Compressed Biceps Autograft Augmentation of Arthroscopic Rotator Cuff Repair.

Rotator cuff repair failure rates continue to be a challenging problem. Various methods of biological and structural augmentation of the rotator cuff have been explored to improve tendon healing after repair. We describe a technique in which biceps tendon autograft is harvested after tenodesis. The biceps tendon is then compressed into a patch that is placed over the repaired rotator cuff tendon. Repurposing the portion of the tendon that is otherwise discarded offers several advantages over other augmentations that have been used, including the biological potential of live autograft tenocytes in the patch, lower cost, and no donor-site morbidity.

Autograft Long Head Biceps Tendon Can Be Used as a Scaffold for Biologically Augmenting Rotator Cuff Repairs.

PURPOSE: We create a viable, mechanically expanded autograft long head biceps tendon (LHBT) scaffold for biologically augmenting the repair of torn rotator cuffs. METHODS: The proximal aspect of the tenotomized LHBTs was harvested from patients during rotator cuff repair surgery and was mechanically formed into porous scaffolds using a surgical graft expander. LHBT scaffolds were evaluated for change in area, tensile properties, and tenocyte viability before and after expansion. The ability of endogenous tenocytes derived from the LHBT scaffold to promote tenogenic differentiation of human adipose-derived mesenchymal stromal cells (ADMSCs) was also determined. RESULTS: Autograft LHBTs were successfully expanded using a modified surgical graft expander to create a porous scaffold containing viable resident tenoctyes from patients undergoing rotator cuff repair. LHBT scaffolds had significantly increased area (length: 24.91 mm [13.91, 35.90] × width: 22.69 mm [1.87, 34.50]; P = .011) compared with the native LHBT tendon (length: 27.16 mm [2.70, 33.62] × width: 6.68 mm [5.62, 7.74]). The structural properties of the autograft were altered, including the ultimate tensile strength (LHBT scaffold: .56 MPa [.06, 1.06] vs. native LHBT: 2.35 MPa [1.36, 3.33]; P = .002) and tensile modulus (LHBT scaffold: 4.72 MPa [-.80, 1.24] versus native LHBT: 37.17 MPa [24.56, 49.78]; P = .001). There was also a reduction in resident tenocyte percent viability (LHBT scaffold: 38.52% [17.94, 59.09] vs. native LHBT: 68.87% [63.67, 74.37]; P =.004). Tenocytes derived from the LHBT scaffold produced soluble signals that initiated ADMSC differentiation into an immature tenocyte-like phenotype, as indicated by an 8.7× increase in scleraxis (P = .040) and a 3.6× increase in collagen type III mRNA expression (P = .050) compared with undifferentiated ADMSC controls. CONCLUSIONS: The ability to produce a viable autologous scaffold from the proximal biceps tendon having dimensions, porosity, mechanical characteristics, native ECM components, and viable tenocytes that produce bioactive signals conducive to supporting the biologic augmentation of rotator cuff repair surgery has been demonstrated. CLINICAL RELEVANCE: This biologically active construct may help to improve the quality of healing and regeneration at the repair site of rotator cuff tears, especially those at high risk for retear.

A comparison of onlay versus inlay glenoid component loosening in total shoulder arthroplasty.

BACKGROUND: Glenoid component loosening is common in total shoulder arthroplasty (TSA), often resulting from the mechanical interaction of glenohumeral components. This cadaveric study was performed to evaluate and to compare commercially available onlay and inlay glenoid prosthetic designs with respect to loading characteristics and loosening. METHODS: Sixteen prescreened cadaveric shoulders (8 matched pairs) underwent either onlay or inlay TSA. We created a custom glenohumeral loading model and used cycles of 5 mm anterior-posterior humeral translation to simulate a rocking-horse loosening mechanism for all testing. Articular TekScan measurements were performed with 9.1 kg (88.9 N) of glenohumeral compression before and after TSA. Fatigue testing was performed with 34.0 kg (333.6 N) of glenohumeral compression using high-definition video to document gross glenoid loosening. Testing ended with gross loosening or a maximum of 4000 cycles. Mean contact area, pressure, and joint reaction force were used to compare the 2 glenoid designs. RESULTS: In both implant types, contact area decreased and pressure increased after TSA (P < .0001). Force increased at the onlay component edge only (P = .0012) compared with native glenoid testing. Force was greater in the onlay vs. the inlay implants (P < .0001). During fatigue testing, all onlay glenoid components exhibited gross loosening at a mean of 1126 cycles (range, 749-1838), whereas none of the inlay glenoid components exhibited gross loosening (P < .0001). CONCLUSION: The inlay glenoid implant exhibited biomechanical characteristics favoring stability and decreased loosening compared with the onlay glenoid implant in this cadaveric model.

Spatiotemporal induction of matrix metalloproteinase-9 transcription after discrete myocardial injury.

Radiofrequency (RF) ablation of the myocardium causes discrete sites of injury. RF scars can expand, altering the extracellular matrix (ECM) structure and the continuity of the electrical syncytium of the adjacent myocardium. Matrix metalloproteinases (MMPs), such as MMP-9, contribute to ECM remodeling. However, whether and to what degree transcriptional induction of MMP-9 occurs after myocardial RF injury and the association with electrical conduction patterns after RF injury remains unexplored. This study examined MMP-9 gene promoter (M9PROM) activation after myocardial RF injury using mice in which the M9PROM was fused to a ß-galactosidase (ß-gal) reporter. RF lesions (0.5-mm probe, 80°C, 30 s) were created on the left ventricular (LV) epicardium of M9PROM mice (n=62) and terminally studied at 1 h, 1 d, 3 d, 7 d, 14 d, and 28 d after RF injury. M9PROM activation was localized through ß-gal staining. The RF scar area and the area of ß-gal staining were measured and normalized to LV area (planimetry). RF scar size increased from 1 h post-RF-injury values by 7 d and remained higher at 28 d. M9PROM activation became evident at 3 d and peaked at 7 d. Electrical conduction was measured (potentiometric dye mapping) at 7 d after RF injury. Heterogeneities in action potentials and electrical impulse propagation coincident with M9PROM activation were observed after RF injury. For example, conduction proximal to the RF site was slower than that in the remote myocardium (0.15±0.02 vs. 0.83±0.08 mm/ms, P<0.05). Thus, a unique spatiotemporal pattern of MMP-9 transcriptional activation occurred after discrete myocardial injury, which was associated with the development of electrical heterogeneity. Therefore, these findings suggest that changes in a key determinant of extracellular matrix remodeling, in addition to changes in myocardial structure, can contribute to arrhythmogenesis around the region of myocardial injury.