We agree with Dr. Rompe's opinion that extracorporeal shock wave must remain in the hands of a physician who understands topographical anatomy and is aware of the potentially destructive effects of high-energy shock wave application.

In our institute, the shock-wave treatment is applied to the insertion of the supraspinatus tendon. It can be identified by the calcified deposit in a patient with calcified tendinopathy. In patient without a calcified deposit, the focal area is directed to the painful point.

From a review(1) about the blood supply to humeral head, the three major vessels are the arcuate artery, branches from the posterior circumflex, and the rotator cuff. Obstruction of the muscular supply and arcuate artery will precipitate necrosis. The damage may be to one of these three vessels or their branches.

Compromise of the blood supply to the humeral head can occur in one of four ways: disruption of blood vessels; injury to or compression of the arterial walls; arterial obstruction such as thrombosis and embolism; and venous outflow obstruction(2). Injuries to the vascular supply can also be classified by their site of action: intraosseous -extravascular; intraosseous-arterial; extraosseous-arterial; and venous(3). We can not identify the exact location of injury in our case.

Osteonecrosis typically follows the chronic administration of high- dose steroids, but it is impossible to predict in which patients the disease will develop. Usually, shock-wave treatment for rotator cuff tendinopathy is quite safe. We reported a case of osteonecrosis after shock-wave treatment to alert readers about this possible side effect, especially when high-energy shock wave was applied.

References:

1. Rowe LJ, Yochum TR. Hematologic and vascular disorders. In: Essentials of skeletal radiology. Philadelphia: Lippincott Williams & Wilkins; 2005. p 1484-5.

2. Mankin HJ. Nontraumatic necrosis of bone (osteonecrosis). N Engl J Med 1992;326:1473-79.

3. Hungerford DS. Pathogenetic considerations in ischemic necrosis of bone. Can J Surg 1981;24:583-8.

To The Editor:

The authors have reported a case of humeral head osteonecrosis three months after shock wave treatment to the shoulder. Theoretically, it is certainly possible that shock waves can disrupt any arterial blood supply by destroying vessels with the focal area. However, before drawing conclusions, some questions remain to be answered.

Apparently, high-energy shock waves were applied. As no calcifying tendinitis was evident in this particular case, where were the shock waves directed and how did the authors confine the area of shockwave therapy to the pathology?

RCTs have shown only an effect of shock wave treatment for tendinitis of the rotator cuff when there was a calcific deposit. In these cases the focal area is directed to the deposit which usually is located close to the major tubercle, at the insertion of the supraspinatus tendon. The MRI presented in the article show osteonecrosis at the ANTERIOR part of the humeral head, which is where the subscapularis tendon and the biceps tendon are located. Was shock wave treatment applied to the anterior aspect of the shoulder? Only then, compromise of the anterior circumflex artery is imaginable.

In conclusion, it is good that the authors point out a "maybe" threat by extracorporeal shock wave treatment. It must be clear, that shock wave treatment must remain in the hands of a physician who understands topographical anatomy and is aware of the potentially destructive effects of high-energy shock wave application. This is why shock wave treatment with an energy flux density greater 0.3 mJ/mm² per shock are to be avoided outside of controlled clinical trials.

The author(s) of this letter to the editor did not receive payment or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the author(s) are affiliated or associated.

We thank Dr.Wang for his comments. In our Institute, the depth of extracorporeal shockwave treatment for the shoulder tendonopathy is 0.5 to 1.0cm.

Osteonecrosis results from interruption of the normal blood supply to bone leading to cell death. Interruption of blood flow can be caused by intraluminal obstruction secondary to thromoembolism, sludging of blood cells, or stasis; vascular compression (vasospasm); or the physical disruption of the vessels. We agree that the insertion site of supraspinatus tendon into the greater tuberosity is far away from the anterior circumflex artery. However, if the branches of the anterior circumflex artery are damaged by the shockwave, osteonecrosis may occur. The extraosseous and intraosseous blood supply to the adult humeral head have been studied(1). There is a consistent ascending branch of the anterior humeral circumflex artery that enters the proximal humerus at the upper end of the bicipital groove or by way of its branches into the adjacent greater and lesser tuberosities. Once intraosseous, a single vessel or multiple vessels pursue a tortuous posteromedial course just below the epiphyseal scar; the single vessel has been termed the arcuate artery of Laing. The intraosseous artery has a rich periosteal vascular network but few anastomoses exist. This finding has been confirmed recently(2). The subchondral bone of the humeral head is especially vulnerable to thrombotic and embolic phenomenon, because the arterioles in this area become sinusoids that turn 180¢X to return to the intraosseous circulation and the lack of collateral blood flow also enhances this vulnerability(3).

In our patient, the osteonecrosis was diagnosed with magnetic resonance imaging three months after extracorporeal shock-wave treatment. As we mentioned in our paper, we cannot completely exclude the possibility of idiopathic osteonecrosis in our patient. However, the timing of the finding on magnetic resonance imaging in relation to the extracorporeal shock-wave treatment strongly supports our assumption that the shock-wave therapy was the cause.

References:

1. Laing PG. The arterial supply of the adult humerus. J Bone Joint Surg Am 1956;38:1105-16.

2. Gerber C, Schneeberger AG, Vinh TS. The arterial vascularization of the humeral head. J Bone Joint Surg Am 1990;72:1486-94.

3. Hasan SS. Romeo AA. Nontraumatic osteonecrosis of the humeral head. Journal of Shoulder & Elbow Surgery. 2002;11:281-98.

To The Editor:

The authors have reported a case of humeral head osteonecrosis after extracorporeal shockwave treatment to the shoulder, and allege shockwave as the cause. While congratulating the authors on their article reporting an extremely rare case report, I must raise several questions and concerns.

1. In the treatment of rotator cuff tendinopathy of the shoulder, the shockwave treatment should be focused at an appropriate depth (usually 1.5 to 2.5 cm) to the tendon-bone junction (insertion) of the rotator cuff tendon around the greater tuberosity, ensuring that the shockwave impulses do not reach or penetrate the bone. Do we know the depth of shockwave penetration in this case report?

2. The authors speculate that vascular damage to the anterior humeral circumflex artery by the shockwave may have been a possible cause of the resulting humeral head osteonecrosis. However, in normal anatomy, the insertion site of supraspinatus tendon into the greater tuberosity is far away from the anterior circumflex artery. Therefore, the possibility of shockwave injury to the anterior circumflex artery is not likely.

3. Based on the follow up, subsequent treatment, and outcome of this patient, one might question the accuracy of the initial diagnosis. It may have been possible that osteonecrosis was present at the time of the initial treatment even with a negative MRI. It seems that the authors' attribution of humeral head osteonecrosis to shockwave application, in this case report, is purely speculative.

The author(s) of this letter to the editor did not receive payment or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the author(s) are affiliated or associated.