Primary OA is a disease that originates in hyaline articular cartilage, causing its progressive destruction and alteration of the subchondral bone. Articular geometry is slowly altered through cartilage remodeling, capsular and synovial thickening, marginal osteophyte formation, subchondral sclerosis, and subchondral cyst formation.

The role of systemic and local biomechanical and biochemical alterations is under investigation. Genetics, aging, bone density, muscle weakness, joint laxity, and obesity have all been cited as possible etiologic factors in the development of OA (1,2). Although aging and repetitive microtrauma have been shown to alter articular cartilage, normal lifelong joint use has not been shown to cause degeneration (2). Changes in osteoarthritic cartilage do not parallel the changes in the cartilage of a normal aging adult, implying genetic and molecular etiologies. An underlying imbalance in the cytokine-mediated anabolic and catabolic processes of articular cartilage regeneration appears to have some role (3).

Mechanical factors also play an important role in the pathogenesis of cartilage destruction. The interstitial water supports approximately 95% of a compressive load in normal cartilage (2). In osteoarthritic cartilage, water content and permeability increase as the hydrophilic proteoglycan content decreases. The hydraulic strength proportionately decreases, subjecting the collagen matrix to a greater proportion of the applied loads. Compressive joint reaction forces across the elbow have been shown to reach six times body weight during throwing or heavy pounding, which belies the assumption that the elbow is not a weightbearing joint (4).

Alterations in joint biomechanics can cause an increase in the joint reaction force. Chronic strain from heavy repetitive motion has been shown to cause laxity of the elbow’s stabilizing collateral ligaments (5). Cartilage injury from repetitive microtrauma can cause a localized thickening of the subchondral bone at the expense of uncalcified hyaline cartilage thickness (2). Cartilage thinning leads to an altered ability to resist normal shear forces and compressive loading, accelerating joint degeneration in the effected compartment.

A disparity exists between the wear patterns of normal aging elbows and those requiring surgical intervention. Goodfellow and Bullough provide a description of the pattern of wear in 28 cadaver elbows of varying age (6). They report a consistent and progressive erosion of the radiocapitellar joint in all specimens with a relative sparing of the ulnohumeral articulation. In contrast, Morrey found that of 15 elbows undergoing surgical treatment, all displayed significant ulnohumeral disease, whereas radial head osteophytes were present in only seven (7). One hypothesis for this disparity would state that attenuation of the medial collateral ligament, from repetitive stress, or an altered joint line, from pediatric fracture, caused a chronic alteration in medial joint reaction force. The ulnohumeral joint must then increase its contribution to joint stability at the expense of altered loading patterns. This situation is analogous to the valgus extension overload seen in the pitching elbow with posteromedial ulnohumeral impingement and posterior osteophyte formation (8). Edge loading and olecranon impingement decrease the weightbearing surface of the articulation, causing an uneven distribution of compressive stresses (9). Damage to the cartilage and hypertrophy of the subchondral bone accelerate the progression to OA by the aforementioned mechanisms.

Two studies have reported the incidence of primary symptomatic OA in the elbow joint to be approximately 2% to 8% (10, 11, 12). Stanley reported on the prevalence of primary elbow OA in 1,000 consecutive patients attending a fracture clinic. All cases of previous periarticular elbow fracture, multiple joint OA, and posttraumatic arthritis were excluded. It was discovered that more than 10% of those involved with heavy labor had primary OA of the elbow and none were younger than 40 years of age. A report by Doherty and Preston emphasized the high association between elbow and metacarpophalangeal involvement in the axial digits (62%), which may strengthen the association to the repetitive microtrauma hypothesis (13).

Patients with primary OA frequently present with activityrelated joint pain and restriction of motion. A definable periarticular or ligamentous injury may be recalled, but most have no recollection of prior injury. Middle-aged males are many times more likely to be afflicted than females, with the dominant extremity involved in 54% to 90% of cases (10,13, 14, 15, 16). Approximately 60% to 80% report an occupation or proclivity for an activity that involves a heavy repetitive use of the dominant arm (10,15). Individuals who use the upper extremities for prolonged crutch ambulation or wheelchair mobility have been diagnosed with OA in the elbow as well (7).

Malunited intraarticular fractures of the distal humerus, radial head, and olecranon can result in posttraumatic arthritis. When open reduction and internal fixation (ORIF) are required, anatomic restoration of the injured articular surface is the primary goal. Residual articular incongruity can result in accelerated cartilage wear at a rate dependent on the residual malalignment and the demand placed on the elbow. Osteochondral or chondral defects can thwart even the best articular reductions and result in accelerated wear of the opposing articular surface. Periarticular deformity, particularly in the coronal plane, can result in accelerated joint wear by altering the forces across the elbow.

Residual elbow instability following traumatic injury can also lead to progressive cartilage wear and joint space narrowing. The elbow joint is highly constrained and does not tolerate alterations in stability without consequence. Minor alterations in ulnohumeral biomechanics secondary to ligamentous attenuation can lead to accelerated ulnohumeral degeneration.

Posttraumatic arthritis is particularly troublesome because it often affects a younger active patient population. Many years of heavy use are to be expected, and early advanced arthritis can adversely affect a patient’s ability to resume a previous occupation, often with significant social consequences. Unfavorable outcomes after reconstruction are often associated with multiple surgeries, infectious complications, instability, deformity, and bone loss (4,21, 22, 23, 24, 25).

The primary lesion in rheumatoid disease is an invasive inflamed synovium. The exact pathogenesis of synovial hyperplasia, angiogenesis, and pannus formation remains elusive to investigators. Both genetic and infectious models have been postulated and investigated. The strong association with the human leukocyte antigen (HLA)-DR4 locus has been investigated for therapeutic and diagnostic significance. There is general agreement on the idea that genetically susceptible individuals exposed to an unknown environmental agent produce a cytokine-mediated autoimmune response that leads to the clinical manifestations seen in RA (3,40,41).

With advanced disease, a tumorlike expansion of highly invasive and immature fibroblastlike cells, or pannus, forms on the inner lining of the inflamed synovium. Cartilage destruction, in its earliest phases, occurs at the periphery of the joint where the cartilage and bone interface the invading synovial pannus. Inflammatory mediators and enzymes found in the synovial fluid sustain the continued destruction of cartilage, overlying tendons, ligaments, and bone (41). Periarticular osteopenia occurs early in the disease process. As cartilage and ligamentous support is destroyed, joint space narrowing progresses and instability may present. In the end stages of aggressive, poorly treated disease, significant bone loss and tissue attrition can cause ankylosis or a flail elbow.

JRA is a distinct entity from adult-onset RA. Currently, the cause is unknown. Although 5% to 10% will have a disease course that is similar to the adult form, in most children, the immunogenetics, clinical course, and outcomes will be different than the adult-onset disease. It is divided into three clinically distinct forms: systemic onset (Still’s disease), polyarticular JRA, and pauciarticular JRA.

The seronegative spondyloarthropathies represent a wide range of diseases involving the axial and peripheral joints. A strong association with the HLA-B27 histocompatibility complex is found in AS and Reiter’s syndrome.

A diagnosis of inflammatory arthritis is frequently made prior to presentation to the orthopedist. However, clinical suspicion should be aroused when a patient presents with symmetric polyarticular arthralgias without the typical signs of OA. Signs of systemic manifestations of inflammatory arthritides should be actively pursued if the diagnosis is unclear. Nearly two-thirds of all patients with RA will develop involvement of the elbow joint (30,31). Pain, stiffness, and loss of function in the rheumatoid elbow continue to be the most common indications for TEA (25,35, 36, 37,42).

Perhaps the most important factor to be considered prior to surgical treatment of the synovial-based arthritides is that medical therapy has been maximized. In most cases, synovial-based arthritides respond to medical remitting agents. That having been said, approximately 10% of patients with RA will have a progressive aggressive disease pattern that does not respond to current medical therapies. Many patients will present with polyarticular disease, and functional restoration should take a stepwise approach. Patients with highly aggressive rheumatoid disease, or those requiring long-term immunosuppressive medications, should be considered immuno-deficient and treated accordingly. Perioperative consultation with a medical physician should be obtained.

Surgical management of the extremity with multiple symptomatic joints deserves special consideration. Priority should be placed on the joints with the greatest pain and functional disability, or on the hand and wrist if all joints are equally symptomatic (39,47). Whether priority is placed on the shoulder or elbow when symptoms are similar is a topic of some debate. Although one report states that elbow arthroplasty should precede shoulder arthroplasty (48), Connor, Morrey, and Neel feel that in most cases, the shoulder arthroplasty should take precedence over the elbow (47,49). Deep infection after TEA or interval
glenoid bone loss could potentially preclude total shoulder arthroplasty.

Nutrition is also a concern when dealing with patients with chronic catabolic inflammatory diseases. Malnutrition, as evidenced by serum albumin, prealbumin, and transferring values, should be diagnosed and aggressively treated to maximize the intrinsically poor healing potential of these patients.