Skip to main content
NCBI home page
JSES Reviews, Reports, and Techniques logoLink to JSES Reviews, Reports, and Techniques
. 2025 Jan 15;5(2):243–250. doi: 10.1016/j.xrrt.2024.12.005

The Buford complex: a review of embryology, imaging, technical considerations, and clinical significance

Jay Moran a, Peter Y Joo a, Kinjal Vasavada a, Ryan Cheng a,b,∗, Sarah Levitt a, Joseph E Manzi c, Saarang Patel a, Robert Cecere b, Jack Porrino a,d, Lee D Katz a,d, Andrew E Jimenez a, Michael J Medvecky a
PMCID: PMC12047549  PMID: 40321863

Abstract

The Buford complex, defined as a cord-like middle glenohumeral ligament with an absence of the anterosuperior labrum, is the rarest anatomical labral variant of the shoulder and occurs in 1.5% to 6.5% of the general adult population. Misidentifying the Buford complex for a pathological anterosuperior labral tear can result in pain, stiffness, and limited external rotation if accidentally surgically repaired. While the Buford complex was historically thought to be a benign anatomical variant, recent evidence has suggested that patients with a Buford complex may be at a higher risk for sustaining superior labrum anterior-posterior tears compared to those without a Buford complex. In addition, it remains unknown if the Buford complex is a congenital variant or one that pathologically develops from untreated shoulder instability in early childhood. Given these recent findings and their potential implications on management, it is important for surgeons to have a thorough understanding of the Buford complex. The current review aims to describe the anatomy, development, preoperative imaging, technical considerations, and clinical significance of the Buford complex.

Keywords: Buford complex, Middle glenohumeral ligament, Anterosuperior labrum, Shoulder anatomy, Embryology, Anatomic variants

Improvement in diagnostic technology, such as higher resolution 3 Tesla magnetic resonance imaging (MRI), magnetic resonance arthrography, and arthroscopy, has enhanced the anatomical knowledge of glenohumeral joint. As a result, anatomical variants of the labrum, capsule, and glenohumeral ligaments (GHLs) within the shoulder and their associated pathologies have been better defined and understood in recent years.2,9,21,23, 24, 25, 26 The GHLs, which can vary in origin, size, and appearance, are thickenings of the shoulder capsule that attaches to the glenoid and stabilizes the humerus as it moves away from the midline.9 The middle glenohumeral ligament (MGHL) is a specific anterior stabilizer that extends off the articular side of the subscapularis muscle, attaches at the 3 o’clock position on the glenoid, and contributes to the upper portion of the anterior labrum.

The Buford complex, a rare congenital or developmental anatomic variant, has both an absent anterosuperior labrum from the 1 to 3 o’clock position on the glenoid and an MGHL that is thickened and commonly described as cord-like.20,23,28 The unusual appearance of the Buford complex may lead a surgeon to misinterpret this variant with a sublabral foramen or a pathological anterosuperior labral detachment. In 1994, Williams et al was first to describe the Buford complex and reported on an aberrantly repaired cord-like MGHL to the anterior glenoid rim which resulted in severely restricted range of motion that necessitated multiple revision procedures for lysis of adhesions.28 Since William’s original report, it was universally accepted within the orthopedic community that Buford complexes are benign anatomical variants that should be left in situ.

More recent clinical studies have suggested that patients with a Buford complex are at a higher risk of sustaining superior labrum anterior-posterior (SLAP) tears when compared to control shoulders without a Buford complex.5,14 Furthermore, it remains unknown if the Buford complex is a congenital variant or one that pathologically develops from untreated shoulder instability in early childhood. This newer evidence has called into question the prior dogma of the seemingly benign finding of the Buford complex, and some have proposed modified surgical techniques that address the Buford complex in the setting of SLAP tears. Given these recent findings and their potential implications on management, it is important for surgeons to have a thorough understanding of the Buford complex. The current review aims to describe the anatomy, development, preoperative imaging, technical considerations, and clinical significance of the Buford complex.

Anatomy

The soft-tissue portions of the glenohumeral joint consist of the capsule, the 3 GHLs, and the labrum. The GHLs consist of the superior glenohumeral ligament (SGHL), MGHL, and the inferior glenohumeral ligaments (IGHLs) (Fig. 1). The SGHL has been found to have the most consistent anatomy of all the GHLs, with 90% to 98% of patients containing this ligament with varying degrees of thickness.9 Anatomically, the SGHL runs from the superior aspect of the labrum and coracoid process to the superior portion of the lesser tuberosity of the humerus at the medial ridge of the intertubercular fossa. The SGHL traverses along and around the long head of the biceps brachii tendon and blends in with the coracohumeral ligament. From a functional standpoint, the SGHL acts as a sling for the humerus, preventing anterior-inferior translation of the humerus relative to the glenoid when the arm is in an adducted and externally rotated position.9

Figure 1.

Figure 1

Open in a new tab

Drawing of the lateral view of the labral-ligamentous complex to illustrate the normal anatomy of the joint, including the superior glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and the anterior and posterior bands of the inferior glenohumeral ligament (IGHL). Note the insertion of the long head of the biceps tendon (BT) in the superior labrum.

In contrast to the SGHL, the MGHL has the most variability in terms of diameter, shape, and attachments and is seen in 60% to 85% of individuals.9,27,28 For the majority of patients, the MGHL commonly arises inferior to the SGHL at the anterosuperior labrum and inserts into the anatomic neck of the humerus just medial to the lesser tuberosity. The MGHL can be absent in up to 37% of specimens studied, and the origin of the MGHL has been found to arise from various areas of the labrum, the SGHL, the long head of the biceps tendon, or various combinations.3,9,27,28 When the MGHL is present, it acts to resist anterior and posterior translation of the humerus in 45° of abduction with external rotation.9,27

The IGHL is also present in the majority of individuals (72% to 93%) and is the thickest GHL consisting of 2 bands—the posterior and anterior bands—that make up the borders of the axillary pouch.9,27 The ligament originates at the anterior-inferior and posterior-inferior margins of the glenoid labrum, and attaches to the inferior aspect of the anatomical neck of the humerus. Biomechanically, the anterior band of the IGHL restricts anterior and inferior translation of the humerus in 90° of abduction and in external rotation, whereas the posterior band of the IGHL restricts posterior and inferior translation of the humerus when held in adducted and internally rotated position.9,27

The labrum is a fibrocartilaginous structure that circumferentially attaches to the glenoid rim, and also provides a site of attachment for the GHLs. It has been hypothesized that the anterosuperior labrum may be derived from a different embryological origin compared to the rest of the labrum due to the increased susceptibility to injury and variation in this area.11,19,22 The anterosuperior labrum increases the stability of the shoulder by increasing the glenoid depth and maintaining a negative intra-articular pressure within the glenohumeral joint. Anatomically, the anterosuperior labrum is variable with reports demonstrating a mobile labrum in 26% of patients, a sublabral foramen in 11.9%, complete absence of labral tissue in the anterosuperior region in 1.5%, and a sublabral recess in as many as 85% of shoulders.21 It is important to note that a sublabral foramen is defined as complete detachment of the labrum from the glenoid, while a sublabral recess or sulcus is characterized as a labrum that is lifted off the glenoid at the articular surface but maintained with a deeper attachment.16,21

Anterosuperior glenoid variants often include both the labrum and the MGHL and have been classified as type I: cord-like MGHL without sublabral foramen, type 2: sublabral foramen without a cord-like MGHL, type 3: sublabral foramen with a cord-like MGHL, and type 4: absent anterosuperior labrum with the anterior aspect of the superior labrum continuous with a cord-like MGHL (Buford complex).12 A study by Ilahi et al arthroscopically evaluated 334 shoulders, and found that 35.3% had an anterosuperior glenoid variant, of which 27.1% were type 1, 22.9% were type 2, 28.8% were type 3, and 21.2% were type 4.12 The type 4 anterosuperior glenoid variant is called the Buford complex (Fig. 2).

Figure 2.

Figure 2

Open in a new tab

Anterosuperior glenoid anatomical variants: (A) Standard, classical anatomy of the region. (B) Type 1, variant with a cord-like MGHL and no sublabral foramen. (C) Type 2: variant with a sublabral foramen but without a cord-like middle glenohumeral ligament. (D) Type 3: variant with a sublabral foramen with a cord-like middle glenohumeral ligament. (E) Type 4 (Buford complex): variant with an absent anterosuperior labrum and the anterior aspect of the superior labrum continuous with a cord-like middle glenohumeral ligament. MGHL, middle glenohumeral ligament.

The true prevalence of the Buford complex has been widely debated, with reports ranging from 0.3%-9%.5,6,13,17,19,26,28 The discrepancy is likely due to differences in patient inclusion criteria in these studies, with most studies retrospectively evaluating only patients who had received arthroscopic shoulder surgery, with or without shoulder instability. Furthermore, it is probable that the variation is a result of nonuniformity in nomenclature and recognition of this complex, as some studies used the terminology of “Buford complex” for a cord-like MGHL but had no mention of an absent anterosuperior labrum (Fig. 3).

Figure 3.

Figure 3

Open in a new tab

Depicts the Buford complex with an absent anterosuperior labrum and a “cord-like” middle glenohumeral ligament. BT, biceps tendon; SGL, superior glenohumeral ligament; MGL, middle glenohumeral ligament; IGL, inferior glenohumeral ligament.

Embryological/development of the Buford complex

The SGHL is the first GHL to form from the capsular tissue embryologically. Before 10 weeks of age, Gardner and Gray noted that the SGHL is first seen in an embryo, with a thickening of the capsule region deep to the supraspinatus tendon.11 The low variability in the SGHL across populations may be due to this being the first structure to form. The SGHL did not appear as a free band in any of the fetal specimens studied, but rather as a thickened area of the capsule.

Around this time, the labrum also forms from 6 weeks to 8 weeks.10,11 Interestingly, at 8 weeks, a deficient area of the anterior superior labrum deep to the coracoid process is seen, while the rest of the circumference continues to develop. It has been postulated that the anterior superior labrum is derived from the synovial mesenchyme, separate from the rest of the labrum, as this portion forms later and does not adhere to the cartilage of the glenoid at this stage.10,11,21 Further anatomic studies have shown that this stage is where the variability branches with most individuals developing a continuous labral ring that later attaches fully to the glenoid, some developing the ring but without attachment (sublabral foramen), and others remaining completely deficient of the anterior superior labrum.8,10,11

By 12 weeks, the labrum is noted to be thickened, except in the anterior superior aspect, where it appears to be meniscus-like.11,21 The MGHL also forms around this time and originates from a similar attachment as the SGHL, with 2 distinct condensations of the capsule. The first appears as a fold of the capsule and the second as cellular tissue that attaches to the subscapularis muscle. By the 13th week, all GHLs are more sharply defined. The MGHL has variability as a free band or as a thickening of the capsule, which is dependent on the location of the subscapular bursa.8,10,11 Interestingly, the subscapular bursa develops separately from the rest of the shoulder joint, unlike most bursae in the shoulder joint which are present early in the fetal period and develop along with the other components of the joint.6 At around 16 weeks, the subscapular bursa usually starts communicating with the cavity between the SGHL and MGHL, forming a subscapular recess.6 If the subscapular bursa was located between the SGHL and the MGHL, the synovial tissue surrounded the MGHL, and it appears as a free band. Otherwise, it appears as a thickening of the capsule that is continuous and inseparable from the SGHL and IGHL.

The cord-like MGHL in the Buford complex may be a result of the subscapular bursa surrounding the MGHL early on in embryological development.11 Gardner and Gray found that the appearance of the MGHL as a discrete band was due to the presence and location of the bursal openings into the joint cavity, with the MGHL appearing thick when the opening for the subscapularis bursa was not present between the superior and middle ligaments.11 The embryological link between the location of the subscapular bursa and the anterior superior labrum has not yet been examined. Interestingly, just as the MGHL has been reported as the most variable GHL in adult shoulders, Gardner and Gray reported that the MGHL is the most variable in appearance of the fetal capsular ligaments.11 It is thought that the variations of the GHLs could be attributed to the dissociated and irregular collagen fiber organization in the capsular region between the subscapularis and supraspinatus muscles, and this fibrous tissue maturing into more organized tissue and ligaments is a result of the stresses on the tissue.17 The MGHL was usually thinner and more difficult to discern as a distinct structure, which could potentially be related to the higher variability in development.17

By week 16, the labrum changes in microscopic appearance, with the superior aspect becoming more fibrous and vascular, while the rest of the labrum takes on a more fibrocellular appearance.21 Embryologic arthroscopic studies have found variability in detachment of the anterior superior labrum from the glenoid and reported a prevalence of 10%.22 While there is evidence that shoulder variations arise early on during fetal development, there remains a paucity of imaging or arthroscopic studies on the early development of the shoulder ligaments or labrum and the derivatives of these structures that cause such variability.

The embryological developmental patterns can result in anatomic variants isolated to one shoulder, both shoulders, and even different variants in both shoulders.12 Ilahi et al reported 13 patients who underwent bilateral shoulder arthroscopy and reported 8 of them had a variant in at least 1 shoulder and only 4 of them had variants in both shoulders.12 Of the 4 patients with variants in both shoulders, only 1 patient had symmetric morphology with the Buford complex present bilaterally, while the other 3 patients had different anterosuperior glenoid variants.12

Finally, it is relatively unknown whether the Buford complex is a developmental variant or a congenital variant. Recent literature has postulated that the Buford complex may be developmental in nature and a result of shoulder instability in early childhood rather than a benign congenital abnormality. In 2024, Scott et al examined the prevalence of Buford complexes and sublabral foramens in 122 children (mean age of 6.4 years) who underwent MRI for an indication other than glenohumeral instability and reported that one showed evidence of a sublabral foramen, while none showed evidence of a Buford complex. The authors used a published rate of 6.5% for sublabral foramen and Buford complex in adults to calculate the expected rates in their patient population of children. Their reported results significantly differed from the expected 8 and 23 children who should have had a Buford complex or sublabral foramen, respectively.20 This evidence potentially suggests that the Buford complex could be developmental in nature from early childhood instability; however, more evidence, especially arthroscopic evaluation rather than MRI, is needed to further build on these findings.

Identification on preoperative imaging

MRI is widely used to assess various soft tissue pathologies of the shoulder.25 Magnetic resonance arthrogram (MRA) is considered the gold standard and most sensitive modality for diagnosing labral pathologies.5 This was demonstrated by Bents and Skeete who reported that MRA has a 93% sensitivity for non-Buford complex SLAP tears and 100% sensitivity for SLAP lesions in patients with Buford complexes.5 However, with the improvement in MRI technology, such as magnet strength, optimized coils, and improved signal to noise, the popularity and trend of obtaining an MRA has decreased substantially over the last decade.1 Regardless of conventional MRI versus MRA, MRI is an important step for recognizing a Buford complex and associated pathologies during the preoperative period.

Shoulder MRIs are commonly obtained with a 1.5 or 3 T magnet strength scanner using a phased-array shoulder coil with the patient laying supine with their arm in slight external rotation.25,26 The Buford complex is best seen on axial images.25,26 Tuite et al examined the sensitivity of MRI for diagnosing the Buford complex in patients with arthroscopic confirmation and noted a sensitivity of 0.94 and a specificity of 0.80, with an accuracy of 0.90.25,26

It is important to distinguish between labrum tears and normal anatomical variants. Labral tears can present with imaging characteristics such as a lateral orientation of the abnormal high-signal intensity on oblique coronal images, irregular margins, more than 2 mm depth of separation from the glenoid articular surface, and/or extension of the abnormal signal posterior to the biceps tendon.22 On the other hand, normal variants demonstrate medially oriented high-signal intensity on oblique coronal images, smooth margins, minimal separation, and normal dark labral signal.

The location of an anterior labrum variant or tear, whether it is below or above the 3 o’clock position, may provide valuable evidence for identifying a Buford complex on MRI.18,25,28 Multiple studies have reported that absent anterior-superior labrum in a Buford complex should not extend inferior to the anterior glenoid notch, which is between the 2 and 3 o’clock positions, and divides the upper one-third of the glenoid from the lower two-thirds.25,28 In agreement with Palmer et al, Tuite et al reported that only 6% of patients with arthroscopically confirmed Buford complexes or sublabral foramens had absent labrum that extended inferiorly past the anterior glenoid notch.18,21,25,26 An unattached or absent anterior-superior labrum that is isolated above this point on MRI appears to be highly indicative of anatomical variant.18,21,25,26 In addition, identification of the thick or cord-like MGHL on oblique sagittal images can aid in confirming the diagnosis of Buford complex on MRI (Fig. 4).

Figure 4.

Figure 4

Open in a new tab

MRI arthrogram T1W-FS demonstrating the Buford complex. (A) Axial image demonstrating Buford complex (yellow arrow) and sublabral foramen (white arrow). (B) Sagittal image demonstrating cord-like middle glenohumeral ligament (yellow arrow) and sublabral foramen (white arrow). MRI, magnetic resonance imaging.

Clinical relevance and technical considerations

It is important to note that identification of the Buford complex is best done at the time of arthroscopy (Fig. 5).20 As previously mentioned, it is still unknown whether the Buford complex is a benign congenital variant or a pathological one that develops from an untreated shoulder injury or instability in early childhood. Scott et al recently speculated that early shoulder injury during childhood or adolescence may result in separation of the anterosuperior labrum and glenoid.20 Moreover, the robust healing potential of children allows the separated labrum to join with the MGHL to form a cord-like structure. Further comparative anatomic studies are needed to prove this concept, as it is only speculative in nature. 20

Figure 5.

Figure 5

Open in a new tab

Demonstrates an arthroscopic image from the posterior viewing portal of the Buford complex with (i) absence of anterior-superior labrum, (ii) cord-like middle glenohumeral ligament. A = glenoid surface; B = humeral head. This image is from an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).7

The clinical association between Buford complex and SLAP tears has been reported in various adult studies to date.5,12,13 Ozer et al examined 3129 consecutive shoulder arthroscopies and reported on 83 (2.65%) patients with SLAP tears and Buford complexes.17 In their analysis, the patients with a Buford complex had significantly greater odds of SLAP lesions compared to those without a Buford complex.17 However, clinical outcomes were not compared between the 2 groups.

Kaptan et al examined 843 shoulder arthroscopies and reported that SLAP lesions accompany Buford complex significantly more frequently than all other types of MGHL variants.14,17 Similarly, a recent systematic review examined 20 studies that reported on morphological features of the glenoid labrum, consisting of 7601 shoulders.4 The authors reported that a Buford complex was seen in 3.0% of patients and that these individuals had a relative risk of 2.4 (95% confidence interval: 1.3-4.7) of developing SLAP lesions, especially type II, whereas such risk for patients with a sublabral recess and sublabral foramen were not statistically significant.4 In comparison to all other anatomic variants, these findings suggest that the Buford complex may be a predisposing factor for sustaining a SLAP lesion and highlights the need for a high index of suspicion and thorough SLAP tear evaluation in patients with a Buford complex that are undergoing shoulder arthroscopy.4,14,17,20 Figure 6 demonstrates an MRI example from our institution of a patient with a Buford complex and SLAP tear.

Figure 6.

Figure 6

Open in a new tab

(A) Axial image demonstrating Buford complex (absent anterosuperior labrum and cord-like middle glenohumeral ligament, (yellow arrow)) with a SLAP tear extending into posterior labrum (white arrow). (B) Sagittal image demonstrating MGHL (yellow arrow) and SLAP tear (white arrow). SLAP, superior labrum anterior-posterior; MGHL, middle glenohumeral ligament.

There are various hypotheses on why a Buford complex could increase the chances of sustaining a SLAP tear. Biomechanically, the labrum is a system of parallel collagen fibers around the glenoid that typically works to disperse forces into hoop stresses at the periphery.23,24 The absent anterosuperior labrum and cord-like MGHL in a Buford complex can prevent an even load dispersion which leads to a more concentrated force applied to the biceps origin and superior labrum. From a clinical standpoint, this may predispose the superior labrum-biceps complex to injury when paired with acute trauma or chronic overuse mechanisms.

Since William’s original report in 1994,28 it was universally accepted that Buford complexes should undergo a standard SLAP repair without altering the Buford complex anatomy. This dogma is still the most common practice today. However, given the recent notion that Buford complexes are developmental or predispose patients to SLAP tears, leaving the Buford complex unaltered may leave the patient with the same anatomy that predisposed them to a SLAP tear in the first place. While only speculative in nature, this could increase the risk for retearing or revision surgery after SLAP repair.

It is important to note that SLAP repairs have generally fallen out of favor to biceps tendinosis; however, there is a paucity of literature that has reported on the surgical management of SLAP tears in the setting of a Buford complex. In 2011, Crockett et al sought to address the aforementioned concern and reported outcomes on 21 patients with Buford complexes and type II SLAP lesions that were treated with a modified arthroscopic repair in an effort to enhance fixation and reduce postsurgical forces on the SLAP repair.6 In their technique, the biceps anchor and superior labrum were repaired to the superior glenoid rim with 2 labral anchors. It is important to note that this SLAP repair in association with a Buford complex variant has limited or no labral tissue present anterior to the biceps anchor to repair, unlike other variants. The next step of the technique involved using the proximal segment of the cord-like MGHL to augment the SLAP repair anterior to the biceps anchor. One to 2 anchors were placed at the edge of the anterosuperior glenoid rim, and the sutures are passed through the body of the proximal robust MGHL, leaving 25% of the tissue on the medial side of the suture and 75% on the lateral side. The sutures were then tightened and the proximal end of the cord-like MGHL was brought into apposition to the glenoid. Finally, the distal MGHL was completely transected just distal to the repair site on the glenoid at the equator to prevent loss of external rotation.6

Crockett’s repair technique has 3 proposed advantages over standard SLAP repairs that leave the Buford anatomy untouched: (1) transection of the cord-like MGHL decreases the concentrated forces of the MGHL pulling at the superior labrum and biceps anchor, (2) repairing the proximal segment of the cord-like MGHL to the anterior glenoid rim enhances the SLAP repair and biceps anchor, and (3) transection and releasing of the MGHL mitigates the risk of impaired external rotation due to tightened cord-like MGHL.6 For their cohort, the mean Constant score increased from 39.7 preoperatively to 85 postoperatively at a mean of 44 months of follow-up.

The main concern with transection of the MGHL is anterior instability of the shoulder. It is generally accepted that the anterior band of the IGHL is the primary stabilizer against anterior dislocation, and not necessarily the MGHL. Crockett et al reported no loss of function, instability, or revision surgery in their cohort, and it is important to note that these findings were appreciated in 5 overhead college and 12 recreational athletes.6 While these outcomes are promising, the limitations of this study included inadequate long-term follow-up, single surgeon (vs. multiple surgeons) data, and lack of a comparison group. Recently, Cunningham et al published a technical article in 2024 on arthroscopic stabilization for anterior traumatic glenohumeral instability associated with a Buford complex.7 In their note, the cord-like MGHL is used to reconstruct a neo-labrum, associated with an anteroinferior GHL application. The authors advocated that glenohumeral stabilization using the cord-like MGHL of the Buford complex may be an efficient alternative to a bone block procedure.7 Nevertheless, higher-level studies are needed to compare standard SLAP repair techniques as well as treatment with biceps tenodesis for patients with SLAP tears and Buford complexes to better guide management.

Finally, there are also limited studies that have reported on isolated MGHL injuries in patients with a Buford complex and subsequent surgical treatment. Lee et al reported on a 50-year-old female who presented with 9 months of persistent shoulder pain and stiffness and was diagnosed with an isolated tear at the insertion site of the cord-like MGHL in Buford complex.15 The patient successfully underwent arthroscopic suture anchor repair of the cord-like MGHL back to its insertion site on the superior labrum. At 2-year follow-up, the patient demonstrated full range of motion and excellent clinical outcome scores. Further studies are also needed to assess if there is a role to repair isolated injuries to the Buford complex, as the current data have minimal validity and confined to low-evidence studies.

Conclusion

The Buford complex is the rarest anatomical labral variant of the shoulder and has been reported to occur in 1.5% to 6.5% of the general population. Confusing the Buford complex for a pathological labrum detachment can result in pain, stiffness, and limited external rotation after surgical repair. While once thought to be a benign variant, clinical studies have shown a significant association with type II SLAP tears. In these scenarios, surgical repair techniques can involve only the SLAP tear or the SLAP tear and components of the Buford complex. Given the limited data on this pathological combination, further clinical research is needed to guide proper surgical management.

Disclaimers:

Funding: No funding was disclosed by the authors.

Conflicts of interest: Jack Porrino is in the editorial or governing board of Arthritis and Rheumatology, Current Problems in Diagnostic Radiology, and Radiology Case Reports. Lee Katz is a paid consultant for Stryker. The other authors, their immediate families, and any research foundation with which they are affiliated have not received any financial payments or other benefits from any commercial entity related to the subject of this article.

Footnotes

Institutional review board approval was not required for this review article.

References

  • 1.Arora S., Popkin C.A., Wong T.T. Trends in MR arthrogram utilization at a tertiary care academic center. Curr Probl Diagn Radiol. 2023;52:346–352. doi: 10.1067/j.cpradiol.2023.02.002. [DOI] [PubMed] [Google Scholar]
  • 2.Beltran J., Bencardino J., Mellado J., Rosenberg Z.S., Irish R.D. MR arthrography of the shoulder: variants and pitfalls. Radiographics. 1997;17:1403–1412. doi: 10.1148/radiographics.17.6.9397454. discussion 1412-1405. [DOI] [PubMed] [Google Scholar]
  • 3.Beltran J., Bencardino J., Padron M., Shankman S., Beltran L., Ozkarahan G. The middle glenohumeral ligament: normal anatomy, variants and pathology. Skeletal Radiol. 2002;31:253–262. doi: 10.1007/s00256-002-0492-1. [DOI] [PubMed] [Google Scholar]
  • 4.Benes M., Kachlik D., Kopp L., Kunc V. Prevalence of the anterosuperior capsulolabral anatomical variations and their association with pathologies of the glenoid labrum: a systematic review and meta-analysis. Arch Orthop Trauma Surg. 2023;143:6295–6303. doi: 10.1007/s00402-023-04932-9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Bents R.T., Skeete K.D. The correlation of the Buford complex and SLAP lesions. J Shoulder Elbow Surg. 2005;14:565–569. doi: 10.1016/j.jse.2005.01.002. [DOI] [PubMed] [Google Scholar]
  • 6.Crockett H.C., Wingert N.C., Wright J.M., Bonner K.F. Repair of SLAP lesions associated with a Buford complex: a novel surgical technique. Arthroscopy. 2011;27:314–321. doi: 10.1016/j.arthro.2010.09.005. [DOI] [PubMed] [Google Scholar]
  • 7.Cunningham G., Cochard B., Martz P., Brandariz R. Shoulder stabilization technique using the medial glenohumeral ligament in patients with the Buford complex. Arthrosc Tech. 2024;13:102871. doi: 10.1016/j.eats.2023.10.013. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Fealy S., Rodeo S.A., Dicarlo E.F., O'Brien S.J. The developmental anatomy of the neonatal glenohumeral joint. J Shoulder Elbow Surg. 2000;9:217–222. [PubMed] [Google Scholar]
  • 9.Fox A.J.S., Fox O.J.K., Schär M.O., Chaudhury S., Warren R.F., Rodeo S.A. The glenohumeral ligaments: Superior, middle, and inferior: anatomy, biomechanics, injury, and diagnosis. Clin Anat. 2021;34:283–296. doi: 10.1002/ca.23717. [DOI] [PubMed] [Google Scholar]
  • 10.Gardner E. The prenatal development of the human shoulder joint. Surg Clin North Am. 1963;43:1465–1470. doi: 10.1016/s0039-6109(16)37130-4. [DOI] [PubMed] [Google Scholar]
  • 11.Gardner E., Gray D.J. Prenatal development of the human shoulder and acromioclavicular joints. Am J Anat. 1953;92:219–276. doi: 10.1002/aja.1000920203. [DOI] [PubMed] [Google Scholar]
  • 12.Ilahi O.A., Cosculluela P.E., Ho D.M. Classification of anterosuperior glenoid labrum variants and their association with shoulder pathology. Orthopedics. 2008;31:226. doi: 10.3928/01477447-20080301-18. [DOI] [PubMed] [Google Scholar]
  • 13.Ilahi O.A., Labbe M.R., Cosculluela P. Variants of the anterosuperior glenoid labrum and associated pathology. Arthroscopy. 2002;18:882–886. doi: 10.1053/jars.2002.36119. [DOI] [PubMed] [Google Scholar]
  • 14.Kaptan A.Y., Özer M., Alim E., Perçin A., Ayanoğlu T., Öztürk B.Y., et al. The middle glenohumeral ligament: a classification based on arthroscopic evaluation. J Shoulder Elbow Surg. 2022;31:e85–e91. doi: 10.1016/j.jse.2021.07.026. [DOI] [PubMed] [Google Scholar]
  • 15.Lee B.I., Kim Y.B., Won S.H., Hwang S.C., Choi S.W., Nho J.H., et al. Isolated tear of the cord-like middle glenohumeral ligament in Buford complex: a case report. Medicine (Baltim) 2017;96 doi: 10.1097/MD.0000000000008604. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Marcon G.F., Macedo T.A. Artifacts and pitfalls in shoulder magnetic resonance imaging. Radiol Bras. 2015;48:242–248. doi: 10.1590/0100-3984.2013.0006. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Özer M., Kaptan A.Y., Ataoglu M.B., Cetinkaya M., Ayanoglu T., Ince B., et al. The Buford complex: prevalence and relationship with labral pathologies. J Shoulder Elbow Surg. 2021;30:1356–1361. doi: 10.1016/j.jse.2020.08.037. [DOI] [PubMed] [Google Scholar]
  • 18.Palmer W.E., Brown J.H., Rosenthal D.I. Labral-ligamentous complex of the shoulder: evaluation with MR arthrography. Radiology. 1994;190:645–651. doi: 10.1148/radiology.190.3.8115604. [DOI] [PubMed] [Google Scholar]
  • 19.Rao A.G., Kim T.K., Chronopoulos E., McFarland E.G. Anatomical variants in the anterosuperior aspect of the glenoid labrum: a statistical analysis of seventy-three cases. J Bone Joint Surg Am. 2003;85:653–659. doi: 10.2106/00004623-200304000-00011. [DOI] [PubMed] [Google Scholar]
  • 20.Scott J.A., Dwek J.R., Cheng K.Y., Bryan T.P., Edmonds E.W. The Buford complex redefined: a pathologic morphology in sheep's clothing. Orthop J Sports Med. 2024;12 doi: 10.1177/23259671241252834. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Smith C., Funk L. The glenoid labrum. Shoulder Elbow. 2009;2:87–93. doi: 10.1111/j.1758-5740.2010.00050.x. [DOI] [Google Scholar]
  • 22.Tena-Arregui J., Barrio-Asensio C., Puerta-Fonollá J., Murillo-González J. Arthroscopic study of the shoulder joint in fetuses. Arthroscopy. 2005;21:1114–1119. doi: 10.1016/j.arthro.2005.05.013. [DOI] [PubMed] [Google Scholar]
  • 23.Tirman P.F., Feller J.F., Palmer W.E., Carroll K.W., Steinbach L.S., Cox I. The Buford complex--a variation of normal shoulder anatomy: MR arthrographic imaging features. AJR Am J Roentgenol. 1996;166:869–873. doi: 10.2214/ajr.166.4.8610565. [DOI] [PubMed] [Google Scholar]
  • 24.Tischer T., Vogt S., Kreuz P.C., Imhoff A.B. Arthroscopic anatomy, variants, and pathologic findings in shoulder instability. Arthroscopy. 2011;27:1434–1443. doi: 10.1016/j.arthro.2011.05.017. [DOI] [PubMed] [Google Scholar]
  • 25.Tuite M.J., Blankenbaker D.G., Seifert M., Ziegert A.J., Orwin J.F. Sublabral foramen and buford complex: inferior extent of the unattached or absent labrum in 50 patients. Radiology. 2002;223:137–142. doi: 10.1148/radiol.2231010896. [DOI] [PubMed] [Google Scholar]
  • 26.Tuite M.J., Orwin J.F. Anterosuperior labral variants of the shoulder: appearance on gradient-recalled-echo and fast spin-echo MR images. Radiology. 1996;199:537–540. doi: 10.1148/radiology.199.2.8668808. [DOI] [PubMed] [Google Scholar]
  • 27.Willen J., Mooney M., Andrews K., Ebraheim N. The glenohumeral ligaments: anatomy, clinical presentation, and review of the literature. J Orthop Ther. 2018;189:1. doi: 10.29011/2575-8241.000089. [DOI] [Google Scholar]
  • 28.Williams M.M., Snyder S.J., Buford D. The Buford complex--the "cord-like" middle glenohumeral ligament and absent anterosuperior labrum complex: a normal anatomic capsulolabral variant. Arthroscopy. 1994;10:241–247. doi: 10.1016/s0749-8063(05)80105-7. [DOI] [PubMed] [Google Scholar]

Articles from JSES Reviews, Reports, and Techniques are provided here courtesy of Elsevier

RESOURCES