Background: Patellar tendon ruptures have a reported incidence of 0.68 per 100,000 person-years in the general population. The epidemiology of surgically treated patellar tendon ruptures in the US military has yet to be reported, which would provide opportunity for identification of risk factors for these otherwise healthy and active patients. Purpose: To determine the incidence of patellar tendon rupture in the Military Health System (MHS) population and to analyze demographic patterns, surgical fixation methods, and rerupture rates. Study Design: Case-control study; Level of evidence, 3. Methods: We utilized the MHS Data Repository (MDR) to identity active-duty military servicemembers surgically treated for patellar tendon rupture between 2010 and 2015. Records were reviewed for demographic information, injury characteristics, fixation technique, and occurrence of rerupture. Risk factors for rupture were calculated using Poisson regression based on population counts and demographic data obtained in the MDR. Risk factors for rerupture and return to duty were analyzed via univariate analysis and multivariate regression. Results: A total of 504 operatively treated primary patellar tendon repairs in 483 patients were identified, with an overall incidence of 6 per 100,000 person-years. Mean age was 33.6 years (range, 17-54 years) and 98% of patients were male. Fixation method was 81% bone tunnels and 7% suture anchors, and 12% were unknown. Black race had a higher relative rate ratio for rupture compared with the race categories White (9.21; P < .0001) and Other (3.27; P < .0001). The rupture rate was higher in 35- to 44-year-old patients compared with those aged 18 to 24 years ( P < .0001), 25 to 34 years ( P < .0001), and 45 to 64 years ( P = .004). Return to full previous level of activity occurred in 75.8% of patients, 14.6% returned to activity with limitations, and 9.5% were medically separated. The rerupture rate was 3%. Fixation method, tobacco usage, body mass index, and race were not significant risk factors for rerupture. Conclusion: The incidence of patellar tendon rupture in the US military population is substantially higher than has been reported in the civilian population. Among military personnel, men, Black servicemembers, and those aged 35 to 44 years were at highest risk for patellar tendon rupture. Three-quarters of patients were able to return to full activity without limitations. The rerupture rate was low and unaffected by fixation method.

Peripheral Nerve Injury (PNI) represents a major clinical and economic burden. Despite the ability of peripheral neurons to regenerate their axons after an injury, patients are often left with motor and/or sensory disability and may develop chronic pain. Successful regeneration and target organ reinnervation require comprehensive transcriptional changes in both injured neurons and support cells located at the site of injury. The expression of most of the genes required for axon growth and guidance and for synapsis formation is repressed by a single master transcriptional regulator, the Repressor Element 1 Silencing Transcription factor (REST). Sustained increase of REST levels after injury inhibits axon regeneration and leads to chronic pain. As targeting of transcription factors is challenging, we tested whether modulation of REST activity could be achieved through knockdown of carboxy-terminal domain small phosphatase 1 (CTDSP1), the enzyme that stabilizes REST by preventing its targeting to the proteasome. To test whether knockdown of CTDSP1 promotes neurotrophic factor expression in both support cells located at the site of injury and in peripheral neurons, we transfected mesenchymal progenitor cells (MPCs), a type of support cells that are present at high concentrations at the site of injury, and dorsal root ganglion (DRG) neurons with REST or CTDSP1 specific siRNA. We quantified neurotrophic factor expression by RT-qPCR and Western blot, and brain-derived neurotrophic factor (BDNF) release in the cell culture medium by ELISA, and we measured neurite outgrowth of DRG neurons in culture. Our results show that CTDSP1 knockdown promotes neurotrophic factor expression in both DRG neurons and the support cells MPCs, and promotes DRG neuron regeneration. Therapeutics targeting CTDSP1 activity may, therefore, represent a novel epigenetic strategy to promote peripheral nerve regeneration after PNI by promoting the regenerative program repressed by injury-induced increased levels of REST in both neurons and support cells.

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