Humeral head avascular necrosis: etiology, diagnosis, and management

Elisabeth Kaza; Garret Neel; Scott Feeley; Kelly Kilcoyne; Daniel Song

doi:10.5397/cise.2025.00493

Clin Shoulder Elb > Volume 28(4); 2025 > Article

Kaza, Neel, Feeley, Kilcoyne, and Song: Humeral head avascular necrosis: etiology, diagnosis, and management

Current Concept

Clinics in Shoulder and Elbow 2025; 28(4): 517-528.

Published online: August 26, 2025

DOI: https://doi.org/10.5397/cise.2025.00493

Humeral head avascular necrosis: etiology, diagnosis, and management

Elisabeth Kaza¹

, Garret Neel²

, Scott Feeley²

, Kelly Kilcoyne²

, Daniel Song²

¹Uniformed Services University of the Health Sciences, Bethesda, MD, USA

²Department of Orthopedic Surgery, Walter Reed National Military Medical Center, Bethesda, MD, USA

Correspondence: Elisabeth Kaza Uniformed Services University of the Health Sciences, 4301 Jones Bridge Rd, Bethesda, MD 20814, USA
Tel: +1-571-393-4056 Email: elisabeth.kaza@usuhs.edu

Received: May 8, 2025 Revised: June 23, 2025 Accepted: June 30, 2025

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Humeral head avascular necrosis (AVN) can cause significant shoulder morbidity and represents the second most common site of nontraumatic osteonecrosis after the femoral head. The pathophysiology centers on disrupted blood supply, ultimately leading to bone death and structural compromise. It is associated with various etiologies, including trauma, iatrogenic factors, hematologic conditions, lifestyle factors, certain environmental exposures, and systemic diseases. Diagnosis relies on a combination of clinical assessment and radiographic evaluation, with magnetic resonance imaging serving as the most sensitive modality for early detection. The Cruess classification system guides treatment decisions. Although conservative measures are used in early stages, they carry a risk of progression, as they do not alter the disease course—unlike surgical techniques such as core decompression. Arthroplasty is reserved for later stages with evidence of collapse, with research suggesting that the use of pyrocarbon in hemiarthroplasty may help reduce glenoid erosion. This review provides a comprehensive overview of humeral head osteonecrosis, emphasizing its etiology, clinical evaluation, imaging findings, and treatment strategies. It highlights the growing support for early operative intervention over conservative management, emerging treatment modalities such as biologic augmentation and allografting, and promising new materials like pyrocarbon in hemiarthroplasty to mitigate glenoid erosion.

Key Words: Avascular necrosis; Shoulder surgery; Systematic review; Shoulder arthroplasty; Core decompression

INTRODUCTION

Humeral head avascular necrosis (AVN) is characterized by the progressive death of bone tissue due to compromised blood supply, which can lead to significant pain and functional impairment [1-3]. The pathogenesis of humeral head AVN is multifactorial, with a variety of etiological factors ranging from trauma and iatrogenic insults to systemic conditions and lifestyle influences [4-9]. Early diagnosis is crucial for preventing joint collapse and optimizing outcomes [10,11]. This review provides an overview of humeral head AVN, focusing on its epidemiology, etiology, pathophysiology, diagnostic evaluation, and current management strategies. This update is critical due to the disease's morbidity and recent therapeutic developments, which include growing support for early operative intervention, use of biologic augments and allografts, and the introduction of new arthroplasty materials such as pyrocarbon to mitigate glenoid erosion.

EPIDEMIOLOGY

The annual incidence of osteonecrosis appears to be increasing, with nationwide Danish data showing a rate of 3.9 per 100,000 inhabitants in 1995 and 5.5 in 2012, which can be partly attributed to an increase in steroid use [12]. Humeral head AVN accounts for a small but growing portion of cases, with nationwide Korean data showing an increase from 0.13 per 100,000 person-years in 2008 to 0.33 in 2018 [13]. Female patients account for 53% of all osteonecrosis cases, but this proportion rises to 61.8% for humeral head osteonecrosis specifically [12,13]. The femoral head is the most common site, accounting for about 80% of cases [12], followed by the humeral head, which accounts for about 10% of all osteonecrosis cases [10]. Approximately 5% of patients with glenohumeral arthritis also have underlying osteonecrosis [14], and about 5% of all shoulder arthroplasties are performed to treat humeral head AVN [6].

PATHOPHYSIOLOGY

AVN, or osteonecrosis, occurs when the blood supply to bone tissue is disrupted, leading to cell death and bone deterioration [13]. The pathophysiology of osteonecrosis was described by Mankin [1,2]. The blood supply to bones is maintained by two primary mechanisms: the internal medullary supply, which provides blood to the medullary cavity and inner cortex, and the external periosteal supply, which originates from the periosteum and supplies the outer cortex. Disruption of either supply can lead to osteonecrosis. In the medullary cavity, disrupted blood flow causes the death of trabecular bone and other local cells, which are primarily lipocytes in adults. The breakdown of lipocytes releases free fatty acids, which acidifies the environment and leads to the release of calcium hydroxyapatite crystals that form insoluble precipitates. When osteonecrosis occurs in a joint, such as the humeral head, corticocancellous osteonecrosis occurs. Blood supply disruption results in the death of trabeculae and subchondral bone, which is not particularly prone to calcification because it has fewer lipocytes than the medullary cavity. Instead, microfractures accumulate, leading to uncontrolled repair processes.

Ultimately, disrupted blood supply to the humeral head can lead to progressive collapse and glenohumeral joint arthritis [3]. The anterior humeral circumflex artery and posterior humeral circumflex artery (PHA) are the main sources of blood supply to the humeral head, with the PHA providing 64% of the overall supply and most of the blood to three of the four quadrants of the humeral head [15]. It also has the most sizable intraosseous anastomoses, supplied from the deep brachial artery [4,16]. The superomedial aspect of the humeral head is most susceptible to AVN due to both its relatively poor blood supply and the mechanical stress it endures, so it is the most common initial site of necrosis [4,17].

ETIOLOGY

There is a wide variety of causes of humeral head AVN, and Table 1 summarizes some of the most common ones [8,18-20].

Trauma

The incidence of posttraumatic humeral head AVN ranges up to 35% [21], primarily due to mechanical disruption of the blood supply, with proximal humeral fractures being one of the most common associations [22]. Among these fractures, the four-part proximal humerus fracture has the highest incidence of osteonecrosis, ranging from 15%–30%, largely attributed to damage to the anterior and posterior circumflex arteries [23].

Surgical Risk Factors

Surgical procedures are a known risk factor for humeral head AVN, with evidence from several case reports suggesting that this complication occurs within the first year following surgery [6,21,24-28]. A prospective study by Hertel et al. [24] evaluated 100 cases of proximal humerus fractures that were treated with open surgery and reported that 55 cases progressed to AVN. That study identified calcar extension of less than 8 mm, high medial hinge displacement, and basic fracture type as the strongest predictors of AVN.

In contrast, a retrospective study by Campochiaro et al. [21] reviewed 267 proximal humerus fractures managed with open reduction and internal fixation. Unlike Hertel et al. [24], Campochiaro et al. [21] found that metaphyseal head extension and medial hinge displacement were unreliable predictors of AVN. Instead, their findings highlighted poor reduction quality and inadequate maintenance of the reduction as key factors associated with AVN development.

Growing evidence suggests a link between orthopedic procedures, including internal fixation [6,25,26] and arthroscopic rotator cuff repair [27], and traumatic humeral head osteonecrosis. A systematic review found that the deltopectoral approach for humeral head internal fixation had a significantly higher AVN rate (odds ratio, 4.06) than the anterolateral deltoid-split approach [26]. A larger incision and extensive soft tissue dissection are required for the deltopectoral approach, leading to a greater risk of blood vessel damage. Conversely, the deltoid-split approach minimizes dissection and avoids areas with significant blood vessels [26]. However, a subsequent meta-analysis that incorporated additional studies found no significant difference in AVN rates between the two approaches [28].

Medications and Substance Abuse

Corticosteroid use is the most commonly reported nontraumatic cause of humeral head AVN, with its prevalence in AVN cases ranging up to 38% [4,8]. A retrospective study of 215 shoulders found that osteonecrosis developed on average 15 months after steroid initiation [29]. The pathogenesis of corticosteroid-induced AVN is primarily explained by two theories: one suggests that corticosteroids increase circulating fats, leading to fat emboli that disrupt bone circulation, and the other posits that corticosteroids promote adipogenesis, fat cell hypertrophy, osteocyte apoptosis, and reduced osteoclast and osteoblast differentiation, resulting in increased intraosseous pressure and vascular compression [8,18,23]. Corticosteroids have also been implicated in angiogenesis inhibition and the induction of a hypercoagulable state that further contribute to thrombosis and vascular insufficiency [6].

Interestingly, genetic predisposition could play a role. Seven genetic variants that increase susceptibility to corticosteroid-induced osteonecrosis have been identified [18]. In patients with acute lymphoblastic leukemia who are being treated with glucocorticoids, polymorphisms in the ACP1 gene, which helps regulate lipid levels and osteoblast differentiation, and in the GRIN3 and GRIK1 genes, which encode glutamate receptor subunits that can ultimately affect the activation of osteoblast receptors, have been associated with an increased risk of osteonecrosis [30,31]. Other genes that have been implicated include VDR, TYMS, SERPINE1, and BCL2L11, although results for those genes have been mixed [32].

The pathogenesis of alcohol-induced osteonecrosis is thought to parallel that of corticosteroid-induced osteonecrosis. Alcohol abuse has been associated with elevated baseline cortisol levels, increased bone cholesterol content, and fat emboli formation, all of which contribute to vascular disruption [8,18,23]. Evidence suggests that excessive alcohol consumption has direct toxic effects on osteocytes [8]. Animal studies have demonstrated that chronic alcohol intake promotes adipogenesis and suppresses hematopoiesis, impairing bone homeostasis [6]. Moreover, alcohol-induced vascular changes, including venous stasis and increased intraosseous pressure, have been implicated in the progression to bone necrosis [23].

Hematologic

Hematologic conditions, particularly sickle cell disease, are well-established causes of osteonecrosis due to impaired blood circulation. Sickle cell disease is an autosomal recessive genetic disorder caused by a mutation in the β-globin gene [33]. Sickle-shaped red blood cells have impaired rheology, leading to aggregation within blood vessels and blood flow obstruction that ultimately causes microinfarcts, tissue ischemia, and subsequent bone necrosis [6,18,33,34]. Bedair et al. [34] described how these infarcts typically occur in the medullary cavities and epiphyses, with hypoxic cell death causing the disruption of cell membranes, apoptosis of osteocytes, and impaired phagocytosis. This process results in the development of osteosclerotic strands, bone marrow edema, and bone loss that ultimately leads to bone collapse.

In general coagulopathy, Von Willebrand factor and tissue factor activate platelets and the coagulation cascade to form clots [35]. Assouline-Dayan et al. [8] expanded on the role of coagulopathy in osteonecrosis, noting that various etiologies—particularly familial thrombophilia, hypersensitivity reactions, organ rejection, bacterial endotoxins, antiphospholipid antibodies, pancreatitis, pregnancy, and malignancy—can lead to microvascular coagulation, venous thrombosis, and arterial occlusion, which all contribute to AVN.

Infectious

Infectious causes of humeral head AVN have been identified, particularly in the context of meningococcemia complicated by disseminated intravascular coagulation (DIC) [36] and human immunodeficiency virus (HIV) [37]. Meningococcal endotoxin triggers a cascade of harmful effects that can lead to DIC. It activates coagulation factors and prompts the release of granulocyte procoagulant materials and inflammatory cytokines such as tumor necrosis factor-alpha and interleukin-1. This process ultimately damages endothelial cells and activates platelets and the complement system, setting the stage for DIC [38].

Borges et al. [39] reviewed the records of 73 HIV-positive patients with AVN and found that AIDS-defining illnesses, opportunistic infections, and cancers were independently associated with an increased risk of osteonecrosis. HIV has been associated with elevated immunoglobulin E (IgE) [40], which is one significant factor in the multifactorial link between HIV and osteonecrosis. Higher IgE correlates with increased Th2-type cytokines in HIV patients, and they contribute to the destabilization and rupture of atheromatous plaques. IgE also activates platelets by binding to FcεRI and FcεRII receptors. This binding initiates a cascade that leads to thrombin activation, thrombin-antithrombin III complex formation, and the development of intravascular thrombi and emboli [37].

Metabolic

Metabolic derangement can compromise the vasculature and perfusion of the humeral head. Gaucher disease is an autosomal recessive lysosomal storage disorder caused by mutations on chromosome 1q22 that lead to β-glucocerebrosidase (β-glucosidase) deficiency [41]. It leads to an inability to break down glucocerebroside and thus to an abnormal accumulation of it in macrophage lysosomes, which are termed “Gaucher cells” [5]. This accumulation of lipid-laden Gaucher cells in the bone marrow is hypothesized to cause osteonecrosis by elevating intraosseous pressure or directly compressing vessels [18,23].

Environmental

Dysbarism is caused by sudden pressure changes, which can lead to nitrogen-induced adipose injury and air emboli that obstruct the humeral head vasculature. For example, during a dive, increased pressure causes continuous nitrogen uptake into the blood. Upon resurfacing, those nitrogen bubbles rapidly expand, which can injure adipose tissue and collapse vessels, ultimately leading to AVN [5,6,18,23]. Prompt hyperbaric treatment is crucial for preventing dysbarism osteonecrosis, with delays longer than 6 hours linked to elevated rates of disease [42].

Clinical Presentation

AVN of the humeral head is often indolent and asymptomatic in its early stages, leading many patients to present with advanced disease at the time of diagnosis. Pain is typically the first symptom, and patients sometimes experience a painful "click" during shoulder movement as a result of joint incongruity, the presence of a cartilage flap, or large loose bodies within the joint. The pain often disrupts sleep, significantly impairs range of motion (ROM), and limits the ability to do physical work. In later stages of the disease, physical examination can reveal tenderness to palpation and pain, particularly with arm abduction or elevation to 90°, which places the maximal load on the glenohumeral joint [3-6,9].

IMAGING

Radiographs are typically the first imaging modality used to evaluate humeral head AVN, though they have limitations in detecting early disease (Fig. 1A). Standard radiographic views include the anteroposterior, axillary, and Grashey views of both internal and external rotation [5]. Radiographs are sufficient for diagnosing late-stage disease [3], and findings can include cystic and sclerotic changes, subchondral lucency (often referred to as “crescent sig,” shown in Fig. 1B, D, and F), and signs of joint collapse or degenerative changes [6,14]. To improve detection, additional imaging modalities such as magnetic resonance imaging (MRI), selective angiography, and skeletal scintigraphy can be used [8].

MRI is highly sensitive and specific for diagnosing AVN, with reported sensitivities and specificities of 99% [6,14]. It excels in detecting early changes (Fig. 1C, E), making it ideal for screening, diagnosis, and monitoring progression after treatment. Key MRI findings suggestive of AVN include osseous low-signal intensity on T1-weighted images and high-signal intensity on T2-weighted images, often with joint effusion [6]. Additional signs include a low-intensity signal in osteonecrotic regions on both T1 and T2 images and the "double-density" sign, characterized by a low signal line at the periphery of the lesion with a more centrally located high-signal band, on T2 images. Gadolinium-enhanced MRI is particularly effective for assessing osteonecrosis, which demonstrates no increase in uptake after contrast administration [8].

The extent of humeral head involvement on MRI correlates with the risk of collapse [4]. Sakai [17] evaluated 46 shoulders and found that 11/12 lesions that had a necrotic angle greater than 90° on both mid-oblique coronal spoiled gradient recalled echo pulse sequence (SPGR) images and mid-oblique sagittal SPGR progressed to humeral head collapse, whereas 34/34 lesions with a necrotic angle less than 90° did not collapse (Fig. 2).

Other imaging modalities include skeletal scintigraphy, single photon emission computed tomography (SPECT), and CT. Skeletal scintigraphy is useful for the early diagnosis of AVN due to its sensitivity to increased osteoblastic activity and blood flow, but it can miss advanced disease due to decreased metabolism from lack of blood flow. SPECT is also used, but it has low resolution, making it difficult to differentiate AVN from conditions such as fractures or osteoporosis [8]. CT is rarely used for AVN diagnosis, but it can detect subchondral fractures [6].

CLASSIFICATION

The progression of shoulder AVN was first described by Cruess as a modification of the Ficat classification for AVN of the femoral head (Table 2) [43]. Stage I is characterized by a normal radiographic appearance. In stage II, sclerosis and a mottled pattern emerge on the humeral head, with well-localized subchondral osteolytic defects. Stage III is marked by the crescent sign, indicating the coalescence of subchondral lesions and the beginning of subchondral bone collapse. Stage IV involves the collapse of the subchondral bone, when necrotic bone is resorbed by blood vessels from adjacent healthy bone, creating a void above the necrotic area. This process causes the articular cartilage to reattach to the collapsed bone, resulting in joint incongruity. Finally, stage V represents the complete degeneration of the glenohumeral joint, leading to advanced joint destruction.

The inter- and intra-rater reliability of the Cruess system has not been studied directly, but the Ficat classification on which it is based has been found to have high inter- and intra-rater reliability ranging from 0.85–0.9 [44]. Classification and staging are used to guide treatment choices, and accuracy has been shown to have significant effects on patient outcomes [44]. Decompression is generally the treatment of choice in the pre-collapse stages [3,10,11,14,45,46], and arthroplasty or resurfacing is used for the post-collapse stages [11,47-49].

NONOPERATIVE TREATMENT

Conservative treatments that address the underlying pathology through lifestyle changes, such as reducing alcohol and corticosteroid use when feasible, can be used for stages I and II of osteonecrosis. Other options include symptomatic management through activity modification, physical therapy, nonsteroidal anti-inflammatory drugs, hyaluronic acid, and cortisone injections [4,14,50,51]. However, conservative management is largely ineffective. For example, a retrospective review of 30 shoulders with AVN treated conservatively found that only half had satisfactory global, pain, function, and satisfaction outcomes at the 10-year follow-up, and the other half had very poor outcomes and went on to have surgery or significant dysfunction [52]. A systematic review comparing nonoperative treatment with core decompression for avoiding arthroplasty found that the mean success rate of core decompression was 76.6% in stages I through III, whereas the success rate for nonoperative treatment was only 10.3% [10]. Overall, studies indicate that conservative management generally yields poor outcomes across all stages of AVN [10], with the results being particularly unfavorable as the disease progresses beyond stage II [4,6].

SURGICAL TREATMENT

A wide range of procedures is used to treat AVN of the humeral head: arthroscopic debridement, core decompression, vascularized bone grafting, resurfacing, and arthroplasty.

Arthroscopic Debridement

Arthroscopic debridement and related techniques have shown positive results for early-stage AVN of the humeral head, especially stages I–III [53,54]. However, this technique is seldom used in isolation. It is most often used in conjunction with core decompression techniques because it does not alter the underlying pathophysiology.

Core Decompression

Core decompression is a widely used treatment for early-stage AVN, particularly stages I and II, that aims to relieve intraosseous pressure and improve blood flow by drilling tunnels into the necrotic bone, a process that stimulates neovascularization [3,45]. Various approaches, such as lateral percutaneous with fluoroscopy and an open anterior approach, are used (Fig. 3) [3,6,45].

Both the arthroscopic and open techniques for core decompression have been shown to significantly improve function, reduce pain, and prevent arthroplasty [55-59], and they have also been found to be efficacious in the pediatric population [50]. One systematic review indicated that core decompression is most effective in the early, pre-collapse stages, with success rates declining in more advanced stages [11]. That finding is supported by a study that used the University of California, Los Angeles (UCLA) shoulder rating system to evaluate 64 shoulders treated with open core decompression. Success was defined as achieving at least 24 out of 30 points on the UCLA rating system and preventing arthroplasty. The results showed a success rate of 94% in stage I, 88% in stage II, 70% in stage III, and only 14% in stage IV [55]. It is critical to counsel patients on the effects that core decompression appears to have on the natural history of AVN. In patients with stage I and II AVN, delaying surgery and simply monitoring symptoms can be problematic because the progression of symptoms often comes with collapse, progression to stage III AVN, and the need for more invasive procedures.

Core decompression has been coupled with biologic augments; however, the results of such augmentation have been somewhat contentious. Various techniques, including calcium phosphate augmentation, bone marrow aspirate concentrate injection, and autografts, have been described [14,46,60-63]. Calcium phosphate replaces necrotic bone with a sound structure, encouraging revascularization and reossification [60]. Bone marrow aspirate introduces multipotent mesenchymal stem cells that can differentiate into new bone and potentially halt osteonecrosis progression [61].

Both vascularized and nonvascularized bone grafts have been used in the treatment of osteonecrosis, although their use in humeral head AVN is limited. Vascular bone grafts have been described in the use of femoral head AVN as a way to provide structural support, enhance revascularization and osteogenic potential, and arrest the progression of necrosis. Non-vascularized bone grafts lack the ability to revascularize the necrotic area, but they can nevertheless promote bone remodeling and healing [64,65].

Case studies show promising outcomes with vascularized scapula grafts for the treatment of humeral head AVN. For example, a 17-year-old female with stage III AVN had full ROM and pain resolution 73 months after a vascularized scapula graft was placed [62]. Another case report indicates favorable outcomes in a 27-year-old male 36 months after the procedure [64]. The scapula offers anatomical advantages, including a 14-cm lateral border of straight cancellous bone and two pedicles, the circumflex scapular artery, and the angular branch of the thoracodorsal artery [65]. The procedure involves harvesting the graft with its vascular supply, and then inserting it through a bone tunnel to support the subchondral bone [62,64].

Several studies have also shown good outcomes with fibular strut allografts. This procedure involves drilling a hole into the necrotic lesion and inserting a fibular strut allograft to stabilize the bone and prevent collapse [66]. A retrospective review of eight pre-collapse and six post-collapse shoulders treated with core decompression and fibular allograft strut placement found similar pre- and postoperative ROM and functional scores between the two groups, although two stage II shoulders and one stage IV shoulder were ultimately converted to hemiarthroplasty (HA) [67].

Arthroplasty

Various types of arthroplasty have been used to treat AVN of the humeral head, including HA, anatomic total arthroplasty (aTSA) and reverse total shoulder arthroplasty (rTSA). These options are typically reserved for cases of subchondral collapse after joint preservation has failed (Fig. 4).

Both HA and aTSA generally yield satisfactory outcomes for humeral head AVN. Both have demonstrated significant improvements in pain and ROM for high-grade AVN [47,48,68-70]. The choice between HA and aTSA depends on several characteristics of the disease and its etiology. aTSA is generally recommended for stage V AVN, cases with glenoid cartilage wear, and posttraumatic AVN, which often is accompanied by glenoid cartilage degeneration [6,11,49], whereas HA is generally recommended for atraumatic AVN with preserved glenoid cartilage [49]. Schoch et al. [22,71] evaluated differences in patients undergoing aTSA and HA for both atraumatic and posttraumatic AVN. They found that HA tended to have lower revision rates than aTSA and that aTSA offered better pain improvement than HA in posttraumatic AVN, where glenoid erosion was present. However, increased complication and revision rates were also found in patients undergoing aTSA for posttraumatic AVN or corticosteroid-induced AVN, compared with patients undergoing HA or aTSA for other etiologies [68,72]. Although HA was found to have lower revision rates, the causes for revisions differed between the groups. One retrospective study of 64 shoulders treated with either aTSA or HA found the complication rate to be 22% in the aTSA group and only 8% in the HA group [68]. aTSA complications are typically related to instability, glenoid loosening, or humeral loosening, whereas HA complications are typically related to glenoid wear [11,47,48,68]. Despite those differences, both aTSA and HA have good long-term survival, with a 10-year survivorship rate of 80% [46].

Because glenoid erosion is one of the most common complications of HA, with incidence rates of up to 72%, pyrocarbon has been explored as a humeral head material to mitigate this risk [73]. In vitro studies have demonstrated its superior cartilage preservation, compared with cobalt-chromium and ceramic [74]. Furthermore, wear simulation against cortical bone showed that 5 million cycles of pyrocarbon produced significantly less damage to the bone counterface than cobalt-chromium did after only 320,000 cycles [75]. Pyrocarbon also exhibited substantially lower linearized bone penetration (0.28 mm/million cycles) than cobalt-chromium (12.6 mm/million cycles) in these in vitro wear tests [75]. Additional clinical research supports the reduction of glenoid erosion with pyrocarbon. A study of nine patients who underwent HA for humeral head AVN revealed an average glenoid erosion of 1.4 mm over a mean follow-up of 3.6 years [76]. The observed average erosion rate of approximately 0.4 mm per year aligns with the 0.3 mm per year of glenoid erosion reported for pyrocarbon hemiarthroplasties in conditions such as osteoarthritis. This contrasts sharply with cobalt chromium humeral head resurfacing. A separate study reviewing 38 cases, 5 of which had humeral head AVN, found an average of 5.5 mm of glenoid erosion after a mean follow-up of 5.5 years—equating to about 1 mm per year. That demonstrates a significant 60%–70% reduction in erosion with pyrocarbon compared with cobalt chromium implants, though it is important to note the small sample sizes [77,78].

Typically, rTSA is reserved for cases with rotator cuff insufficiency, while aTSA remains the more common choice for younger patients without rotator cuff insufficiency [49]. Nonetheless, rTSA provides outcomes comparable to aTSA for treating humeral head AVN [6,49]. Studies indicate that rTSA generally results in greater improvements in abduction, pain relief, and overall function than aTSA, whereas aTSA produces greater improvements in internal rotation, though the differences are often modest [49]. Notably, rTSA carries a lower risk of complications than aTSA in cases in which clinical factors limit the use of conventional aTSA [6,49]. The reported complications of rTSA include infection, dislocation, acromial fracture, and scapular fracture [49,79], whereas aTSA is more commonly associated with instability, as well as humeral and glenoid component loosening [11,47,48,68]. A systematic review of 12 studies shows that both procedures are effective for humeral head AVN, with success rates from 54% to 100%. This wide variability stems from the differing definitions of success used across studies, which included UCLA scores, Neer rating system scores, patient satisfaction, radiological scales, and the prevention of reoperation [11]. The research for rTSA for humeral head AVN is limited, but that might change because rTSA has been increasing in popularity, and its indications have been expanding [80].

CONCLUSIONS

AVN of the humeral head is a multifactorial condition with various underlying etiologies that range from trauma and orthopedic procedures to medications and hematologic disorders, among many others. Despite its relatively rare occurrence, the disease's progressive nature and the risk of joint collapse underscore the importance of early diagnosis and appropriate management. Cruess's staging system remains a crucial tool for classifying disease severity and guiding both nonoperative and surgical interventions. Although conservative treatment can help with symptom management in the early stages, outcomes worsen as the disease advances, and advanced disease requires surgical interventions such as core decompression, bone grafting, or arthroplasty. Future research should continue to explore advances in treatments such as biologic augmentation and pyrocarbon arthroplasty, as well as advanced imaging techniques to enhance early detection and improve the long-term outcomes of patients with humeral head AVN.

NOTES

Author contributions

Conceptualization: EK, GN, SF, DS. Writing – original draft: EK, GN. Writing – review & editing: E EK, GN, SF, KK, DS. All authors read and agreed to the published version of the manuscript.

Conflict of interest

None.

Funding

None.

Data availability

None.

Acknowledgments

None.

Fig. 1.

Paired radiographic (A, B), T1-weighted (C, D), and T2-weighted (E, F) magnetic resonance imaging (MRI) images of a 29-year-old male with sickle cell disease. The left column (A, C, E) shows images taken before bilateral core decompression. The right column (B, D, F) shows images taken 3 years later, demonstrating the progression of avascular necrosis and development of a crescent sign (indicated by red arrows). Note that the initial MRI sequences (C, E), which were acquired approximately 1 month after the initial radiograph (A), offer better sensitivity than plain radiographs for detecting the early signs of avascular necrosis. The outcome following subsequent hemiarthroplasty is shown in Fig. 4.

Fig. 2.

Measuring the necrotic angle on the mid-oblique sagittal view: point O marks the center of the humeral head, points A and B mark the two endpoints of the necrotic lesion. The necrotic angle is defined as <AOB [17].

Fig. 3.

A 27-year-old male with left shoulder stage II osteonecrosis with preoperative anteroposterior and Grashey views (A, B). An arthroscopic evaluation was performed under fluoroscopy to triangulate the placement of a drill guide for core decompression (C). The final intraoperative fluoroscopy demonstrated the appropriate placement of bone marrow aspirate concentrate into the pathologic region, indicated by the red arrow (D). Radiographs taken 14 months postoperatively demonstrate improved radiographic appearance without subchondral collapse (E, F).

Fig. 4.

Postoperative axial and anteroposterior radiographs from a 29-year-old male with sickle cell disease who received pyrocarbon hemiarthroplasty to treat progressive humeral head avascular necrosis 3 years after core decompression. Significant pain relief and improved range of motion were observed 3 months after hemiarthroplasty

Table 1.

Most common etiologies of humeral head AVN

Etiology	Example
Trauma	Proximal humeral fracture, internal fixation, arthroscopic rotator cuff repair
Iatrogenic	Corticosteroids
Hematologic	Sickle cell disease, coagulopathy
Substance abuse	Excessive alcohol consumption
Infectious	Meningococcemia, human immunodeficiency virus
Metabolic	Gaucher’s disease
Environmental	Dysbarism
Other	Pancreatitis [18], systemic lupus erythematosus [8], vascular endothelial growth factor-inhibitors [19], influenza vaccine [20]

AVN: avascular necrosis.

Table 2.

Cruess classification of humeral head avascular necrosis with characteristic imaging appearance [6,8,43,50,51]

	Stage	Radiographic appearance
Pre-collapse	Stage I	Normal radiographic appearance
Pre-collapse	Stage II	Cystic or sclerotic changes without collapse
Post-collapse	Stage III	Crescent sign, subchondral fracture plane
	Stage IV	Collapse of subchondral bone, flattening of the humeral head
	Stage V	Glenohumeral joint degeneration and arthritis

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