Faculty Bibliography

Deep soft-tissue infection occurs infrequently after rotator cuff repair surgery. We retrospectively reviewed the clinical presentation in 14 patients whose rotator cuff repair was complicated by an early deep infection (<6 weeks). The functional outcome after treatment in 12 of these patients was analyzed at a mean follow-up of 37.5 months (range, 11-122 months). The diagnosis of infection was most often made within 3 weeks from the date of surgery (mean, 18 days; range, 3-41 days). Common presenting symptoms included localized wound erythema and drainage. The blood leukocyte counts were usually normal, but the erythrocyte sedimentation rates and C-reactive protein levels were elevated. A mean of 2.6 surgical debridements were required to clean the wound effectively in each case. Eight of twelve patients were dissatisfied at final assessment. Most patients reported reasonably good relief of pain, but they had residual shoulder stiffness and weakness. Retention of suture anchors in the humeral head did not preclude successful eradication of the infection

Preoperative evaluation for a total shoulder arthroplasty includes 2-dimensional analysis of the glenoid through either standard radiographs or computed tomography (CT) images. Recent evidence suggests that these 2-dimensional images may actually misrepresent the 3-dimensional (3D) anatomy of the glenoid. Because 3D reconstructions of CT images allow 3D visualization and analysis of the scapula as a free body, we hypothesized that they can reflect the true anatomy of the glenoid more accurately. To test this hypothesis, we obtained various glenoid morphometric measurements from excised cadaveric scapulae as well as their respective 3D CT images. On average, the glenoid version angles measured from the 3D CT images were within 1.0 degrees +/- 0.7 degrees (mean +/- SD) of those from the actual specimen (95% confidence limit, <2.2 degrees for all observers). These measurements from the 3D CT images showed high interobserver and intraobserver reliability (interobserver and intraobserver correlation coefficients, 0.983 and 0.978, respectively). Similarly, measured glenoid surface width and length from the 3D CT images were within 1.8 +/- 1.2 mm and 1.4 +/- 1.1 mm, respectively, of those from the actual specimen. In addition, we were able to estimate the glenoid surface area as well as the glenoid vault volume from the 3D CT images. These values were 8.67 +/- 2.73 cm2 and 11.86 +/- 5.06 cm3, respectively. The mean glenoid vault volume with respect to its surface area was 1.35 +/- 0.24 cm3/cm2 (range, 1.06-1.91 cm3/cm2). These data suggest that 3D CT images can accurately reflect the true anatomy of the glenoid and that they can provide valuable information regarding the glenoid surface and vault. As such, 3D CT images may prove to be a useful tool during the preoperative evaluation for a total shoulder arthroplasty, particularly in patients with significant glenoid bone loss

Treatment of patients with complex multifactorial diseases can be clarified by the development of clear, evidence-based treatment guidelines or algorithms. This article presents a detailed algorithm for the management of patients who present with persistent shoulder pain secondary to rotator cuff disorder, adhesive capsulitis, or glenohumeral osteoarthritis. The algorithm includes both nonpharmacologic and pharmacologic interventions and provides a stepwise approach for managing patients' care. While 'treatment pathways' are set forth for these specific disorders, the algorithm also provides a common nonoperative protocol for general shoulder conditions that should help simplify patient management and guide clinicians to alternative therapies

A variety of pathological conditions affect the acromioclavicular joint and the surrounding structures. For each of these, different procedures have been described with varying degrees of success. This article focuses on contemporary procedures. The acromioclavicular joint can be reapproximated using one of three stabilization techniques: (1) primary fixation across the acromioclavicular joint, (2) secondary stabilization of the joint by recreating the anatomic linkage between the distal clavicle and the coracoid process, or (3) dynamic stabilization of the joint by creating an inferiorly directed force on the distal clavicle. These methods are not mutually exclusive and may be combined in a single operative setting to produce a final construct with superior mechanical stability

A general feature of the developing nervous system is the activity-dependent rearrangement of genetically defined, synaptic connections. A parallel process occurs at the developing neuromuscular junction as activity-dependent synapse withdrawal reduces the initial polyneuronal innervation of individual muscle fibers to a mononeuronal innervation within the first few weeks after birth. Because members of the neurotrophin gene family influence motor neuron differentiation and survival, we examined whether or not they also influence synaptic rearrangements in neonatal muscles. We found that treatment with brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), or neurotrophin-4/5 (NT-4/5) causes the transient retention of multiple synaptic contacts on neonatal myofibers. However, the combination of both electrophysiological and histological assays revealed that the majority of such supernumerary synaptic contacts are functionally inactive or 'silent.' There also occurs an increase in the number of retracting axons. Because BDNF mRNA is expressed in developing muscle and the trkB tyrosine kinase receptor for BDNF is expressed by neonatal motor neurons, our results suggest that BDNF may play an endogenous role in the refinement of synaptic connectivity that occurs in skeletal muscles after birth

We show that leukemia inhibitory factor (LIF) plays a physiological role in the programmed withdrawal of synapses from neonatal muscles. First, LIF mRNA is present in embryonic skeletal muscle and is developmentally regulated. We detect high levels of LIF mRNA at embryonic day 17 (E17) in mouse hind leg muscles. The content of LIF mRNA falls 10-fold between E17 and birth and then remains low in the neonate and adult. The decrease in LIF mRNA in skeletal muscle coincides with the end of secondary myogenesis and the completion of the adult number of myofibers. Second, treatment of the mouse tensor fascia latae (TFL), a superficial muscle of the hind leg, with LIF from birth (100 ng/day), transiently delays the withdrawal of excess inputs from polyneuronally innervated myofibers by approximately 3 days. The midpoint of the process is shifted from 7.5 +/- 10.2 +/- 0.6 days of age. LIF treatment delays synapse withdrawal by altering its timing without an appreciable effect on its rate. Third, in mice homozygous for a disruption of the LIF gene, the midpoint in the reduction of multiply innervated TFL myofibers occurs 1 day earlier, at 6.5 +/- 0.5 days of age. Muscle fiber number is unchanged in LIF null mice. Treatment with LIF does not alter the rate of neonatal growth, the number of muscle fibers in the TFL, or the reappearance of inputs that have been eliminated. Instead, LIF appears to delay maturation of the motor unit by transiently delaying the onset of synapse withdrawal. We hypothesize that this is a necessary component of a selective process that will operate simultaneously and equally on multiple, competing motor units

The mutation gly93-->ala of Cu,Zn superoxide dismutase (SOD) is found in patients with familial amyotrophic lateral sclerosis and causes motor neuron disease when expressed in transgenic mice. The progression of clinical and pathological disease was studied in a line of mice designated G1H. Clinical disease started at 91 +/- 14 days of age with fine shaking of the limbs, followed by paralysis and death by 136 +/- 7 days of age. Pathological changes begin by 37 days of age with vacuoles derived from swollen mitochondria accumulating in motor neurons. At the onset of clinical disease (90 days), significant death of somatic motor neurons innervating limb muscles has occurred; mice at end-stage disease (136 days) show up to 50% loss of cervical and lumbar motor neurons. However, neither thoracic nor cranial motor neurons show appreciable loss despite vacuolar changes. Autonomic motor neurons also are not affected. Mice that express wild-type human Cu,Zn SOD remain free of disease, indicating that mutations cause neuron loss by a gain-of-function. Thus, the age-dependent penetrance of motor neuron disease in this transgenic model is due to the gradual accumulation of pathological damage in select populations of cholinergic neurons