Posterolateral rotatory instability (PLRI) is the most common type of elbow instability. It is caused by an insufficiency of the lateral ligamentous complex, which consists mainly of the radial collateral ligament (RCL) and the lateral ulnar collateral ligament (LUCL).

Investigate the influence of serial sectioning of the lateral ligamentous complex on elbow stability in a cadaveric model of PLRI.

Kinematics of six fresh frozen cadaveric elbow specimens were measured by digitizing anatomical marks with a Microscribe 3DLX digitizing system (Revware Inc, Raleigh, NC). Each specimen was tested under four conditions: Intact, LUCL tear, LUCL and RCL tear, and complete Tear (LUCL, RCL and capsule tear). Each specimen was tested in 30°, 60° and 90° elbow flexion angles. Varus- laxity was measured in supination, pronation, and neutral forearm rotation positions and total forearm rotation was measured with 0.3 Nm of torque. Statistical significant differences between the conditions were detected using a two-way ANOVA with Tukey's post-hoc test.

The radial head dislocated in all specimens in LUCL and RCL tear and Comp but not in LUCL tear. Total forearm ROM did not increase form intact to LUCL tear (p>0.05) but significantly increased in LUCL and RCL tear (p=0.0002) and complete tear (p<0.0001) in all flexion angles. Additionally, ROM in LUCL tear significantly differed from LUCL and RCL tear and complete tear (p=0.0027 and p=0.0002). A similar trend was seen with the varus angle. While there was a significant difference when the intact condition was compared to both the LUCLand RCL tear and complete tear conditions (p<0.0001 and p<0.0001), there was no difference between the intact and LUCL tear conditions.

LUCL tear alone is not sufficient to cause instability and increase ROM and varus angle, meanwhile the increase of ROM and varus angle with additional capsular tear was not significant compared to LUCL and RCL tear. The increase of ROM after LUCL and RCL tear is an unknown symptom of PLRI.

Disturbed muscular architecture, fatty infiltration and muscular atrophy remain irreversible in chronic rotator cuff tears (RCT) even after repair. Poly-[ADP-ribose]-polymerase 1 (PARP-1), a nuclear factor involved in DNA damage repair, has shown to be a key element in the up-regulation of early muscle inflammation, atrophy and fat deposition. We therefore hypothesized that the absence of PARP-1 would lead to a reduction in muscular architectural damage, early inflammation, atrophy and fatty infiltration subsequent to combined tenotomy and neurectomy in a PARP-1 knock-out mouse model.

PARP-1 knock-out (KO group) and standard wild type C57BL/6 (WT group) mice were randomly allocated into three different time points (1, 6 and 12 weeks, total n=72). In all mice the supraspinatus (SSP) and infraspinatus (ISP) tendons of the left shoulder were detached and the SSP muscle was denervated according to a recently established model. Macroscopic muscle weight analysis, retraction documentation using macroscopic suture, magnetic resonance imaging, immunohistochemistry gene expression analysis using real time qPCR (RTqPCR) and histology were used to assess the differences in muscle architecture, early inflammation, fatty infiltration and atrophy between knock out and wild type mice in the supraspinatus muscle.

The SSP did retract in both groups, however; the KO muscles and tendons retracted less than the WT muscles (2.1±21mm vs 3.4±0.41mm; p=0.02). Further assessment of muscle architecture demonstrated that the pennation angle was significantly higher in the KO groups at 6 and 12 weeks (28±5 vs 36±5 and 29±4 vs 34±3; p<0.0001). Combined Tenotomy and neurectomy resulted in a significant loss of muscle mass in both groups compared to the contralateral unoperated side (KO group 62±11% and WT group 52±11%, p=0.04) at 6 weeks. But at 12 weeks postoperatively, there was a significant increase in muscle mass to near normal levels in KO group compared to the WT group (14±6% and 42±7% lower muscle mass respectively; p<0.0001) and less fatty infiltration (12.5 ± 1.82% and 19.6 ± 1.96%, p=0.027). Immunohistochemistry revealed a significant decrease in the expression of inflammatory, apoptotic, adipogenic and muscular atrophy genes at both the 1 week and 6 weeks time points, but not at 12 weeks in the KO group compared to the WT group. This was confirmed by histology.

Our study is the first to show that knocking out PARP-1 leads to decreased loss of muscle architecture, early inflammation, fatty infiltration and atrophy after combined tenotomy and neurectomy of the rotator cuff muscle. Although the macroscopic muscles reaction to injury is similar in the first 6 weeks, its ability to regenerate is much greater in the PARP-1 group leading to a near normalization of the muscle substance and muscle weight, less retraction, and less fatty infiltration after 12 weeks.

Insufficiency of the lateral collateral ligamentous complex causes posterolateral rotatory instability (PLRI). During reconstruction surgery the joint capsule is repaired, but its biomechanical influence on elbow stability has not been described. We hypothesized that capsular repair reduces ROM and varus angle after reconstruction of the lateral collateral complex.

Six fresh frozen cadaveric elbow specimens were used. Varus laxity in supination, pronation and neutral forearm rotation with 1 Nm load and forearm rotaitonal range of motion (ROM) with 0.3 Nm torque were measured using a Microscribe 3DLX digitizing system (Revware Inc, Raleigh, NC). Each specimen was tested under four different conditions: Intact, Complete Tear with LUCL, RCL and capsule tear, LUCL/RCL reconstruction + capsule repair and LUCL/RCL reconstruction only. Reconstruction was performed according to the docking technique (Jones, JSES, 2013) and the capsule was repaired with mattress sutures. Each condition was tested in 30°, 60° and 90° elbow flexion. A two-way ANOVA with Tukey's post-hoc test was used to detect statistical differences between the conditions.

Total ROM of the forearm significantly increased in all flexion angles from intact to Complete tear (p<0.001). ROM was restored to normal in 30° and 60° elbow flexion in both reconstruction conditions (p>0.05). LUCL/RCL Reconstruction + capsule repair in 90° elbow flexion was associated with a significantly lower ROM compared to intact (p=0.0003) and reconstruction without capsule repair (p=0.015). Varus angle increased significantly from intact to complete tear (p<0.0001) and restored to normal in both reconstruction conditions (p>0.05) in 30° and 60° elbow flexion. In contrast varus angle was significantly lower in 90° elbow flexion in both reconstruction conditions compared to intact (both p<0.0001).

Reconstruction of the lateral collateral complex restores elbow stability, ROM and varus laxity independent of capsular repair. Over tightening of the elbow joint occurred in 90° elbow flexion, which was aggravated by capsular repair. Over all capsular repair can be performed without negatively affecting elbow joint mobility.