What are the academic and demographic characteristics of orthopaedic spine surgery division chiefs?

Background: To our knowledge no analysis of academic orthopedics division chiefs (DC) exists in the current orthopedic literature. Serving as a Division Chief may be a career milestone or an opportunity to lead and transition to additional leadership roles. Our objective is to answer the following questions (1) Are there academic characteristics common to Spine divisions chiefs? (2) Are there demographic characteristics common to Spine division chiefs? (3) Do most Spine division chiefs train at certain fellowships? Methods: Allopathic residency program websites were used to locate DC and Division Co-Chiefs (DCC). Academic characteristics evaluated included: H-index, academic rank, number of degrees, additional leadership titles, the availability of fellowship training and service as past/current society president and participation in travelling fellowships. Demographic characteristics including gender and race were collected. Years since completions of fellowship and which fellowship program the DC/DCC trained at were collected. Results: 102 DC/DCC were identified and had an average H-index of 22.1. The majority (48%) had an academic rank of Professor, 29% Associate Professor, 16% Assistant Professor and 8% rank could not be identified. 45% had additional leadership positions within their department and 18% had additional graduate degrees. Two institutions had designations of co-chiefs. The majority (57%) offered spine fellowships at their institution. The majority of DC were males (99%) and White (72.5%). On average the DC/DCC were 19.5 years past their fellowship completion. 19% participated in at least one travelling fellowship and 14% served as a president of a Spine or Orthopaedic Society. Conclusions: Spine surgery division chiefs are 99% male, with a rank of Professor and trained at select fellowship programs. Nearly half of spine surgery division chiefs held concurrent administrative roles in the department and 14% have served as President of a spine or Orthopaedic society. There is room to Improve on the gender and ethnic/racial diveristy of spine surgery division chief leadership.

Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair.

Bone fracture is a growing public health burden and there is a clinical need for non-invasive therapies to aid in the fracture healing process. Previous studies have demonstrated the utility of electromagnetic (EM) fields in promoting bone repair; however, its underlying mechanism of action is unclear. Interestingly, there is a growing body of literature describing positive effects of an EM field on mitochondria. In our own work, we have previously demonstrated that differentiation of osteoprogenitors into osteoblasts involves activation of mitochondrial oxidative phosphorylation (OxPhos). Therefore, it was reasonable to propose that EM field therapy exerts bone anabolic effects via stimulation of mitochondrial OxPhos. In this study, we show that application of a low intensity constant EM field source on osteogenic cells in vitro resulted in increased mitochondrial membrane potential and respiratory complex I activity and induced osteogenic differentiation. In the presence of mitochondrial inhibitor antimycin A, the osteoinductive effect was reversed, confirming that this effect was mediated via increased OxPhos activity. Using a mouse tibial bone fracture model in vivo, we show that application of a low intensity constant EM field source enhanced fracture repair via improved biomechanical properties and increased callus bone mineralization. Overall, this study provides supporting evidence that EM field therapy promotes bone fracture repair through mitochondrial OxPhos activation.

Bone morphogenic protein-2 signaling in human disc degeneration and correlation to the Pfirrmann MRI grading system.

BACKGROUND CONTEXT: Back and neck pain secondary to disc degeneration is a major public health burden. There is a need for therapeutic treatments to restore intervertebral disc (IVD) composition and function. PURPOSE: To quantify ALK3, BMP-2, pSMAD1/5/8 and MMP-13 expression in IVD specimens collected from patients undergoing surgery for disc degeneration, to correlate ALK3, BMP-2, pSMAD1/5/8 and MMP-13 expression in IVD specimens to the 5-level Pfirrmann MRI grading system, and to compare ALK3, BMP-2, pSMAD1/5/8 and MMP-13 expression between cervical and lumbar degenerative disc specimens. STUDY DESIGN: An immunohistochemical study assessing ALK3, BMP-2, pSMAD1/5/8, and MMP-13 expression levels in human control and degenerative IVD specimens. METHODS: Human IVD specimens were collected from surgical patients who underwent discectomy and interbody fusion at our institution between 1/2015 and 8/2017. Each patient underwent MRI prior to surgery. The degree of disc degeneration was measured according to the 5-level Pfirrmann MRI grading system. Patients were categorized into either the 1) control group (Pfirrmann grades I-II) or 2) degenerative group (Pfirrmann grades III-V). Histology slides of the collected IVD specimens were prepared and immunohistochemical staining was performed to assess ALK3, BMP-2, pSMAD1/5/8, and MMP-13 expression levels in the control and degenerative specimens. Expression levels were also correlated to the Pfirrmann criteria. Lastly, the degenerative specimens were stratified according to their vertebral level and expression levels between the degenerative lumbar and cervical discs were compared. RESULTS: Fifty-two patients were enrolled; however, 2 control and 2 degenerative patients were excluded due to incomplete data sets. Of the remaining 48 patients, there were 12 control and 36 degenerative specimens. Degenerative specimens had increased expression levels of BMP-2 (p=.0006) and pSMAD1/5/8 (p<.0001). Pfirrmann grade 3 (p=.0365) and grade 4 (p=.0008) discs had significantly higher BMP-2 expression as compared to grade 2 discs. Pfirrmann grade 4 discs had higher pSMAD1/5/8 expression as compared to grade 2 discs (p<.0001). There were no differences in ALK3 or MMP-13 expression between the control and degenerative discs (p>.05). Stratifying the degenerative specimens according to their vertebral level showed no significant differences in expression levels between the lumbar and cervical discs (p>.05). CONCLUSIONS: BMP-2 and pSMAD1/5/8 signaling activity was significantly upregulated in the human degenerative specimens, while ALK3 and MMP-13 expression were not significantly changed. The expression levels of BMP-2 and pSMAD1/5/8 correlate positively with the degree of disc degeneration measured according to the Pfirrmann MRI grading system. CLINICAL SIGNIFICANCE: BMP-SMAD signaling represents a promising therapeutic target to restore IVD composition and function in the setting of disc degeneration.

Inhibition of the mitochondrial permeability transition improves bone fracture repair.

Bone fracture is accompanied by trauma, mechanical stresses, and inflammation - conditions known to induce the mitochondrial permeability transition. This phenomenon occurs due to opening of the mitochondrial permeability transition pore (MPTP) promoted by cyclophilin D (CypD). MPTP opening leads to more inflammation, cell death and potentially to disruption of fracture repair. Here we performed a proof-of-concept study and tested a hypothesis that protecting mitochondria from MPTP opening via inhibition of CypD improves fracture repair. First, our in vitro experiments indicated pro-osteogenic and anti-inflammatory effects in osteoprogenitors upon CypD knock-out or pharmacological inhibition. Using a bone fracture model in mice, we observed that bone formation and biomechanical properties of repaired bones were significantly increased in CypD knock-out mice or wild type mice treated with a CypD inhibitor, NIM811, when compared to controls. These effects were evident in young male but not female mice, however in older (13 month-old) female mice bone formation was also increased during fracture repair. In contrast to global CypD knock-out, mesenchymal lineage-specific (Prx1-Cre driven) CypD deletion did not result in improved fracture repair. Our findings implicate MPTP in bone fracture and suggest systemic CypD inhibition as a modality to promote fracture repair.