Publications

BACKGROUND

Patellar fractures are debilitating injuries that compromise the knee extensor mechanism and are frequently associated with poor outcomes. The purpose of this study was to quantify the functional outcomes of operative treatment of patellar fractures.

METHODS

Functional outcome data on thirty patients with an isolated unilateral patellar fracture were prospectively obtained at three, six, and twelve months postoperatively.

RESULTS

All fractures healed. There were two complications (7%) related to the surgery (wound dehiscence and refracture), and eleven patients (37%) underwent removal of symptomatic implants. The tibial plateau-patella angle demonstrated patella baja in seventeen (57%) of the patients. Anterior knee pain during activities of daily living was experienced by twenty-four (80%) of the patients. Clinical improvement occurred over the first six months. However, functional impairment persisted at twelve months, with objective testing demonstrating that the knee extensor mechanism on the injured side had deficits in strength (-41%), power (-47%), and endurance (-34%) as compared with the uninjured side.

CONCLUSIONS

Despite advances in surgical protocols and acceptable radiographic outcomes, functional impairment remains common after treatment of patellar fractures. Rehabilitation strategies following surgical stabilization of these injuries will be a fruitful area for future clinical research.

Matrix metalloproteinase-2 (MMP-2) is increasingly recognized as a major contributor to progressive cardiac injury within the setting of ischemia-reperfusion injury and ischemic ventricular remodeling. A common feature of these conditions is an increase in oxidative stress, a process that engages multiple pro-inflammatory and innate immunity cascades. We recently reported on the identification and characterization of an intracellular isoform of MMP-2 generated by oxidative stress-mediated activation of an alternative promoter located within the first intron of the MMP-2 gene. Transcription from this site generates an N-terminal truncated 65 kDa isoform of MMP-2 (NTT-MMP-2) that lacks the secretory sequence and the inhibitory prodomain region. The NTT-MMP-2 isoform is intracellular, enzymatically active and localizes in part to mitochondria. Expression of the NTT-MMP-2 isoform triggers Nuclear Factor of Activated T-cell (NFAT) and NF-κB signaling with the expression of a highly defined innate immunity transcriptome, including Interleukin-6, MCP-1, IRF-7 and pro-apoptotic transcripts. To determine the functional significance of the NTT-MMP-2 isoform in vivo we generated cardiac-specific NTT-MMP-2 transgenic mice. These mice developed progressive cardiomyocyte and ventricular hypertrophy associated with systolic heart failure. Further, there was evidence for cardiomyocyte apoptosis and myocardial infiltration with mononuclear cells. The NTT-MMP-2 transgenic hearts also demonstrated more severe injury following ex vivo ischemia-reperfusion injury. We conclude that a novel intracellular MMP-2 isoform induced by oxidant stress directly contributes, in the absence of superimposed injury, to cardiomyocyte hypertrophy. inflammation, systolic heart failure and enhanced susceptibility to ischemia-reperfusion injury.