents had 2925 patient encounters that included 1 or more spinal pain diagnoses. Overall, 2767 patients (95%) received OMT. The probability (95% CI) of residents using OMT was 0.99 (0.98-0.99) for the NMM/OMM residents, 0.66 (0.55-0.77) for the FP/OMT residents, 0.94 (0.88-0.97) for the FP/NMM residents, and 0.997 (0.98-1.0) for the IM/NMM residents. The FP/OMT residents were less likely to manage spinal pain using OMT (P<.001) and documented fewer somatic dysfunction assessments and fewer musculoskeletal assessments (P<.001), but they documented significantly more non-somatic dysfunction assessments (P<.001). When using OMT, the FP/OMT residents diagnosed somatic dysfunction in fewer mean (95% CI) body regions (2.9 [2.4-3.5]) than the NMM/OMM (5.5 [4.9-6.2]), the FP/NMM (5.5 [4.8-6.3]), or the IM/NMM (4.6 [3.4-6.0]) residents (P<.001). The FP/OMT residents also managed fewer mean (95% CI) body regions with OMT (3.5 [3.0-4.1]) than the NMM/OMM (5.7 [5.2-6.3]), the FP/NMM (5.6 [5.0-6.3]), or the IM/NMM (4.7 [3.7-6.0]) residents (P<.001). CONCLUSION: Although the FP/OMT residents used OMT less frequently than the other residents during spinal pain encounters, they provided care for a larger number and a wider variety of non-somatic dysfunction assessments.

Enhanced chondrogenesis and Wnt signaling in PTH-treated fractures.

UNLABELLED: Studies have shown that systemic PTH treatment enhanced the rate of bone repair in rodent models. However, the mechanisms through which PTH affects bone repair have not been elucidated. In these studies we show that PTH primarily enhanced the earliest stages of endochondral bone repair by increasing chondrocyte recruitment and rate of differentiation. In coordination with these cellular events, we observed an increased level of canonical Wnt-signaling in PTH-treated bones at multiple time-points across the time-course of fracture repair, supporting the conclusion that PTH responses are at least in part mediated through Wnt signaling. INTRODUCTION: Since FDA approval of PTH [PTH(1-34); Forteo] as a treatment for osteoporosis, there has been interest in its use in other musculoskeletal conditions. Fracture repair is one area in which PTH may have a significant clinical impact. Multiple animal studies have shown that systemic PTH treatment of healing fractures increased both callus volume and return of mechanical competence in models of fracture healing. Whereas the potential for PTH has been established, the mechanism(s) by which PTH produces these effects remain elusive. MATERIALS AND METHODS: Closed femoral fractures were generated in 8-wk-old male C57Bl/6 mice followed by daily systemic injections of either saline (control) or 30 microg/kg PTH(1-34) for 14 days after fracture. Bones were harvested at days 2, 3, 5, 7, 10, 14, 21, and 28 after fracture and analyzed at the tissue level by radiography and histomorphometry and at the molecular and biochemical levels level by RNase protection assay (RPA), real-time PCR, and Western blot analysis. RESULTS: Quantitative muCT analysis showed that PTH treatment induced a larger callus cross-sectional area, length, and total volume compared with controls. Molecular analysis of the expression of extracellular matrix genes associated with chondrogenesis and osteogenesis showed that PTH treated fractures displayed a 3-fold greater increase in chondrogenesis relative to osteogenesis over the course of the repair process. In addition, chondrocyte hypertrophy occurred earlier in the PTH-treated callus tissues. Analysis of the expression of potential mediators of PTH actions showed that PTH treatment significantly induced the expression of Wnts 4, 5a, 5b, and 10b and increased levels of unphosphorylated, nuclear localized beta-catenin protein, a central feature of canonical Wnt signaling. CONCLUSIONS: These results showed that the PTH-mediated enhancement of fracture repair is primarily associated with an amplification of chondrocyte recruitment and maturation in the early fracture callus. Associated with these cellular effects, we observed an increase in canonical Wnt signaling supporting the conclusion that PTH effects on bone repair are mediated at least in part through the activation of Wnt-signaling pathways.