Mimickers of Hill-Sachs Lesions

Abstract

The purpose of this article is to describe the imaging appearance, etiology, clinical features, and treatment of rare presentations of common bone and joint diseases known to mimic Hill-Sachs lesions. Knowledge of uncommonly encountered manifestations of ankylosing spondylitis, rheumatoid arthritis, septic joint, hyperparathyroidism, hydroxyapatite deposition disease, malignant bone tumors and benign bone cysts which mimic traumatic Hill-Sachs lesions is important for radiologists to guide the clinical care of patients who present with shoulder symptoms.

Traumatic Hill-Sachs lesions are encountered commonly in clinical practice. Radiologists should be aware that several common nontraumatic bone and joint diseases rarely mimic Hill-Sachs lesions. Knowledge of Hill-Sachs lesion mimickers may help to avert a delay in diagnosis or missed diagnosis. This article reviews the diagnostic imaging, etiology, clinical presentation, and treatment of Hill Sachs lesion mimickers; including ankylosing spondylitis, rheumatoid arthritis, septic arthritis, hyperparathyroidism, hydroxyapatite deposition disease, malignant bone tumors and benign bone cysts (Appendix A and B).

Anatomy

The proximal humerus consists of distinct bony regions at the shoulder, including the humeral head, greater and lesser tuberosities (Figure 1). The anatomic neck forms a border that delineates the humeral head from the greater and lesser tuberosities which serve as the anatomic footprint for the insertion of the rotator cuff. The portion of the humeral head which articulates with the scapular glenoid is intracapsular; and the small region without overlying hyaline cartilage, inside the joint capsule and lateral to the hyaline cartilage, is known as the “bare area”[1–3].

Figure 1.

Illustrations of proximal humerus anatomy. (A) Anterior and (B) posterior illustrations of the proximal humerus: 1 = greater tuberosity, 2 = lesser tuberosity, 3 = articular surface of the humeral head, 4 = anatomic neck (dotted line), green = typical location of Hill-Sachs lesions and its mimickers. (C) Location of osseous regions at the proximal humerus in relation to the glenohumeral joint in cross-section (coronal plane): red = cortex of the greater tuberosity, blue = bare area, yellow = subchondral bone of the humeral head, purple = rotator cuff tendon, asterisk = intracapsular space of the glenohumeral joint.

Hill-Sachs Lesions

Hill-Sachs lesions are traumatic impaction fractures of the humeral head. The shoulder dislocates anteriorly in > 90% of cases, and Hill-Sachs lesions occur in 67 to 93% of patients with anterior dislocation [4, 5]. The mechanism for Hill-Sachs lesions is blunt trauma: the dislocated humeral head is displaced in an anterior-inferior-medial direction relative to the scapular glenoid fossa; subsequent strong muscular contractions lead to a violent bony collision between the anteroinferior region of the scapular glenoid rim and the posterior-superior-lateral aspect of the humeral head [4, 5]. The acute clinical presentation is shoulder pain, weakness and limited range of motion; an additional potential long-term complication is shoulder instability [4, 5]. Hill-Sachs lesions are strongly associated with anterior-inferior scapular glenoid fracture, anterior-inferior glenoid labrum tear (Bankart lesion) and joint capsular injury [5, 6]. Hill-Sachs lesions vary in length, width, depth and orientation; and occur anywhere along the superior aspect of the humeral head, bare area and greater tuberosity [5, 7].

A typical set of radiographs in the setting of shoulder trauma includes anteroposterior (AP), axillary, Grashey and scapular Y views; special views such as Stryker notch radiographs may be obtained when a Hill-Sachs lesion is suspected following anterior shoulder dislocation [5, 8]. AP internal rotation and Stryker notch radiographs are particularly useful to measure the size, depth and orientation of Hill-Sachs lesions at the posterolateral aspect of the humeral head [4, 5]. Axillary and Grashey radiographs are helpful to identify associated fractures of the scapular gleniod [8]. On radiographs, Hill-Sachs lesions present as flat- or wedge-shaped impaction fractures at the posterolateral aspect of the humeral head and adjacent greater tuberosity (Figure 2) [4]. CT and MRI provide greater sensitivity than radiographs for detection and characterization Hill-Sachs lesions and additional concomitant bone and soft tissue injures [4, 8]. Loss of the circular contour and lateral flattening of the humeral head on the three superior most axial images through the humerus on CT and MRI are characteristic of a Hill-Sachs lesion in the setting of anterior dislocation [4]. The presence of intramedullary low signal on T1-weighted sequences and bright signal on fluid-sensitive sequences is compatible with bone marrow edema; signifying an acute or subacute clinical presentation, possibly recurrent; while the lack of edema denotes a chronic injury [8]. Radiographs and CT are inferior to MRI in regard to evaluating the chronicity of Hill-Sachs lesions based on imaging, since both have poor sensitivity to detect bone marrow edema in comparison to MRI.

Figure 2.

Hill-Sachs lesions. 53-year-old man after acute fall > 30 feet into water. (A) Anteroposterior (AP) internal rotation shoulder radiograph shows an acute anterior shoulder dislocation. (B) Follow-up AP internal rotation shoulder radiograph shows a Hill-Sachs lesion (arrow) following reduction of the dislocation. 25-year-old man with chronic shoulder instability and history of multiple dislocations. (C) Grashey shoulder radiograph shows a Hill-Sachs lesion (arrow).

Small Hill-Sachs lesions may be not clinically significant or require treatment. Indications for surgical intervention include large size, shoulder instability and/or engagement (“locking”) of a Hill-Sachs lesion onto the anterior glenoid rim of the scapula [5].

Ankylosing Spondylitis

Ankylosing spondylitis (AS) is a seronegative spondyloarthropathy and is associated with HLA-B27. The prevalence among persons of European decent is 0.2%, but is less common in those of African descent [9]. AS typically presents between the ages of 20 and 40 years, and is three times more likely in men [2]. AS classically follows an axial distribution [2, 10] (Figures 3A and 3B). Clinical signs of AS include pain and stiffness of the neck and back, usually with insidious onset lasting greater than 3 months, beginning before the age of 40 years [9]. End stage disease results in bony ankylosis of the sacroiliac joints and a “bamboo spine”, characterized by ossified syndesmophytes bridging the spine disc spaces and osseous fusion of the facet joints [2].

Figure 3.

Ankylosing spondylitis. A 31-year-old man with ankylosing spondylitis complains of multifocal joint pain. (A) Anteroposterior (AP) pelvic radiograph demonstrates complete ankylosis of the right sacroiliac joint (black arrow) and incomplete bony ankylosis of the left sacroiliac joint (white arrow). (B) Lateral cervical spine radiograph demonstrates thin bridging syndesmophytes anteriorly (arrows). (C) AP internal and (D) AP external rotation shoulder radiographs demonstrates a large erosion (arrow) at the posterolateral aspect of the humeral head and greater tuberosity.

Radiographs are the primary imaging modality for AS. In the early stages, CT is more sensitive than radiographs to detect erosions and joint space narrowing [10]. MRI can show the earliest signs of AS, by detecting bone marrow edema at the sacroiliac joints and the spine [11]. AS, in rare cases, may exhibit erosions and bone destruction at the shoulder and hip [10, 12]. In long-standing AS, the “hatchet sign” is a coined term referring to a large erosion at the superolateral aspect of the subchondral bone and bare area of the humerus (Figures 3C and 3D) [13].

Current treatment guidelines recommend non-steroidal anti-inflammatory drugs (NSAIDs) as first-line therapy for symptomatic AS. However, patients who do not respond to NSAIDs may be considered for second-line disease modifying anti-rheumatic drugs (DMARDs); such as tumor necrosis factor inhibitors including adalimumab or etanercept, or an interleukin 17A monoclonal antibody inhibitor such as secukinumab [14, 15].

Rheumatoid Arthritis

Rheumatoid arthritis (RA) affects 1% of the adult population and has an annual incidence rate of 54 cases per 100,000 persons [16]. RA is a common inflammatory arthropathy, typically presenting between ages 30 to 60 years, and is three times more common in women [2, 16]. Seropositive and seronegative rheumatoid factor (RF) forms of RA exist. HLA-DRA is present in nearly 70% of cases, but is less common in seronegative rheumatoid arthritis [16, 17].

Clinical symptoms and signs of RA include joint pain and swelling. Pain is posited to stem from proliferative synovitis and associated joint destruction. Potential long-term complications of RA include vasculitis, Felty syndrome, subcutaneous nodules and interstitial lung disease [17]. Long-standing RA also is associated with rotator cuff tears [18].

The classic distribution of joint space loss and erosions at the carpus and metacarpophalagenal joints on hand and wrist radiographs, and the lack of bone production, help to rule in the diagnosis of RA [2]. Shoulder radiographs may show peri-articular osteopenia, bony erosions and joint space narrowing; and rarely, in long-standing disease, joint arthrodesis [2, 17, 19] Superior subluxation of the humeral head and narrowing of the acromiohumeral interval is consistent with an associated rotator cuff tear [2, 18]. RA rarely causes large intraarticular erosions at the subchondral bone and bare area of the superolateral humeral head (Figure 4A) [19, 20]. MRI is more sensitive than radiographs to detect erosions in RA, with osteitis present in some cases (Figure 4B) [19]. MRI also is more sensitive than radiographs to characterize associated glenohumeral joint synovitis, bicipical synovitis and associated bursitis [19]. Rice body formation in the glenohumeral joint or subacromial subdeltiod bursa provides increased specificity, and limits the differential diagnosis to RA, tuberculosis, and coccidiomycosis [21]. Rice bodies are small hypo-intense foci composed of necrotic collagenous cellular debris on MRI [16, 21].

Figure 4.

Rheumatoid Arthritis. A 37-year-old woman with rheumatoid arthritis and chronic shoulder pain. (A) Anteroposterior external rotation shoulder radiograph shows a large erosion (arrow) at the humeral head and greater tuberosity. (B) Oblique coronal short tau inversion recovery-weighted shoulder MR image shows an erosion with associated osteitis / bone marrow edema at the humeral head (long-thin arrow). Rice-bodies (short-thin arrow) and fluid distend the subacromial subdeltoid bursa, and a high-grade articular surface partial tear of the supraspinatus tendon (short-wide arrow) is present.

Treatment is aimed at managing symptoms and delaying progression of joint damage. DMARDs are the mainstay of treatment. Most patients are treated initially with conventional synthetic DMARDs such as Methotrexate, with monotherapy effective in 25 to 40 % of cases. A 3 to 4 month trial of corticosteroid therapy is often prescribed for patients who suffer from symptomatic flares. If corticosteroids are not effective, a biologic DMARD, such as etanercept, tocilizumab, or adalimumab; or a targeted synthetic DMARD, such as tofacitinib, may be given in combination with Methotrexate [22].

Septic Arthritis

Septic arthritis typically presents as a mono-arthropathy [2]. Early diagnosis and intervention are the preferred course of action in the native joint, before destruction of hyaline cartilage occurs [23]. Nearly 3 to 15% of cases of septic arthritis occur at the shoulder, at a rate of approximately 3,200 cases per year in the United States [24, 25]. Shoulder septic arthritis is a well-known source of morbidity. Since clinical symptoms are usually non-specific, definitive diagnosis is not uncommonly delayed, and effective treatment is often difficult to deliver [24, 26]. The acuity of the disease process may not be recognized by healthcare providers if symptoms of shoulder pain and decreased range of motion are not accompanied by localizing systemic symptoms such as spreading redness, fevers and chills. Immunocompromised patients can present an even greater challenge, as clinical signs may be almost entirely absent [23].

Bacterial Infection (Typical)

Shoulder joint infection occurs in the setting of hematogeneous spread or direct extension from bone or soft tissue [2, 27, 28]. Cases also may occur following therapeutic injections or arthrocentesis for treatment of noninfectious pathologies [27, 28]. Typical bacterial septic arthritis is associated with elevations in white blood cell count, erthytocyte sedimentation rate and C-reactive protein. Diagnosis is established with positive synovial fluid cultures [28]. Staphylococcus aureus is the most common cause of septic arthritis, although infection by a plethora of other bacterial species have been described [2, 27, 28]. Immunocompromised patients and intravenous drug abusers show a higher prevalence of septic arthritis secondary to gram-negative bacteria such as pseudomonas aeruginosa and escherichia coli, as compared to the general population [27].

The earliest finding of septic arthritis on radiographs may be joint space widening, secondary to joint effusion. Subsequent findings over time include joint space narrowing, peri-articular osteopenia, bone erosions and soft tissue swelling [2]. At the shoulder, large erosions at the subchondral bone and bare area of the humerus occur rarely (Figures 5 and 6). CT is more sensitive than radiographs to demonstrate the presence and extent of bony erosion (Figure 6B). On MRI, associated symptoms with septic arthritis include increased T2-weighted signal and decreased signal on T1-weighted images that is representative of osteomyelitis or reactive bone marrow edema (Figure 5C). Additional findings include perisynovial edema, synovial enhancement and hypertrophy, and joint effusion [26].

Figure 5.

Typical bacterial infection. A 38-year-old man with nonspecific shoulder pain for several months developing septic joint of the shoulder caused by methicillin-sensitive staphylococcus aureus. (A) Anteroposterior neutral shoulder radiograph shows no abnormality on initial presentation. (B) Post-operative Grashey shoulder radiograph following incision and drainage (I&D) surgery 4 months later demonstrates an interval development of diffuse peri-articular osteopenia and a large erosion (arrow) at the junction of the greater tuberosity and humeral head. (C) Oblique coronal short tau inversion recovery-weighted shoulder MR image 2 days prior to I&D surgery shows an erosion with associated bone marrow edema at the lateral aspect of the humeral head (arrow). Diffuse peri-articular soft tissue edema is also present.

Figure 6.

Typical and atypical bacterial infection. A 50-year-old woman with endocarditis and septic shoulder joint caused by methicillin-resistant staphylococcus aureus. (A) Anteroposterior neutral shoulder radiograph shows an ill-defined erosion at the humeral head and greater tuberosity (arrow). (B) Contrast-enhanced axial CT image shows a large humeral head erosion (arrow) and a large glenohumeral joint effusion (asterisk). A 55-year-old man with disseminated mycobacterium avium-intracellulare complex and septic shoulder joint. (C) Oblique coronal proton density-weighted and (D) oblique sagittal T1-weighted shoulder MR images show a large erosion involving the greater tuberosity and humeral head (arrows) with associated soft tissue abscess (asterisk).

Atypical Infection

Mycobacterial organisms account for < 3% of musculoskeletal infections and are often overlooked as a cause of septic arthritis. The prevalence may be higher in endemic areas or in patients with known prior infection [29]. Mycobacterium tuberculosis is known to infect bones and joints, but is much more common in the spine than peripheral joints. [29]. Mycobacterium avium-intracellulare complex (MAC) is a rare cause of septic arthritis [30]. Mycobacterial joint infections occur through hematogenous spread or direct extension from infected bone or soft tissue. Atypical joint infections often present with an indolent course. Symptoms may be nonspecific and only consist of long-standing shoulder pain and stiffness [29].

Diagnosis of mycobacterial infections are generally made be culture, Ziehl-Neelsen staining or polymerase chain reaction [29, 31]. Classic radiographic signs of mycobacterial infection include the Phemister triad: severe juxta-articular osteopenia, marginal erosions and gradual joint space narrowing [32]. Atypical bacterial infections rarely are associated with large confluent erosions at the humeral head and greater tuberosity on imaging (Figures 6C and 6D). MRI findings are similar to those seen in typical bacterial infection. The presence of rice-body formation limits the differential diagnosis to tuberculosis, RA and coccidiomycosis [21].

Treatment and Prognosis

Septic arthritis of the shoulder is often a greater challenge to treat as compared to other joints, since patients often have medical co-morbidities. Treatment options include antibiotics and arthrocentesis and/or surgical irrigation and debridement [24]. Standard first-line therapy for methicillin-sensitive staphylococcus aureus infection is with a beta-lactam antibiotic such as nafcillin. First line treatment for methicillin-resistant staphylococcus aureus (MRSA) is daptomycin or vancomycin. Patients with strains of MRSA resistant to first line treatment are treated with combination antibiotic therapy [33]. Tuberculosis is treated with intensive multi-drug antibiotic therapy [34]. MAC requires treatment with a macrolide-based regimen, with parenteral aminoglycosides reserved for with severe disease [35].

Surgical shoulder joint incision and drainage interventions may be indicated in cases with large abscesses, multiple drug resistance and severe joint destruction [29]. Patients often experience subsequent systemic complications regardless of treatment method. Septicemia is a common complication of shoulder joint infection. Also, osteomyelitis, recurrent joint effusion and irreversible joint dysfunction are not uncommon sequelae following septic arthritis of the shoulder [24, 25].

Hyperparathyroidism

End-stage renal disease (ESRD) is common and 85,000 patients receive hemodialysis every year in the U.S. [36]. Parathyroid hormone (PTH) is produced by chief cells in the parathyroid gland and helps to regulate calcium, phosphate and vitamin D homeostasis. PTH promotes osteoclast-mediated bone resorption at the bone surface [37]. Primary hyperparathyroidism is caused typically by an autonomous PTH-hypersecreting parathyroid adenoma or parathyroid gland hyperplasia, and rarely parathyroid gland carcinoma [37]. Renal failure is the most common cause of secondary hyperparathyroidism, a state in which parathyroid glands hypersecrete PTH as a result of dysregulation of normal homeostasis, including hyperphosphotemia and insensitivity to elevated calcium levels [36, 37].

Large erosions centered at the intra-articular bare area of the humeral head have been described in patients with secondary hyperparathyroidism and ESRD treated by long-term hemodialysis [20] (Figure 7). Involvement of the greater tuberosity also has been described, suggested to be related to a bone resorptive process given the extra-articular location [38]. Patients with lateral humeral head erosions stemming from primary and secondary hyperparathyroidism may be incidental findings and entirely asymptomatic [20, 37, 38]. Investigators posit that the lack of associated symptoms for erosions in hyperparathyroidism stems from the mechanism being related to bone resorption rather than synovitis [20, 38]. Dialysis-related amyloidosis is an additional cause of rare erosions at the posterolateral aspect of the humeral head in the setting of ESRD described in the literature, which is a distinct pathologic process from secondary hyperparathyroidism [39].

Figure 7.

Hyperparathyroidism. A 65-year-old woman with long standing end-stage renal disease, secondary hyperparathyroidism and chronic shoulder pain. (A) Anteroposterior internal rotation radiograph and (B) a corresponding unenhanced coronal CT image show a large erosion (long arrow) at the posterolateral aspect of the humeral head, with an associated rotator cuff tear implied by severe narrowing of the acromiohumeral interval. Distal claviclar osteolysis is also present (short arrow).

The radiographic appearance of humeral head erosions in primary and secondary hyperparathyroidism are typically well-defined and commonly bilateral [38]. CT may be more sensitive to demonstrate erosions as compared to radiographs (Figure 7B). The more typical findings of subperiosteal and subchondral bone resorption, brown tumors and chondrocalcinosis may not be readily identifiable at the shoulder [38]. Distal clavicle erosions at the acromioclavicular joint or at the site of attachment of the coracoclavicular ligaments are potential associated findings [20, 36].

First-line treatment and the only cure for primary hyperparathyroidism is parathyroidectomy, while medical therapy with cinacalcet or bisphosphonates is available for non-surgical candidates [40]. Treatment options for secondary hyperparathyroidism include dietary limitation of phosphorus, phosphate binding agents, vitamin D supplementation, and cinacalcet; partial parathyroidectomy is also an additional option [41].

Hydroxyapatite Deposition Disease

Hydroxyapatite deposition disease (HADD), often referred to as calcific tendinitis, is a metabolic deposition of calcium hydroxyapatite in juxta-articular tissues. The shoulder is the most common location, where HADD frequently affects rotator cuff tendons or adjacent bursae [42]. HADD is a commonly encountered imaging finding, present in up to 3% of adults [43]. HADD deposition may be in an intratendinous or peritendinous location. Subsequent resolution of HADD on follow-up imaging also is known to occur [43].

The discovery of HADD on an imaging test is most often as an incidental finding in an asymptomatic individual, but in symptomatic patients HADD accounts for up to 7% of painful acute or chronic shoulder syndromes [43–45]. Additional clinical signs include decreased range of motion, edema, erythema and fever [43]. An active inflammatory process at tendon insertions related to HADD has been posited as the cause of bony cortical erosions. Some investigators hypothesize that the resorptive phase preceding the disappearance of HADD and/or mechanical irritation are the trigger(s) for the acute inflammation that causes symptoms [42, 44].

The radiographic and CT appearance of mineralization in HADD is varied. Foci of HADD can appear amorphous, solid or stippled. A soft tissue calcification with a comet-tale shape also has been described when foci are in an intratendinous location [43, 44]. CT may demonstrate cortical erosion to better advantage than radiography [43, 44]. Aggressive or non-aggressive forms of periosteal reaction are additional potential findings. On MRI, foci of hydroxyapatite deposition disease are low signal on T1-, T2, and intermediate-weighted sequences; and some cases demonstrate associated bone marrow edema [42–44]. MRI also may demonstrate bone marrow edema associated with HADD bone destruction which may not be readily evident on radiography (Figure 8) [43, 44]. Increased intrasubstance signal within tendons also has been described in association with HADD on MRI. Associated bony cortical erosion of the greater tuberosity at the site of attachment of the supraspinatus or infraspinatus tendon is rare [42, 43, 45].

Figure 8.

Hydroxyapatite deposition disease. 58-year-old woman with acute on chronic shoulder pain. (A) Oblique coronal short tau inversion recovery-weighted and (B) oblique coronal proton density-weighted shoulder MR images show low signal deposits of calcium hydroxyapatite (long arrow) eroding into the humeral head and greater tuberosity with associated bone marrow edema (asterisk) and adjacent soft tissue edema. Additional foci of calcium hydroxyapatite are associated with the subacromial subdeltoid bursa and rotator cuff (short arrow). (C) A corresponding Grashey shoulder radiograph depicts a focus of calcium hydroxyapatite (arrow).

Treatment options for symptomatic HADD include conservative methods such as NSAIDs, targeted steroid injections and/or physical therapy; since symptoms related to HADD may be self-limited [43–45]. Patients who fail initial conservative measures may be candidates for ultrasound-guided percutaneous aspiration and lavage or high-energy extracorpeal shock-wave therapy [2, 44, 45]. Surgical intervention by arthroscopy also is a treatment option, and has been suggested to be more effective in patients with intra-osseous foci of HADD. Overall, symptomatic patients with bony erosions are theorized to have a worse prognosis as compared to patients who lack bony erosions [45].

Malignant Bone Tumors

Metastasis, multiple myeloma, leukemia and lymphoma cause the vast majority of malignant bone cancer; primary bone sarcoma is rare, accounting for less than 0.2% of bone malignancy [46]. Age is associated strongly with bone tumors, with metastasis representing the vast majority of malignant bone tumors after the age of 40 years [47]. Metastasis represents the invasion of bone from distant sites, with cancers of breast, prostate, kidney, lung and thyroid the most common [46]. Multiple myeloma is the most frequently encountered primary malignancy of bone, and is the result of abnormal clonal proliferation of malignant plasma cells [48].

Bone tumors are an uncommon cause of pain and stiffness at the shoulder, and may be initially overlooked clinically in favor of more prevalent forms of shoulder pathology, such as rotator cuff disorders and osteoarthritis [49]. Malignant neoplasms can occur anywhere at the proximal humerus including at the diaphysis and metaphysis of the proximal humerus, in addition to involvement of the humeral head, surgical and anatomic necks, and greater and lesser tuberosities [49–51].

On radiographs, malignant bone tumors can present as osteoblastic, osteolytic or mixed type lesions; and often present with ill-defined borders or permeative appearance (Figure 9) [46, 49]. CT is superior to radiographs at defining the extent of cortical destruction, endosteal scalloping, cortical tunneling pattern, mineralized matrix and medullary sclerosis [46, 49, 51]. MRI demonstrates any extra-osseous soft tissue component, medullary space involvement, cortical breakthrough, and enhancement pattern [46, 49, 50]. ¹⁸F-FDG PET/CT shows high standard uptake values in FDG-avid malignant bone masses (Figure 9B) [48, 51]. ¹⁸F-FDG PET/CT, ¹⁸F-FDG PET/MRI, and whole body MRI are useful imaging techniques for staging and characterizing extent of disease [48, 52].

Figure 9.

Metastatic disease. A 57-year-old woman with shoulder pain and metastatic cervical carcinoma. (A) Anteroposterior external rotation shoulder radiograph shows a region of ill-defined lytic bone destruction (arrow) involving the posterolateral proximal humerus with a subtle linear lucent step-off at the junction of the humeral head and greater tuberosity suggesting non-displaced pathologic fracture. (B) ¹⁸F-FDG PET/CT fused image shows intense FDG avidity in the metastasis at the proximal humerus with a standard uptake value of 17.

Tissue diagnosis from core or open biopsy allows for histologic and cytogenetic characterization when the diagnosis is unknown or to confirm metastatic spread of disease [51]. Tissue sampling guides diagnosis and management in cases of malignant primary bone tumors [49, 50]. In some cases, blood tests are helpful to make the diagnosis, as in multiple myeloma. Patients with metastatic disease may receive chemotherapy, immunotherapy, therapeutic radiation and/or surgery; the goals of which are definitive cure or palliation, depending on patients’ malignant tissue type and stage of disease. In cases of primary bone sarcoma, definitive treatment ranges from limb-preserving resection to forequarter amputation, depending on presentation [49]. Strategies for multiple myeloma include autologous stem cell transplantation and chemotherapy [53]. Complications of most malignant bone tumors include pathologic fracture, tumor recurrence or progression, and extensive bone destruction [46, 48, 50].

Benign Bone Cysts

Anterior and posterior bone cysts, cortical and subcortical, are not infrequently identified at the greater tuberosity and the adjacent bare area of the humeral head. Subcortical cysts located at the anterior aspect of the greater tuberosity have a 94% positive predictive value for rotator cuff pathology [1, 54]. Anterior cysts present in nearly one-fourth of shoulders with associated supraspintus and/or infraspinatus tendon pathology, inclusive of tendinopathy, partial-thickness and full-thickness tears [54]. Posterior cysts are 2 to 7 times more common than anterior cysts [54, 55]. Historically, investigators theorized that posterior cysts were age-related, degenerative, and related to rotator cuff pathology. More recent studies have found that posterior cysts lack any significant association with rotator cuff pathology [54, 55]. Jin et al in a study of cadaver shoulders, suggested that cysts associated with the bare area at the posterosuperior humeral head were joint space- associated pseudocysts, that are lined with collagen connective tissue [1]. Williams et al, reported that 94% of posterior cysts communicated with the glenohumeral joint on MR arthrography [55]. An additional hypothesis posits that some posterior cysts are actually vascular channels, while others describe an association with internal impingement of the shoulder [1, 54, 56].

Radiographs and CT show bony cortical irregularities and well-defined subcortical cysts. Cortically-based cysts at the greater tuberosity and bare area of the humeral head are known to mimic erosions associated with inflammatory arthropathy, and rarely also may mimic traumatic Hill-Sachs lesions (Figure 10) [54]. MRI usually demonstrates a sharply marginated lesion with a low signal peripheral rim and fluid signal centrally. Subcortical cysts also may present with adjacent bone marrow edema-like changes. Cysts can present as solitary or multiple lesions, and range from a few millimeters to over one centimeter in diameter [54, 55]. Benign bone cysts typically do not require treatment.

Figure 10.

Benign bone cysts. A 55-year-old man with chronic shoulder pain and decreased range of motion. (A) Grashey shoulder radiograph and (B) a corresponding oblique sagittal T1-weighted shoulder MR image demonstrate a focal bone cyst (arrow) involving the junction of the bare area and greater tuberosity. 57-year-old woman with nonspecific shoulder pain. (C) Grashey shoulder radiograph shows bone cyst formation spanning the junction of the greater tuberosity and humeral head.

Conclusion

Knowledge of the imaging appearance, etiology, clinical features and management of rare presentations of common bone and joint diseases that are known to mimic traumatic Hill-Sachs lesions is important for radiologists to guide the clinical care of patients who present with shoulder symptoms.

Appendix

Appendix A.

Category and Clinical Associations of Hill-Sachs lesions and Mimickers

	Category	Clinical Associations
Hill-Sachs Lesion	Trauma	Anterior shoulder dislocation Shoulder instability
Ankylosing Spondylitis	Spondyloarthropathy	HLA-B27 Neck and back pain and stiffness
Rheumatoid Arthritis	Inflammatory arthropathy	Joint pain and edema
Septic Arthritis	Infection	Monoarthropathy Fevers and chills ↑ White blood cell count Insidious onset at shoulder
Hyperparathyroidism	Metabolic disorder	Renal failure Dialysis ↑ Parathyroid hormone level
Hydroxyapatite Deposition Disease	Mineral deposition disorder	Acute disease (shoulder): Pain, edema, erythema, fever
Malignant Bone Tumor	Malignancy	History of malignancy Insidious onset at shoulder
Benign Bone Cyst	Other	Rotator cuff disease Incidental

Appendix B.

Specific Imaging Signs Associated with Hill-Sachs lesions and Mimickers

	Associated Specific Imaging Signs to Support Diagnosis
Hill-Sachs Lesion	Shoulder: Bankart lesion Anterior-inferior scapular glenoid fracture
Ankylosing Spondylitis	Pelvis: Sacroiliac joint ankylosis Spine: Bamboo spine
Rheumatoid Arthritis	Shoulder: Rice bodies Hands/Wrists: Carpal and metacarpophalangeal joint distribution
Septic Arthritis	Shoulder: Rice bodies (tuberculosis)
Hyperparathyroidism	Shoulder: Distal clavicle osteolysis
Hydroxyapatite Deposition Disease	Shoulder: Rotator cuff hydroxyapatite deposition
Malignant Bone Tumor	Shoulder: Multifocal lesions
Benign Bone Cyst	Shoulder: Rotator cuff tendinopathy Rotator cuff partial- or full-thickness tear