Microscopic histopathology of chronic refractory lateral epicondylitis* WILLIAM

From

REGAN,† MD, LESTER

E.

WOLD,‡ MD,

†private practice, London, Ontario, Canada, the ‡Division of Pathology and ∥Department of Orthopaedics, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, and §private practice, Durham, North Carolina tissue and coined the term &dquo;angiofibroblastic hyperplasia&dquo; to describe this pathologic process. To complicate the description of the micropathology even further, the clear description of the normal tendon injected with steroid shows somewhat similar features, including collagen fiber disruption, lymphocyte infiltration, and lipid-laden histiocytes with fibroblastic proliferation.’,&dquo; The questions remain: What, if any, are the characteristic histologic features of chronic lateral epicondylitis? Do the abnormalities represent an inflammatory or an ongoing degenerative process? Is there evidence of repair? Why is there chronic pain? Does nerve entrapment play a role?12,&dquo;,22 With one exception,&dquo; all previous studies have attempted to answer these questions in a retrospective manner by observing tissue removed at surgery for chronic refractory epicondylitis without use of controls. No reports have systematically and statistically analyzed the features of the surgical specimen versus a control group. Hence, the goal of this study was to define the precise and characteristic histologic features of surgically treated chronic refractory lateral epicondylitis. With single-blind randomization of control and patient specimens, two questions were addressed : 1) are there any typical microscopic pathologic changes characterizing the excised tissue; and 2) is there an objective means of grading the above in an attempt to correlate pathologic features with the pain syndrome encountered clinically to help permit insight to its etiology.’

ABSTRACT The histopathologic features from 11 patients who were treated surgically for lateral epicondylitis were graded and compared to similar tissue from 12 cadaveric specimens. All studies were done by a single pathologist who had no knowledge of the origin of the specimen. The surgical specimens were interpreted as abnormal in all 11 specimens, and all 12 of the control specimens were reported as being without histologic abnormality. Vascular proliferation was present in 10 of 11 and focal hyaline degeneration was recorded in all 11 of the surgical specimens. Neither feature was present in any of the control material (P < 0.001). These data suggest that chronic refractory lateral epicondylitis requiring surgery is a degenerative rather than inflammatory process. This may account for the lack of response to rest and antiinflammatory medication.

spite of its frequency, considerable controversy exists regarding the exact etiology and histopathology of the clinical entity &dquo;lateral epicondylitis.&dquo; While most authors have placed the macroscopic changes at the extensor carpi radialis brevis origin, the microscopic features, which have been widely described, have yet to be precisely defined.’-&dquo; leo,12-15 In

Prior observations have described nous

periostitis,’

subtendi-

granulation tissue,l° or bursitis.16,20 These microscopic

studies of the extensor carpi radialis brevis origin were expanded by Coonrad and Hooper,6 who described tendon necrosis and round cell infiltration with foci of calcification and scar tissue. Recently, Nirschp3-15 described the histopathology as invasion of fibroblasts and vascular granulation *

Presented at the annual meeting of the Canadian

MATERIALS AND METHODS The surgical specimens from 11 consecutive primary procedures for lateral epicondylitis were obtained from two surgeons (BFM and RC). All patients were unequivocally diagnosed as having lateral epicondylitis that was refractory to conservative treatment. The average patient age was 40 years (range, 19 to 56). The time from symptom onset to surgery averaged 26.2 months (range, 7 to 96). Physical

Orthopedic Association,

Toronto, Ontano, June, 1989 1

RALPH COONRAD,§ MD, AND BERNARD F. MORREY,∥ a MD

Address correspondence and reprnt requests to. Bernard F Mayo Clinic, 200 First Street, SW, Rochester, MN 55905

Morrey, MD, 746

747

examination of this group showed typical signs of lateral epicondylitis, including pain localized to the lateral epicondyle. There were no signs of neurologic involvement in any patient. The indication for surgery was chronic pain refractory to conservative treatment (nonsteroidal antiinflammatory medications, activity modification, physiotherapy, and bracing). Ten of 11 had at least 1 cortisone injection with a mean of 3.5 injections (range, 0 to 12). At surgery, macroscopic changes at the origin of the

carpi radialis brevis were observed in all patients. Four of the 11 (36%) had involvement of the common extensor origin as well. The excised specimen was preserved for microscopic analysis in 10% buffered formalin. Twelve unembalmed and radiographically normal cadaveric specimens were used as controls. Age, gender, and clinical status was not available for this group. The extensor carpi radialis brevis tendinous origin was harvested in a manner similar to the operative procedure. Each was marked for proximal-distal orientation and fixed in neutral buffered formalin. All of the specimens were embedded in paraffin prepared in 7 JIm-thick sections and stained with H&E for extensor

histologic analysis. A list of 15 microscopic pathologic features, reported as characteristic of lateral epicondylitis, was collected from the literature (Table 1). All of the specimens were reviewed in a single-blind, randomized manner by a single pathologist (LEW). Each histologic feature was graded subjectively as follows: Grade 0, no involvement; Grade 1, mild involvement ; Grade 2, moderate involvement; and Grade 3, marked involvement. Each characteristic was graded and categorized and a diagnosis was made of lateral epicondylitis or normal tissue. Statistical analysis of all features was performed by nonparametric analysis using the median test.

RESULTS The correct

microscopic diagnosis, with at least one pathologic finding noted in each (Table 2), was made in all 11 of the surgical specimens. None of the controls were incorrectly TABLE 1

Histopathologic

features

reported to be associated with epicondylitis

lateral

interpreted as pathologic. The common features of the surgical specimens included vascular proliferation and hyaline degeneration; fibroblastic proliferation and calcific debris were also regularly seen (Table 2). In the cadaveric controls, there were two cases of isolated vascular proliferation graded as mild with no other abnormal histologic features noted. The highest grade in the surgical specimens was noted for vascular proliferation (Fig. 1); hyaline degeneration tended to be of lower grade, but was present in every patient specimen (Fig. 2). Both changes are statistically different from controls (P < 0.001). Patients with calcific debris (Fig. 3) had received 2, 3, or 12 steroid injections preoperatively and calcific debris was graded as marked in all three. Specifically, none of the 11 surgical specimens demonstrated histologic evidence of subtendinous granulation tissue or inflammatory cells. Only 1 surgical specimen had mild cellular infiltrate and histiocyte response. This was the patient who had received 12 cortisone injections preoperatively. There was no evidence of new or old hemorrhage, tendon necrosis, fibrinoid degeneration, polymorphonuclear leukocytes, lipid-laden histiocytes, lymphocytes, or crystalline debris noted in either operative or control specimens. After single-blind randomization, lateral epicondylitis was correctly diagnosed in all cases and easily distinguished from controls.

DISCUSSION In 1873, Runge first described the clinical entity known as lateral epicondylitis.’ The condition occurs more commonly in nonathletic, middle-aged females’* 9 10,13-15 and generally responds successfully to a variety of conservative regimens.2~s,a,m ~s The percentage of cases that prove resistant to conservative care or the passage of time range from 4% to 10%.2°5’l,ls The extensor carpi radialis brevis origin has been cited by many authors6,7,9,13-15 as the primary site of abnormalities. The average time from symptom onset to surgery ranges from 12 to 51 months.6,15 The traditional indication for surgery has been a failure of nonoperative management, including steroid injection. This is important in the selection process for surgical candidates since the confounding variables of steroid deposition and chronicity will influence the histologic character of the pathologic tissue. There is little question that definitive pathologic changes occur with chronic epicondylitis, as evidenced by the 100% success rate of the pathologist in making the diagnosis from pathologic and control material. That none of the 12 controls was misread as abnormal is strong evidence of the distinctive histologic character of the surgical material. Traditionally, an invasion of round cells, fibroblasts, and vessels in tufts that suggest granulation tissue have been considered pathognomonic of epicondylitis. 10 Another study revealed 9 of 11 patients, with no evidence of macroscopic tear, had microscopic findings of round cell infiltration, scattered foci of calcification, and scar tissue with marginal areas of cystic degeneration.~ This study emphasized tendon necrosis as a feature of epicondylitis. ’:II,+, .,¿,

748 TABLE 2

Histopathologic characteristics of 11 patients operated

&dquo;

See text for grading scale. All specimens deposition, leucocytes, and lymphocytes.

were

rated Grade 0 for fibronoid

for lateral

epicondylitis

degeneration, granulation tissue, fascial necrosis, cryastalline

Figure 1. Vascular proliferation was a regular feature of the surgically treated patients, occurring in 10 of 11 patients in that group, but

was

present in

none

of the control material.

Extensor aponeurotic tendon disruption has been described grossly6,7 and is consistent with our microscopic findings of fibroblastic proliferation and focal hyaline degeneration (P < 0.01). On the other hand, there was no evidence of an inflammatory component in our material. The vascular proliferation has been observed before and has been termed angiofibroblastic hyperplasia by Nirschl and Pettrone&dquo; However, no inflammatory cells were present in our material to justify considering this an inflammatory process. It should be noted that our findings are consistent with the microscopic changes noted in rabbit Achilles tendon injected with steroid,1,21 which show hyaline degeneration without an inflammatory response. The possibility exists, therefore, that the cortisone injections may have contributed to the microscopic spectrum of chronic refractory lateral epicondylitis reported here. In a histologic study of lateral epicondylitis, Sarkar and Uhthoff18 demonstrated mesenchymal cells and a plethora of tenoblasts, representing a reactive state with ongoing repair of a degenerative process. Our study concurs with

Figure 2. Focal hyaline degeneration was present in surgical specimens, but in none of the control tissue.

all 11I

these

observations, revealing evidence of an immature reparative process set in a background of focal hyaline degeneration. The interpretation of these findings does not allow a ready explanation of the cause of pain in this condition. There does appear to be a lack of healing of the initial insult that may be considered analogous to the similar condition of the patellar tendon seen in &dquo;jumper’s knee.&dquo; The lack of an inflammatory response may be caused by the effect of the steroid or the chronicity of the process. This may also be responsible for the lack of tendon healing, which may be the feature that distinguishes those refractory cases requiring surgery. CONCLUSIONS The characteristic histologic features of chronic refractory lateral epicondylitis that requires surgical intervention in-

749

REFERENCES 1. Balasubramaniam P, Prathap K The effect of injection of hydrocortisone into rabbit calcaneal tendon J Bone Joint Surg 54B. 729-734, 1972 2 Bernhang AM The many causes of tennis elbow N Y State J Med 79.

1363-1366,1979 3. Bosworth DM Surgical treatment of tennis elbow A follow-up study J Bone Joint Surg 47A 1533-1536, 1965 4 Bosworth DM The role of the orbicular ligament in tennis elbow J Bone Joint Surg 37A 527-533, 1955 5 Boyd HB, McLeod AC Tennis elbow J Bone Joint Surg 55A 1183-1187, 1973 6 Coonrad RW, Hooper WR Tennis elbow Its course, natural history, conservative and surgical management J Bone Joint Surg 55A 1177-

1182,1973 7

8 9 10 11

Figure 3. Calcific debris (arrow) was seen in only three patients who had an average of 3.7 cortisone injections (range, 2 to 12). clude vascular and fibroblastic proliferation accompanied by focal hyaline degeneration of the aponeurotic origin of the extensor carpi radialis brevis tendon. These changes are more characteristic of a degenerative than an inflammatory process. The injection of steroid may well account, in part, for these changes. It is possible that this histopathologic picture accounts for the lack of response to antiinflammatory medication. It is also possible that those instances without histologic healing remain painful, thus requiring surgery.

12

Cyriax JH

The pathology and treatment of tennis elbow J Bone Joint Surg 18 921-940, 1936 Froimson Al Treatment of tennis elbow with forearm support band J Bone Joint Surg 53A 183-184, 1971 Garden RS Tennis elbow J Bone Joint Surg 43B 100-106, 1961 Goldie I Epicondylitis lateralis humeri (epicondylalgia or tennis elbow). A pathogenetical study Acta Chirg Scand (Suppl) 339 1-119, 1965 Kaplan EB The etiology and treatment of epicondylitis Bull Hosp Jt Dis 29 77-83,1968 Kaplan EB Treatment of tennis elbow (epicondylitis) by denervation J

Bone Joint Surg 41A 147-151,1959 Defining and treating "tennis elbow"Contemp Surg 10 (2):

13 Nirschl RP

13-17,1977 14 Nirschl RP Tennis elbow Orthop Clin North Am 4 787-800, 1973 15 Nirschl RP, Pettrone FA Tennis elbow The surgical treatment of lateral epicondylitis J Bone Joint Surg 61A 832-839, 1979 16 Osgood RB Radiohumeral bursitis, epicondylitis, epicondylalgia (tennis elbow) Arch Surg 4 420-433, 1922 17 Roles NC, Maudsley RH Radial tunnel syndrome Resistant tennis elbow as a nerve entrapment J Bone Joint Surg 548 499-508, 1972 18 Sarkar K, Uhthoff H Ultrastructure of the common extensor tendon in tennis elbow Virchows Arch (Pathol Anat] 386 317-330, 1980 19 Spencer GE, Herndon CH Surgical treatment of epicondylitis J Bone Joint

Surg 35A 421-424, 1953 20 Stack JK Acute and chronic bursitis in the region of the elbow joint Surg Clin North Am 29 155-162, 1949 21 Unverferth LJ, Olix ML The effect of local steroid injections on tendon J Sport Med 1(4) 31-37, 1973 22 Werner C-O Lateral elbow pain and posterior interosseous nerve entrapment Acta Orthop Scand (Suppl) 174. 1-62, 1979

Microscopic histopathology of chronic refractory lateral epicondylitis.

The histopathologic features from 11 patients who were treated surgically for lateral epicondylitis were graded and compared to similar tissue from 12...
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