Arthroscopic Débridement and Glenoidplasty for Shoulder Degenerative Joint Disease

Arthroscopic Débridement and Glenoidplasty for Shoulder Degenerative Joint Disease
Christian J.H. Veillette
Scott P. Steinmann
ANATOMY
  • The normal head-shaft angle is about 130 degrees, with 30 degrees of retroversion.
  • The articular surface area of the humeral head is larger than that of the glenoid, allowing for large normal range of motion.
  • Glenoid version, the angle formed between the center of the glenoid and the scapular body, averages 3 degrees and is critical for stability.
  • The glenoid fossa provides a shallow socket in which the humeral head articulates. It is composed of the bony glenoid and the glenoid labrum.
  • The labrum is a fibrocartilaginous structure surrounding the periphery of the glenoid. The labrum provides a 50% increase in the depth of the concavity and greatly increases the stability of the glenohumeral joint.
  • The glenoid had an average depth of 9 mm in the superoinferior direction and 5 mm in the anteroposterior direction with an intact labrum.4,6
  • Capsuloligamentous structures provide the primary stabilization for the shoulder joint (FIG 1).
    • Within this capsule are three distinct thickenings that constitute the superior glenohumeral ligament, middle glenohumeral ligament, and inferior glenohumeral ligament.
PATHOGENESIS
  • OA may be classified as primary, when there is no obvious underlying cause, or secondary, when it is preceded by a predisposing disorder.
  • Pathology in patients with glenohumeral OA includes a degenerative labrum, loose bodies, osteophytes, and articular cartilage defects in addition to synovitis and soft tissue contractures.
    FIG 1 • Glenoid anatomy. The glenoid has an average depth of 9 mm in the superoinferior direction and 5 mm in the anteroposterior direction with an intact labrum.
  • The disease process in OA of the shoulder parallels that of other joints. Degenerative alterations primarily begin in the articular cartilage as a result of either excessive loading of a healthy joint or relatively normal loading of a previously disturbed joint.11
  • Progressive asymmetric narrowing of the joint space and fibrillation of the articular cartilage occur with increased cartilage degradation and decreased proteoglycan and collagen synthesis.
  • Subchondral sclerosis develops at areas of increased pressure as stresses exceed the yield strength of the bone and the subchondral bone responds with vascular invasion and increased cellularity.
  • Cystic degeneration occurs owing to either osseous necrosis secondary to chronic impaction or the intrusion of synovial fluid.
  • Osteophyte formation occurs at the articular margin in nonpressure areas by vascularization of subchondral marrow, osseous metaplasia of synovial connective tissue, and ossifying cartilaginous protrusions.
  • Fragmentation of these osteophytes or of the articular cartilage itself results in intra-articular loose bodies. In late stages, complete loss of articular cartilage occurs, with subsequent bony erosion.
  • Posterior glenoid erosion is predominant, leading to increased retroversion of the glenoid and predisposing to subluxation and reduction of the humeral head, causing symptoms of instability.
NATURAL HISTORY
  • Information on the natural history of OA in individuals and its reparative processes is limited.
  • Progression of OA is considered generally to be slow (10 to 20 years), with rates varying among joint sites.9
  • No specific longitudinal studies exist on the progression of shoulder OA.
PATIENT HISTORY AND PHYSICAL FINDINGS
  • Typical history for patients with OA is progressive pain with activity over time.
  • In early stages, pain is related to strenuous or exertional activities, but over time, it progresses to activities of daily living. In later stages, pain occurs at rest and at night.
  • Pain may be mistaken for impingement syndrome early in the disease process or rotator cuff disease when symptoms occur in the presence of good motion.
  • Progression of the disease often leads to secondary capsular and muscular contractures with loss of active and passive motion.
  • Mechanical symptoms such as catching and grinding are often reported with use of the shoulder.
  • The pain of shoulder OA can be divided into three types:
    • Pain at extremes of motion: due to osteophytes and stretching of the inflamed capsule and synovium
    • Pain at rest: due to synovitis (pain at night is not the same as pain at rest and may be due to awkward positions or increased pressure)
    • Pain in the mid-arc of motion: usually associated with crepitus and represents articular surface damage
  • Physical examination should include the following:
    • Range of motion: Loss of both active and passive motion consistent with soft tissue contractures. In patients with preserved passive motion but loss of active motion, rotatory cuff pathology should be ruled out.
    • Compression-rotation test: Pain during mid-arc of motion is a potentially poor prognostic indication.
    • Neer test and Hawkins test: Often, patients with OA have positive impingement signs related to articular lesions in the glenohumeral joint or to the synovitis in the joint and subacromial pathology.
    • Supraspinatus evaluation: Weakness may reflect associated supraspinatus tear. Patients with OA may have weakness related to pain inhibition on resistance.
    • Infraspinatus and teres minor evaluation: Weakness may reflect associated posterior rotator cuff tear. Patients with OA may have weakness related to pain inhibition on resistance.
    • Subscapularis evaluation: Weakness may reflect associated subscapularis tear. Patients with OA may have weakness related to pain inhibition on resistance.
IMAGING AND OTHER DIAGNOSTIC STUDIES
Jul 24, 2016 | Posted by in ORTHOPEDIC | Comments Off on Arthroscopic Débridement and Glenoidplasty for Shoulder Degenerative Joint Disease

Full access? Get Clinical Tree

Get Clinical Tree app for offline access