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DOI:10.2214/AJR.05.1477
AJR 2007; 188:1094-1098
© American Roentgen Ray Society


Clinical Observations

Chondrolysis of the Glenohumeral Joint After Arthroscopy: Findings on Radiography and Low-Field-Strength MRI

Timothy G. Sanders1,2, Michael B. Zlatkin1,3, Narayan Babu Paruchuri1,3 and Robert W. Higgins4

1 National Musculoskeletal Imaging, 1930 N Commerce Pkwy., Suite 5, Weston, FL 33326.
2 Uniformed Services University of the Health Sciences, Bethesda, MD.
3 Department of Radiology, University of Miami, Jackson Memorial Hospital, Miami, FL.
4 Amarillo Sports Medicine and Orthopedic Center, Amarillo, TX.

Received August 22, 2005; accepted after revision October 10, 2005.

 
Address correspondence to T. G. Sanders (radmantgs{at}cs.com).


Abstract
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
OBJECTIVE. The purpose of this report is to describe the clinical and imaging findings of chondrolysis of the glenohumeral joint.

CONCLUSION. In the appropriate clinical setting, both radiographs and MR images of the shoulder can be used to establish the diagnosis of chondrolysis of the glenohumeral joint.

Keywords: injury • MRI • musculoskeletal system • shoulder • sports medicine


Introduction
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Rapid-onset chondrolysis is a condition in which widespread chondrocyte death occurs within a joint over a relatively short time. The hip and the knee have been reported to be affected most often. The condition usually follows exposure of the articular cartilage to a substance that is toxic to chondrocytes and causes extensive chondrocyte death. In the knee and hip, exposure to chlorhexidine and methylmethacrylate has been shown to lead to rapid and diffuse chondrocyte death [1-4]. There have been several case reports of rapid-onset chondrolysis of the shoulder after arthroscopy. Although the cause is uncertain, this complication appears to occur most commonly in young patients who have undergone shoulder reconstructive procedures to manage shoulder instability [5-7].

Glenohumeral chondrolysis is devastating and difficult to manage because it typically occurs in young athletes. Extensive loss of articular cartilage progresses to severe osteoarthritis of the shoulder, which causes loss of range of motion and pain with any movement of the involved joint. Treatment is initially supportive, but arthroplasty eventually may be necessary.

We present four cases of rapid-onset chondrolysis of the glenohumeral joint after arthroscopy. Each of the four patients, like five patients described in other reports, was young (14-32 years old) and had undergone arthroscopic surgery for shoulder instability. These four patients all did well during surgery and during the initial postoperative recovery period. There were no reported variations from the standard of care during the arthroscopic procedures. Three months after surgery, one patient began to report limitation of overhead activity and decreased internal rotation. By six months after surgery, two patients began to report decreased range of motion. The fourth patient was lost to follow-up until 2 years after arthroscopy, but when he sought treatment, he had been experiencing pain and decreased range of motion for many months. The common clinical presentation among these four patients was pain out of proportion to that expected in the normal postoperative period and progressive loss of the normal range of motion of the shoulder.


Materials and Methods
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
The cases of four patients in whom rapid-onset chondrolysis of the glenohumeral joint developed after shoulder arthroscopy were retrospectively evaluated (Table 1). Preoperative and postoperative clinical notes and surgical procedure notes were reviewed in each case. All four patients had undergone preoperative MRI of the shoulder, and two patients had undergone preoperative shoulder radiography. After onset of symptoms in the postoperative period, all four patients underwent repeated shoulder radiography, and two patients also underwent follow-up MRI. Each of the imaging studies was reviewed in consensus by two musculoskeletal radiologists.


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TABLE 1: Clinical Information

 

Preoperative MRI examinations showed a fibrous Bankart lesion in patients 1 and 4. Minimal nonspecific cystic changes in the greater tuberosity of the humeral head were found in patient 3, but the findings were otherwise unremarkable. Preoperative MRI of patient 2, a collegiate baseball catcher, revealed findings consistent with the diagnosis of posterior superior glenoid impingement with a superior labral anteroposterior tear that extended into the posterior inferior labrum, minimal partial-thickness undersurface tear of the infraspinatus tendon, and cystic changes within the posterior lateral aspect of the humeral head. In all four patients, preoperative MRI showed normal articular cartilage of the glenohumeral joint with no chondral thinning or surface irregularity and no changes in signal intensity in the subchondral bone marrow. Preoperative radiographs of the shoulders of patients 3 and 4 showed no significant abnormality of the glenohumeral joint. Specifically, the radiographs of both patients showed a normal glenohumeral joint space with no narrowing or cortical irregularity and no subchondral radiolucency or sclerosis. The standard radiographs obtained for each patient in the preoperative and postoperative periods included anteroposterior views with internal and external rotation, a true anteroposterior view of the glenohumeral joint (Grashey view), and an axillary view.


Figure 1
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Fig. 1A —32-year-old man with chondrolysis of shoulder after arthroscopy. Preoperative T1-weighted axial (A) and axial STIR (B) MR images of shoulder show normal articular cartilage (arrows) and subchondral marrow signal intensity.

 


Figure 2
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Fig. 1B —32-year-old man with chondrolysis of shoulder after arthroscopy. Preoperative T1-weighted axial (A) and axial STIR (B) MR images of shoulder show normal articular cartilage (arrows) and subchondral marrow signal intensity.

 


Figure 3
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Fig. 1C —32-year-old man with chondrolysis of shoulder after arthroscopy. T1-weighted axial (C) and axial STIR (D) images 2 years after surgery show extensive joint space narrowing (long arrow) and loss of normal articular cartilage on both sides of joint with cortical irregularity and patchy areas of change in signal intensity in subchondral marrow (short arrows) consistent with subchondral sclerosis and marrow edema involving osseous glenoid process and, to lesser extent, humeral head.

 


Figure 4
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Fig. 1D —32-year-old man with chondrolysis of shoulder after arthroscopy. T1-weighted axial (C) and axial STIR (D) images 2 years after surgery show extensive joint space narrowing (long arrow) and loss of normal articular cartilage on both sides of joint with cortical irregularity and patchy areas of change in signal intensity in subchondral marrow (short arrows) consistent with subchondral sclerosis and marrow edema involving osseous glenoid process and, to lesser extent, humeral head.

 
In each case, the preoperative and postoperative MRI examinations were performed on a 0.2-T system (Magnetom Jazz, Siemens Medical Solutions). Sequences included axial and coronal T1-weighted spin-echo images (TR/TE, 650-750/26; bandwidth, 0.6 Hz; field of view, 159-179 mm; matrix size, 192 x 176; slice thickness, 4.0-5.0 mm; gap, 0.0 mm; acquisition time, 7 minutes 54 seconds), axial and coronal STIR images (1,210-1,380/16; bandwidth, 0.6 Hz; field of view, 159-179 mm; matrix size, 192 x 176; slice thickness, 4.0-5.0 mm; gap, 0.0 mm; acquisition time, 8 minutes 31 seconds), axial gradientecho images (50/18; bandwidth, 0.6 Hz; field of view, 159 mm; matrix size, 192 x 160; slice thickness, 3.1 mm; gap, 0.0 mm; acquisition time, 8 minutes 8 seconds), and sagittal and coronal T2-weighted images (1,920/80; bandwidth, 0.6 Hz; field of view, 159 mm; matrix size, 192 x 168; slice thickness, 4.0 mm; gap, 0.0 mm; acquisition time, 8 minutes 41 seconds).


Results
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Each of the four patients had undergone an arthroscopic procedure for glenohumeral instability as summarized in Table 1. All four patients did well during surgery, and there was no reported variation from the standard of care during the arthroscopic procedure or during the immediately postoperative period. Each patient had the normal expected immediately postoperative course. Three months after surgery, one patient began reporting shoulder pain and limitation of overhead activity with decreased internal rotation. Six months after surgery, two patients began reporting decreased range of motion; however, only one of these patients reported associated pain with shoulder motion. At a postoperative follow-up visit 1 month after surgery, the fourth patient had normal findings and then was lost to follow-up for 2 years. Two years after surgery, the patient returned, reporting that for several months he had experienced decreased range of motion and severe pain with any movement of the shoulder.

All four patients underwent follow-up radiography of the shoulder, and two underwent follow-up MRI at the time of onset of postoperative symptoms. Postoperative MR images of the two patients showed extensive diffuse loss of articular cartilage of the glenoid process and humeral head, the most significant changes being on the glenoid side of the joint (Figs. 1A, 1B, 1C, 1D and 2A, 2B, 2C, 2D). Focal areas of subchondral cortical irregularity were found in the region of the osseous glenoid process and the medial aspect of the humeral head. In addition, focal areas of decreased T1-weighted signal abnormality corresponded to areas of increased and decreased T2-weighted signal intensity in the subchondral region of the glenoid process and medial aspect of the humeral head, likely representing areas of focal subchondral marrow edema and subchondral sclerosis. Minimal glenohumeral joint effusion was found during one examination, and the other examination revealed no substantial accumulation of joint fluid. No evidence of synovitis and no loose body or debris were found within the glenohumeral joint. No marginal osteophyte formation was detected.


Figure 5
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Fig. 2A —19-year-old man with chondrolysis of shoulder after arthroscopy. T2-weighted axial (A) and coronal STIR (B) images show superior labral anteroposterior tear (arrow, B) that extends posteriorly to involve posterior labrum (arrow, A). Articular cartilage and subchondral marrow of both osseous glenoid process and humeral head are normal.

 

Figure 6
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Fig. 2B —19-year-old man with chondrolysis of shoulder after arthroscopy. T2-weighted axial (A) and coronal STIR (B) images show superior labral anteroposterior tear (arrow, B) that extends posteriorly to involve posterior labrum (arrow, A). Articular cartilage and subchondral marrow of both osseous glenoid process and humeral head are normal.

 

Figure 7
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Fig. 2C —19-year-old man with chondrolysis of shoulder after arthroscopy. Axial (C) and coronal (D) T1-weighted images obtained 11 months after surgery show joint space narrowing (long arrow) and loss of articular cartilage with extensive subchondral sclerosis and marrow edema (short arrows) diffusely involving osseous glenoid process and, to lesser degree, medial aspect of humeral head.

 

Figure 8
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Fig. 2D —19-year-old man with chondrolysis of shoulder after arthroscopy. Axial (C) and coronal (D) T1-weighted images obtained 11 months after surgery show joint space narrowing (long arrow) and loss of articular cartilage with extensive subchondral sclerosis and marrow edema (short arrows) diffusely involving osseous glenoid process and, to lesser degree, medial aspect of humeral head.

 

Postoperative radiographs of all four patients showed marked joint space narrowing with extensive subchondral sclerosis and patchy areas of subchondral radiolucency compared with the preoperative radiographs (Figs. 3A, 3B and 4A, 4B, 4C, 4D). Areas of cortical thinning and irregularity also were found. These changes appeared most prominent in the region of the superior glenohumeral joint. The most extensive involvement was found in the areas of the superior medial aspect of the humeral head and the adjacent superior aspect of the osseous glenoid process. No loose intraarticular bodies or marginal osteophytes were found.


Figure 9
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Fig. 3A —18-year-old man with chondrolysis of shoulder after arthroscopy. Preoperative anteroposterior radiograph of shoulder shows normal-appearing glenohumeral joint with joint space (arrows) well preserved.

 

Figure 10
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Fig. 3B —18-year-old man with chondrolysis of shoulder after arthroscopy. Follow-up anteroposterior radiograph 6 months after surgery shows extensive narrowing (long arrows) of joint space. Extensive subchondral sclerosis is present, and subchondral cyst formation (short arrows) involves medial aspect of humeral head and osseous glenoid process.

 

Figure 11
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Fig. 4A —14-year-old girl with chondrolysis of shoulder after arthroscopy. Preoperative anteroposterior (A) and axillary (B) radiographs of shoulder show normal joint space (arrows).

 

Figure 12
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Fig. 4B —14-year-old girl with chondrolysis of shoulder after arthroscopy. Preoperative anteroposterior (A) and axillary (B) radiographs of shoulder show normal joint space (arrows).

 

Figure 13
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Fig. 4C —14-year-old girl with chondrolysis of shoulder after arthroscopy. Follow-up anteroposterior (C) and axillary (D) radiographs 6 months after surgery show extensive joint space narrowing (long arrows) with subchondral sclerosis and cyst formation (short arrows) diffusely involving medial aspect of humeral head and osseous glenoid process.

 

Figure 14
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Fig. 4D —14-year-old girl with chondrolysis of shoulder after arthroscopy. Follow-up anteroposterior (C) and axillary (D) radiographs 6 months after surgery show extensive joint space narrowing (long arrows) with subchondral sclerosis and cyst formation (short arrows) diffusely involving medial aspect of humeral head and osseous glenoid process.

 
The clinical and imaging findings in these four cases were considered diagnostic of glenohumeral chondrolysis. For this reason, histologic evaluation and cultures were not performed. Because of their young ages, these patients were treated with conservative palliative measures, including physical therapy in an attempt to maintain range of motion and pain control with nonsteroidal antiinflammatory drugs. Total shoulder replacement may be necessary.


Discussion
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Abstract
Introduction
Materials and Methods
Results
Discussion
References
 
Chondrolysis is a devastating condition in which cell death of chondrocytes results in irreversible loss of articular cartilage and leads to rapidly progressive and extensive osteoarthritis of the joint. Chondrolysis of the hip was first reported in 1930 and has been reported to involve the shoulder, hip, knee, and ankle [8]. In most instances, the mechanism leading to cell death remains poorly understood. In some cases, however, exposure of the articular surface to a toxic substance is the clear etiologic factor. In nearly all instances, rapid destruction of the articular cartilage occurs on both sides of the joint and leads to the clinical presentation of progressively worsening pain, decreased range of motion, and stiffness of the joint.

Chondrolysis of the hip has been reported after intraarticular leakage of methylmethacrylate in the management of benign subchondral cyst [3]. It also has been reported to occur in the hip after trauma and epiphyseolysis [9]. Chondrolysis has occurred after various hip procedures, including transfer of the greater trochanter and rotational acetabular osteotomy, and after penetration of the articular surface of the femoral head with pins placed through the femoral neck [9]. The exact mechanism leading to chondrocyte death was unclear in most of these cases, but some authors [10, 11] have suggested a mechanism whereby deposition of immunocomplexes causes an autoimmune response against the articular cartilage and synovitis develops. A single case of idiopathic chondrolysis of the ankle after arthroscopy and bupivacaine (Marcaine, Sanofi) pump placement has been reported [11]. No known toxic substance was introduced into the joint in that case. Chondrolysis of the knee after accidental chlorhexidine irrigation during arthroscopy has been reported [1, 2].

There have been only a few case reports of chondrolysis involving the glenohumeral joint. In 1997, two cases were reported after color test-assisted rotator cuff repair. In that procedure, gentian violet was introduced into the joint in an attempt to identify a small fullthickness tear of the rotator cuff that was not readily apparent at surgery [12]. Five cases of glenohumeral chondrolysis have been reported in two separate series.

Although the exact cause of development of chondrolysis is unclear, this condition has been most commonly reported in young patients who have undergone shoulder reconstructive procedures to manage shoulder instability. There has been some suggestion in the literature that glenohumeral chondrolysis may be related to the use of thermal or radiofrequency energy within the glenohumeral joint. One scientific study [7] showed that marked cellular death occurs in human chondrocytes after energy application with radiofrequency probes. However, not every reported case of acute glenohumeral chondrolysis has been associated with exposure to thermal energy [5, 6].

A retrospective review [13] of 14,277 thermal procedures on the shoulder revealed no cases of chondrolysis of the glenohumeral joint. Other causal agents in glenohumeral chondrolysis being considered include use of a bupivacaine pump after shoulder arthroscopy, an unknown infectious agent, and an event during arthroscopy that triggers an immune response and subsequent migration of inflammatory cells into the glenohumeral joint [6, 11]. Use of bioabsorbable materials within the joint, mechanical trauma to the joint during arthroscopy, and chemical trauma to the hyaline cartilage have been suggested as etiologic factors that may be associated with acute chondrolysis of the glenohumeral joint [6]. In each of our four cases, thermal energy was used as either a primary method of capsulorrhaphy or as an adjunct to suture capsulorrhaphy. In these cases, thermal energy may have been an etiologic factor in chondrolysis.

In our series of patients, postoperative radiographs showed rapidly progressive and uniform loss of the glenohumeral joint space. Diffuse subchondral sclerosis was found on both sides of the joint. The subchondral changes in the humeral head appeared most prominent along the medial aspect of the humeral head opposite the superior glenoid process. Focal areas of subchondral cortical irregularity and subchondral cyst formation were found within both the osseous glenoid process and the humeral head. In all four cases, there was a noticeable lack of osteophyte formation, which is a hallmark of osteoarthritis and may be helpful in differentiating this entity from radiographic findings of osteoarthritis.

Findings of glenohumeral chondrolysis on MRI are similar to the radiographic findings: extensive uniform narrowing of the joint space and extensive loss of articular cartilage on both sides of the joint. Once again, the most important area of involvement of the humeral head is the medial border opposite the superior aspect of the glenoid process. Cortical irregularity can be seen on both sides of the joint, focal areas of both increased and decreased T2-weighted signal intensity corresponding to focal areas of low T1-weighted signal intensity. These areas of subchondral change in signal intensity likely represent areas of subchondral marrow edema and sclerosis. A small joint effusion was present in a single case, but no intraarticular debris or loose intraarticular body was identified, and no evidence of synovitis was found on MRI. It is generally accepted that MRI with a highfield-strength magnet more accurately depicts articular cartilage abnormalities. In our cases, however, diffuse chondral loss coupled with underlying cortical irregularity and changes in signal intensity in the subchondral marrow were adequately depicted with a low-field-strength magnet, and we confidently established the diagnosis of chondrolysis of the glenohumeral joint.

Because radiography and MRI showed similar findings in glenohumeral chondrolysis after arthroscopy, radiography alone appears adequate for establishing the diagnosis in the proper clinical setting. However, the main differential possibilities in this clinical setting are those of infectious versus reactive synovitis. These entities typically manifest as a thickened, enhancing capsule, large joint effusion, cartilage loss, subchondral cyst formation and erosions, and MRI may be helpful in differentiating chondrolysis and infectious synovitis if there is clinical concern about infection [14]. These entities were not considered as diagnostic possibilities in our cases, so histologic evaluation and cultures were not performed.

At times, the interpreting radiologist may not have the history of recent arthroscopic surgery or the preoperative studies for comparison. In these cases, the presence of centrally located chondrolysis with subchondral marrow edema and sclerosis in the absence of osteophyte formation, a relative absence of joint effusion, and synovitis are important imaging features that can help differentiate chondrolysis from other entities, such as osteoarthritis, juvenile rheumatoid arthritis, and septic arthritis.

Chondrolysis of the glenohumeral joint is a devastating postoperative complication that can occur after shoulder arthroscopy. Radiologists should be aware of this complication because in the proper clinical setting the radiographic and MRI findings of chondrolysis are quite specific.


References
Top
Abstract
Introduction
Materials and Methods
Results
Discussion
References
 

  1. Van Huyssteen AL, Bracey DJ. Chlorhexidine and chondrolysis in the knee. J Bone Joint Surg Br 1999;81 : 995-996[CrossRef][Medline]
  2. Douw CM, Bulstra SK, Vandenbroucke J, Geesink RG, Vermeulen A. Clinical and pathological changes in the knee after accidental chlorhexidine irrigation during arthroscopy: case report and review of the literature. J Bone Joint Surg Br 1998;80 : 437-440[CrossRef][Medline]
  3. Leclair A, Gangi A, Lacaze F, et al. Rapid chondrolysis after intra-articular leak of bone cement in treatment of a benign acetabular subchondral cyst: an unusual complication of percutaneous injection of acrylic cement. Skeletal Radiol 2000;29 : 275-278[CrossRef][Medline]
  4. Rowe LJ, Ho EK. Idiopathic chondrolysis of the hip. Skeletal Radiol 1996;25 : 178-182[CrossRef][Medline]
  5. Levine WN, Clark AM, D'Alessandro DF, Yamaguchi K. Chondrolysis following arthroscopic thermal capsulorrhaphy to treat shoulder instability. A report of two cases. J Bone Joint Surg Am2005; 87:616 -621[Free Full Text]
  6. Petty DH, Jazrawi LM, Estrada LS, Andrews JR. Glenohumeral chondrolysis after shoulder arthroscopy: case report and review of the literature. Am J Sports Med 2004;32 : 509-515[Free Full Text]
  7. Caffey SC, McPerson E, Moore B, Hedman T, Vangsness CT Jr. Effects of radiofrequency energy on human articular cartilage. Am J Sports Med 2005; 33:1 -5
  8. Duncan JW, Nasca R, Schrantz J. Idiopathic chondrolysis of the hip. J Bone Joint Surg Am 1979;61 : 1024-1028[Abstract/Free Full Text]
  9. Abril JC, Calvo E, Castillo F, Alvarez L. Chondrolysis of the hip after transfer of the greater trochanter. J Pediatr Orthop 1998; 18:242 -245[CrossRef][Medline]
  10. Garcia AD, Fernandez PL, Gonzalez MP, et al. Idiopathic chondrolysis of the hip: long-term evolution. J Pediatr Orthop 1999; 19:449 -454[CrossRef][Medline]
  11. Bojescul JA, Wilson G, Taylor DC. Idiopathic chondrolysis of the ankle. Arthroscopy 2005;21 : 224-227[Medline]
  12. Tamai K, Higashi A, Cho S, Yamaguchi T. Chondrolysis of the shoulder following a "color test"-assisted rotator cuff repair: a report of two cases. Acta Orthop Scand1997; 68:401 -402[Medline]
  13. Wong KL, Williams GR. Complications of thermal capsulorrhaphy of the shoulder. J Bone Joint Surg Am 2001;83 [suppl 2]:151 -155[Medline]
  14. Weishaupt D, Schweitzer ME. MR imaging of septic arthritis and rheumatoid arthritis of the shoulder. Magn Reson Imaging Clin N Am 2004; 12:111 -124[CrossRef][Medline]

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