Radiographic osteolysis after total shoulder arthroplasty (TSA) remains a challenging clinical entity, as it may not initially manifest clinically apparent symptoms but can lead to clinically important complications, such as aseptic loosening. A thorough consideration of medical history and physical examination is essential to rule out other causes of symptomatic TSA—namely, periprosthetic joint infection—as symptoms often progress to vague pain or discomfort due to subtle component loosening. Once confirmed, nonoperative treatment of osteolysis should first be pursued given the potential to avoid surgery-associated risks. If needed, the current surgical options include glenoid polyethylene revision and conversion to reverse shoulder arthroplasty. The current article provides a comprehensive review of the evaluation and management of osteolysis after TSA through an evidence-based discussion of current concepts.
The annual incidence of primary anatomical and reverse shoulder arthroplasty (RSA) procedures performed in the United States has increased by 103.7% between 2011 to 2017, with the incidence of RSA increasing 191.3% over the same time period [
Gradual osteolysis around the glenoid or humeral components and loosening of either the glenoid or humeral components can result in instability and loss of function [
The purpose of the current article is to present a comprehensive review of the current concepts in the pathogenesis, evaluation, and management of osteolysis after anatomical TSA and RSA. In the first half of this article, the pathogenesis of osteolysis and the evolution in implant design intended to avoid osteolysis are presented. In the second half of this article, we discuss our approach to evaluating and managing osteolysis treatment through an evidence-based analysis of the literature.
This study did not require approval by the institutional review board at the Hospital for Special Surgery. And, consent was not required for any aspects of this study.
Implant wear occurs primarily at the articular interface, generating debris that results in the destruction of surrounding tissue secondary to inflammation. The destruction is two-fold: damage to the articulating surface of the prosthesis can be detrimental to implant stability, and the debris generated by implant wear can drive inflammation [
Phagocytosis of debris less than twelve 12 µmmicrometers in diameter by macrophages underlies the primary pathogenesis of periprosthetic osteolysis; however, the specific inflammatory response is dictated by the quantity and quality of the particulates regarding size, surface area, and composition. Further, the relative concentration of debris, rather than simply the number of particles, dictates the magnitude of the inflammatory response [
Cement debris resulting in larger particulates not amenable to phagocytosis is associated with giant cell recruitment and toll-like receptor (TLR) stimulation, which, in turn, activates the inflammatory nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) cascade [
Histologic findings of periprosthetic osteolysis include inflammatory cells (lymphocytes, histiocytes, plasma cells, giant cells, and macrophages), which may contain identifiable particulate debris; clefts containing strongly birefringent polyethylene debris; and scalloped edges where cement has been resorbed. Interestingly, Kepler et al. [
Detritic synovitis is an inflammatory response to intraarticular debris, which causes more widespread osteolysis beyond the periprosthetic space, resulting in implant loosening or pathologic fracture [
High amplitude micromotion increases the abhorrent space between the prosthesis and bone, resulting in fibrous ingrowth [
Several biomechanical studies have investigated the implications of high amplitude micromotion on the glenoid component in both anatomical TSA and RSA, although
Notching of the inferior border of the scapula was historically a considerable source of osteolysis in RSA, though the development of lateralized glenospheres and increased awareness of the importance of glenoid positioning has decreased the incidence of this phenomenon. Mechanical notching is described as repetitive contact between the humeral implant and scapula, leading to progressive abrasive wear [
Variations in component composition, component positioning, and stem length have been the mainstay approach to reducing implant wear and associated debris, inflammation, and osteolysis. Cemented all-polyethylene glenoid components are associated with 83% or greater survival rates at year 10 of follow-up; however, wear and revision rates vary between polyethylene models [
Research investigating the means to reduce osteolysis surrounding humeral implants has largely focused on stem length and implant composition. Bell et al. [
Comprehensive postoperative follow-up and physical evaluation should be performed in the setting of new-onset pain following TSA regardless of the time from the index procedure. The most sensitive indicator of osteolysis following TSA is new-onset or persistent pain [
Importantly, the timing, quality, responsiveness, location, and duration of symptoms can provide more insight into the potential pathology. For example, pain secondary to glenoid or humeral osteolysis is generally experienced when sleeping or first initiating movement (start-up pain) of the shoulder and is diffuse in nature, whereas well-localized pain over the posterosuperior aspect of the shoulder may represent an acromial stress fracture. Pain in the proximal part of the upper extremity can indicate humeral component loosening. Patients should also be asked about wound issues and drainage after the index surgery, as this may elevate indolent infection as a cause of symptoms. Concern for possible osteolysis and aseptic loosening should be raised for patients who report years of symptom-free shoulder function postoperatively followed by new-onset pain or reduced function.
The physical exam should be performed systematically and include inspection, palpation, range of motion, strength, and provocative maneuvers where appropriate. Specifically, the surgical incision and skin around the shoulder should be assessed. The presence of effusion, erythema, or swelling may indicate chronic inflammation or infection. Diffuse tenderness to palpation around all areas of the shoulder in the absence of other findings may signify a chronic pain syndrome.
The extent of passive and active range of motion should be assessed, with particular attention directed towards instability, impingement, or pain along short arcs of motion. Patients with osteolysis that begin to experience early subsidence may experience loss of function. Atrophy or deformity in the setting of a primary anatomical TSA may suggest compromise of the rotator cuff. Finally, a thorough neurovascular exam should be assessed to rule out neurovascular compromise as the etiology of pain and dysfunction.
Though osteolysis is characteristically a chronic process associated with night or start-up pain, it is notable that early osteolysis may manifest non-characteristic symptoms. Therefore, in the setting of painful TSA, early osteolysis should still be considered with a thorough evaluation of routine radiographic imaging. Indeed, early osteolysis that is rapidly progressive without identification and treatment can result in glenoid loosening, subsidence, and early failure.
In all scenarios where a patient presents with a painful TSA, standard laboratory testing including complete blood count, erythrocyte sedimentation rate, and C-reactive protein measurement should be obtained. If these raise suspicion for infection, such as if the synovial leukocyte count exceeds 2,000 and is composed of at least 70% polymorphonuclear leukocytes [
Postoperative radiographs are the first-line imaging modality to evaluate for osteolysis in the proximity of either the glenoid or humeral components. Standard views of the shoulder, including anteroposterior, Grashey, lateral, and axillary views, should be obtained. The examiner should evaluate radiographs for radiolucencies and stress shielding adjacent to the glenoid and humeral components. Comparison to prior radiographs should be made when available, particularly when monitoring the progression of previously diagnosed osteolysis. The examiner may observe implant loosening, malpositioning, or subsidence. Particular attention should be focused on the location of the humeral head, as proximal migration may indicate a supraspinatus tear, and anterior displacement may suggest a tear of the subscapularis.
In non-cemented humeral components, radiolucent lines often occur at the tip of the prosthesis, whereas radiolucencies commonly develop along the proximal and midbody aspects of the stem in cemented humeral components. In some smaller series with 10 years of follow-up, over 50% of patients developed radiolucencies, most often in association with glenoid wear and polyethylene debris [
It also appears that the choice of humeral fixation technique is not associated with osteolysis on radiographs. A recent randomized controlled trial with a mean 38-month follow-up period reported a 0.74% incidence of radiolucencies ≥2 mm in three or more zones, which did not significantly differ between cemented and non-cemented humeral component cohorts [
Unfortunately, radiolucent lines on plain radiographs do not always reliably diagnose loosening, particularly during long-term follow-up, as some series report the presence of radiolucent lines in up to 80% of radiographs at 10 years of follow-up [
In cases of osteolysis following RSA, notching of the polyethylene liner against the inferior border of the scapula should be assessed. This mechanical impingement can potentially lead to a high level of particulate debris, leading to osteolysis in both the glenoid and the humerus. In severe cases, significant osteolysis can occur at the inferior glenoid, directly affecting baseplate fixation. In the evaluation of osteolysis after RSA, component malposition should be recognized early and potentially revised to prevent further osteolysis.
It is important to remember that osteolysis is a biological phenomenon rather than a clinical condition. Osteolysis, in and of itself, is frequently an asymptomatic finding identified in routine postoperative imaging. For patients without clinical symptoms who present with imaging findings of mild osteolysis, nonoperative management with close follow-up is appropriate. Serial clinical and radiographic evaluations are recommended to identify the early development of symptoms and radiographic evidence of osteolysis progression or implant loosening.
Surgical management of osteolysis is reserved for patients who manifest clinical symptoms directly attributable to osteolysis and aseptic loosening, such as pain, dysfunction, or shoulder instability, in the absence of an active or indolent infection. A particular treatment strategy must consider (1) the size, location, and chronicity of osteolysis; (2) the suspected source of loosening (i.e., glenoid vs. humeral component, as well as component malpositioning); (3) the patient’s primary subjective complaint; and (4) the patient’s functional status. The task of identifying an appropriate treatment is made challenging by the paucity of high-level, direct comparative studies of available treatment options. Given that the existing surgical treatments vary in invasiveness and the anticipated duration of recovery and that revision shoulder arthroplasty outcomes are generally inferior to the outcomes of primary arthroplasty, a shared decision-making process is essential to ensure that the chosen intervention matches the patient’s goals and expectations (
For patients with symptomatic osteolysis and evidence of glenoid loosening following anatomical TSA or RSA, nonoperative treatment is generally reserved only for patients that are poor surgical candidates and medically unfit for surgery. This approach relies on secondary stabilizers to maintain the functional integrity of the shoulder. To solidify the surrounding soft tissue architecture, nonoperative treatment consists of a 4–6-week period of sling immobilization during which active and passive range of motion are deferred. Whereas all surgical treatment options to be discussed in this article carry a significant risk for complications, non-surgical management mitigates the risk of surgery-related complications. In a retrospective analysis of 79 patients diagnosed with aseptic glenoid loosening following RSA, Ladermann et al. [
In postoperative anatomical TSA patients with isolated aseptic glenoid loosening and suspected infection, arthroscopic removal of the polyethylene glenoid component offers an appealing surgical option [
Another commonly employed surgical treatment option for aseptic glenoid loosening following anatomical TSA is revision anatomical TSA with reimplantation of another polyethylene glenoid [
In the setting of a failed anatomical TSA due to osteolysis or glenoid component loosening, conversion to RSA affords several advantages over revision anatomical TSA (
Humeral component loosening secondary to osteolysis surrounding the humeral implant is exceedingly rare. In a radiographic study of 395 shoulders that previously underwent either hemiarthroplasty or total arthroplasty, 43% of shoulders demonstrated evidence of osteolysis at either the greater tuberosity or calcar [
There are limited data available to guide clinicians in the management of aseptic glenoid loosening following RSA. As mentioned, nonoperative treatment should be pursued as a first-line treatment option in minimally symptomatic patients. For patients unable to tolerate nonoperative management, glenoid loosening should be treated with revision of the glenosphere. Ladermann et al. [
Osteolysis following primary TSA is a challenging clinical entity that causes up to 80% of complications. The pathogenesis of osteolysis is a macrophage-mediated response to debris from the TSA construct that is further facilitated by micromotion. A thorough history and physical examination are essential to rule out other causes of symptomatic TSA—namely, periprosthetic joint infection. Though radiographs remain the gold standard imaging modality in this setting, they remain insensitive for detecting radiolucent lines and early osteolysis, with limited evidence suggesting that CT may be a more efficacious modality for diagnosis. Once confirmed, nonoperative treatment of osteolysis should first be pursued given the potential to avoid surgery-associated risks, and limited data suggesting outcomes may be similar to that of reoperations. Current options for reoperations include glenoid polyethylene revision and conversion to RSA. Future studies are warranted to better define the indications and long-term outcomes of these procedures, though RSA currently appears to be the most reliable option given the evidence available.
Proposed treatment algorithm for the evaluation and management of patients with osteolysis after total shoulder arthroplasty. CBC, complete blood count; ESR, erythrocyte sedimentation rate; CRP, c-reactive protein.
Eighty-year-old male with a prior surgical history of left anatomical total shoulder arthroplasty (TSA) at an outside hospital in 2018 who presented with three years of increasing left shoulder pain and discomfort, especially with physical activity. Physical examination demonstrated the skin over the left shoulder to be intact, and a well-healed surgical incision was observed. The range of motion was 80° of forward flexion, 45° external rotation, and internal rotation to the L4 vertebrae. (A-D) Internal rotation, (B) external rotation, and (C) axillary and (D) outlet radiographs at this time demonstrated a previous anatomical TSA with chronic bony remodeling of the glenoid and anterior dislocation of the humeral component with associated proximal humeral osteolysis. The patient was indicated to undergo conversion to an reverse shoulder arthroplasty.
Eighty-two-year-old healthy female with prior surgical history of a left reverse shoulder arthroplasty (RSA) at an outside hospital on September 24, 2017 and subsequent right RSA at an outside hospital on May 30, 2018 who presented with a chief complaint of left shoulder pain. She stated that the pain began 2 weeks prior to evaluation after being pulled by her dog while holding its leash. She localized the pain to the anterior aspect of the shoulder without radiation. Upon physical exam, the skin over the left shoulder was intact, and a well-healed surgical incision was noted. The range of motion was 140° of forward flexion, 45° of external rotation, and internal rotation to the L1 vertebrae. (A-C) Anteroposterior (A), internal rotation (B), and axillary (C) radiographs at that time demonstrated radiolucencies around the humeral stem and the glenoid baseplate. Though osteolysis was suspected, the decision was made to first rule out low-grade infection and further evaluate the shoulder with a computed tomography (CT) scan. Her erythrocyte sedimentation rate was 6 mm/hr, C-reactive protein level was 0.6 mg/L, and her white blood cell count was 6.8 thousand/uL, which were not concerning for infection. (D-I) Evaluation of this CT scan on axial (D, E), coronal (F, G), and sagittal (H, I) views demonstrated two separate radiolucencies around the medial aspect of the proximal humeral component, which were concerning for osteolysis with aseptic loosening. On March 9, 2021, the patient underwent revision RSA with a Tornier Ascend Flex lateralized 36 glenosphere and +6 poly with centered 0 tray. (J-L) At 8-week postoperation, she was noted to be recovering well with forward flexion to 130°, external rotation to 30°, and acceptable component positioning on anteroposterior (J), internal rotation (K), and axillary (L) views.