Shoulder pain is common in high-level athletes playing overhead or contact sports (7). Diagnosis of shoulder injuries is often straightforward in young active patients; however, atypical etiologies of shoulder pain also must be considered (6,76,7). Hypoplasia or dysplasia of the glenoid has previously been considered a rare anatomic anomaly and is associated with shoulder pain or instability in athletes (16). Many patients with this condition can be asymptomatic, so the true prevalence is likely underestimated (8,138,13). Plain x-ray findings are virtually diagnostic, and these include a smooth glenoid surface with incomplete ossification and dysplasia of the scapular neck or a notched (dentate) glenoid surface (13). Additional bony abnormalities can include dysplasia of the humeral head and hooking of the distal clavicle (8,138,13). Hypertrophied labral tissue is a common magnetic resonance imaging (MRI) finding in these patients, and a spectrum of labral tears has been described (14,1614,16). Prognosis for return to play in a contact sport for symptomatic patients has been generally unfavorable. There is only one previous case report about an American football player with glenoid hypoplasia, and this individual was unable to continue his sport due to pain. Here, we present the case of a 20-year-old varsity offensive lineman originally seen for recurring stingers and in whom the diagnosis of glenoid hypoplasia was incidentally noted. This individual never required surgery and successfully completed all four seasons of college football. We hope to highlight the fact that patients with this condition can succeed in contact sports at the collegiate level and thereby help physicians frame the discussion when counseling future patients with hypoplasia of the glenoid.
A 20-year-old right hand-dominant college football offensive lineman and military cadet presented midseason with the complaint of a right-sided “stinger” from a lateral blow to the neck. He reported having experienced one ipsilateral stinger from a similar mechanism while in high school 2 years earlier, but his symptoms were mild and he never required treatment. He was asymptomatic during his freshman season of collegiate football, and this instance was the only recurrence since high school. His symptoms were consistent with a transient neuropraxia, lasting less than 5 min, without any associated neck pain or shoulder instability.
Physical examination results demonstrated a well-developed individual, with significant muscle bulk and tone (Fig. 1). The shoulders were asymmetric in appearance, with a downward sloping deformity more prominent on the right. The patient had full, pain-free range of motion of the neck and shoulders, 5 out of 5 strength in the bilateral upper extremities, and a negative Spurling test result. There were no physical findings suggestive of instability, impingement, or rotator cuff pathology.
Radiographs of the cervical spine at the time of injury were normal, with no suggestion of stenosis. Radiographs of both shoulders showed hypoplasia of the glenoid necks bilaterally (Fig. 2). There was a jagged appearance of the articular surfaces bilaterally with slight widening of the inferior aspect of the glenohumeral joint space on the right. The patient was counseled regarding the incidentally noted shoulder findings, which were pathognomonic for glenoid hypoplasia, and he admitted that his shoulders did feel sore at times; however, because the patient’s primary complaint was recurrent stingers and there was no suggestion of cervical pathology, no formal restrictions were placed on his activities. He was treated with nonsteroidal anti-inflammatory drugs (NSAID) and completed the remainder of the season without incident.
The following season, he began to experience mild right shoulder pain while playing. Subjective exacerbating factors included overhead or forward flexed and loaded positions, and he sustained a third stinger. He described his symptoms as mild and never missed a game. However, the medical staff expressed concern about the new onset of shoulder pain and a possible connection between the recurrent stingers and the more severe glenoid hypoplasia on the right side. The patient agreed to undergo advanced imaging studies to better evaluate the right shoulder and guide any further treatment recommendations. Computed tomography (CT) scan with three-dimensional reconstructions showed congruency of the acromioclavicular joint but confirmed hypoplasia of the posterior osseous glenoid and scapular neck (Fig. 3). MRI of the right shoulder revealed thickening of the glenoid articular cartilage, hypertrophy of the overlying labrum with a tear of the posterior/inferior aspect, and associated complex paralabral cyst formation (Fig. 4). These studies were extremely useful in more fully appreciating the altered shoulder anatomy and in educating the patient and his parents about the potential treatment options, including possible surgical repair versus debridement of the labral tear and decompression of the paralabral cyst.
He declined surgical intervention but received physical therapy for shoulder strengthening and was prescribed NSAIDs to be used as needed. Despite the patient’s symptoms, he continued to excel in the football field and at his required military training.
Glenoid hypoplasia may be more common than previously thought (8). Many patients are asymptomatic, and the overall incidence may be underestimated (8,138,13). Most patients are male, and the findings are most often bilateral (13). Symptomatic patients may present with chronic shoulder pain, symptoms of multidirectional instability, and limitations in motion (13,14,1613,14,1613,14,16).
The specific developmental etiology of glenoid hypoplasia remains largely unknown. It is a developmental abnormality consisting of dysplasia of the scapular neck and irregularity of the articular surface. It is often associated with changes in the labrum, cartilaginous structures, and humeral head (11). Ossification of the scapula begins in utero (4), and fusion of the two glenoid ossification centers is typically finished by puberty. It has been hypothesized (4,9,104,9,104,9,10) that arrest of ossification of the inferior glenoid apophysis is implicated in the attenuation and dysplasia of the scapular neck and glenoid, but a recent study utilizing advanced imaging has suggested that this arrest would insufficiently explain some magnetic resonance findings of fibrocartilaginous or fatty infiltration in the bony glenoid defect (13). An association with muscular dystrophy, obstetrical trauma, or infection also has been suggested as an etiology (11,13,1611,13,1611,13,16), and there have been reported cases of affected first-degree family members that may suggest an autosomal-dominant inheritance pattern (6,10,156,10,156,10,15). Of note, this patient’s younger brother now also plays varsity college football and does not have glenoid hypoplasia.
Treatment of glenoid hypoplasia is largely driven by patients’ symptomatology. Patients with significant instability are managed with physical therapy for strengthening of the shoulder girdle stabilizers, rotator cuff, and deltoid muscles, similar to instability patients without associated dysplasia of the glenoid articulation (2,13,162,13,162,13,16). In patients with symptomatic labral pathology, surgical management may consist of debridement of hypertrophic tissue or repair of associated tears (13), which may be augmented by bony reconstruction utilizing osteotomy or grafting to restore articular anatomy as indicated (8,138,13). However, there is no standard association between bony and soft tissue abnormalities in patients with glenoid hypoplasia, and the spectrum of labral pathology may range from intrasubstance tears to complete detachment of the labrum from the glenoid (5,135,13). Only two cases of perilabral cyst formation related to glenoid hypoplasia have been previously reported in the literature (13). An association between glenoid dysplasia and subsequent development of degenerative joint disease (DJD) of the glenohumeral joint has been described (8,128,12); however, the role of arthroscopic surgery has not been elucidated in these patients, and reported results have not shown significant benefit (7). Finally, surgical considerations in shoulder arthroplasty in late-stage DJD secondary to glenoid hypoplasia are significant (1,31,3) and beyond the scope of this case report.
There is only a single previous case report involving an intercollegiate offensive lineman with glenoid hypoplasia, and this individual could not keep playing due to pain despite surgical intervention (7). Our case is unique insofar as the glenoid dysplasia was an incidental finding in a patient who presented with recurrent stingers but successfully completed 4 years of college football at the offensive lineman position. He never missed a game or practice due to shoulder pain, although he did become mildly symptomatic as an upperclassman. The authors feel this case might help frame future discussions when physicians encounter contact sport athletes with this condition. Also, it is the first case reported in which recurrent stingers and glenoid hypoplasia are mentioned together. Given the significant downward sloping appearance of this patient’s shoulder, there may be an anatomic basis for an association between his recurrent stingers and glenoid hypoplasia. However, this hypothesis remains to be investigated.
The exact incidence of glenoid hypoplasia remains unknown, but in symptomatic patients, it can cause significant limitation and morbidity (7,8,13,167,8,13,167,8,13,167,8,13,16). Despite bilateral glenoid hypoplasia, dominant-sided labral tear and associated paralabral cyst formation (one of only three similar cases reported in the literature), the patient in our case report was able to compete for 4 years as a college football lineman and currently serves as an active-duty Marine officer. Conservative management can be successful in these patients, and in-depth patient counseling regarding all treatment options must be a priority for physicians managing patients with this condition.
The authors declare no conflicts of interest and do not have any financial disclosures. This article does not contain reproduced copyrighted materials. No external funding was received in support of this study.
The views expressed in this manuscript are those of the authors and do not reflect the official policy of the Department of Army, Department of Defense, or the U.S. government. All authors are employees of the U.S. government. This work was prepared as part of their official duties and as such, there is no copyright to be transferred.
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