Wall Of Bursa Research Articles

Ultrastructure of the subacromial bursa in painful shoulder syndromes.

In order to determine if inflammation of the subacromial bursa or "bursitis" is as common an occurrence as believed in painful conditions of the shoulder, eight bursae were obtained during surgery from 3 cases of calcifying tendinitis, 2 of tight coracoacromial ligament, 2 of rotator cuff tear and 1 of acromioclavicular osteoarthritis. In the cases of calcifying tendinitis, tight coracoacronial ligament and rotator cuff tear the morphological changes mainly consisted of a numerical increase in cells throughout the bursal wall along with proliferation of endothelial cells in the vascular channels. All of the cells including the endothelial had densely packed, intermediate type filaments in their cytoplasm but no appreciable diminution of metabolic organelles. Lipid droplets were abundant in the extracellular connective tissue of the bursae from the cases with rotator cuff tear. In contrast to the other cases, the bursa from the case of acromioclavicular osteoarthritis showed widespread fibrin deposition in association with cell necrosis. In none of the cases did inflammatory leukocytic cells infiltrate bursal tissue. We conclude, that the subacromial bursa tends to undergo proliferative or degenerative changes in rotator cuff tendinopathies but bursal inflammation with polymorphonuclear cell infiltrate does not occur commonly.

The intermetatarsophalangeal bursa--its significance in Morton's metatarsalgia.

The intermetatarsophalangeal bursa was investigated by dissection, radiography and injection. In the web spaces between the second and third and the third and fourth digits the bursa lies superior to the transverse metatarsal ligament but projects distally to it, closely applied to the neurovascular bundle. Tissue from the web spaces of patients with classical Morton's metatarsalgia often shows lymphocytic infiltration, with additional fibrinoid necrosis of the bursal wall. It is suggested that inflammatory changes in this bursa could account for the pathological and histological findings in this condition. The bursa in the most lateral web space does not extend beyond the ligament and is not in contact with the neurovascular bundle, which may explain the rarity of symptoms in this space.

The operative cure of hallux valgus and bunions

The main basic factors in the etiology of hallux valgus and bunions are the adduction of the metatarsal bone of the big toe and the obliquity of its tarsometatarsal joint. The conspicuous and obvious causes of the discomfort and disability are the valgus of the big toe, bony overgrowth at the base of the big toe and the overlying bursa or bunion. The author's operation aims to correct all of the pathological changes without disturbing the function of the big toe joint or the weight bearing surface of the head of the first metatarsal. The adduction of the first metatarsal bone is corrected by the removal of a double wedge from the tarsometatarsal joint, the mobilization of the metatarsal bone and the manual approximation of the first and the second metatarsal. The overgrowth of bone on the head of the metatarsal and the bunion are excised through a separate incision. The correction of the valgus of the big toe is assured by securing to the metatarsal bone a tongue of strong tissue, consisting of bursal wall and capsule, which is attached to the base of the phalanx. Care is exercised not to remove or in any way disturb the articulating portion of the head of the metatarsal bone. This accomplishes two results, namely, the support of the forefoot is not altered and the mobility of the big toe is not diminished. By bringing the big toe into line with the inner border of the foot, the sesamoid bones are returned to their normal relation to the head of the metatarsal, and the dorsal and plantar tendons of the big toe are brought into a normal or nearly normal position, where they can function properly.

So-Called Calcifying Subacromial Bursitis

Codman, in 1906, was the first to describe the symptom-complex which he designated as “subacromial bursitis.” He had not found any calcareous deposits in the cases he then reported. The following year Painter and Baer both reported cases of calcareous deposits and, in the light of present-day knowledge, they were probably both in error in stating that the deposits were situated in the wall of the bursa. They each reported having excised the entire subdeltoid bursa in four cases. Unfortunately many writers have wrongly followed their lead and described the deposits as occurring in the wall of the subacromial bursa and advised total excision of the bursa. Codman was the first to point out that the deposit is located beneath the bursa, in or on the supraspinatus tendon. It is most important for surgeons to realize that the deposit is not in the bursa but beneath its floor, in, on, or even under the supraspinatus tendon, otherwise they are likely to miss it at operation as did Painter in two of his four early operations, in which he reported excision of the subdeltoid bursa, and as did Stern, who probably limited his search to the interior of the bursa. Some confusion has arisen in the literature because various authors use the terms “subacromial bursa” and “subdeltoid bursa” as synonymous and interchangeable, whereas others regard them as separate entities. Experience has shown that there is only the one bursa and the general trend of opinion is to call it “subacromial.” The subacromial bursa is nearly as large as the palm of the hand of the individual in whom it is located, and, except for a small projection beneath the deltoid muscle, lies between the acromion process and the head of the humerus, where it is inaccessible for the complete excision so commonly and wrongly advised by numerous writers. In many of the cases with typical acute or chronic symptoms that are studied carefully at operation, the opened subacromial bursa is found to be entirely free from any pathologic changes, and the deposit is found in or even under the supraspinatus tendon. It, therefore, seems obvious that the symptoms must be caused by the tendon lesion and that the term “bursitis” is really a misnomer. Often a localized or rarely a diffused bursitis may co-exist and is probably induced by the adjacent tendon lesion, but the symptoms in no way differ from the cases in which the tendon alone is affected. Codman believes the deposits are due primarily to acute traumatic rupture of a few fibers of the supraspinatus tendon, with the occurrence at the site of rupture of a hematoma in which calcium salts are deposited.