My Orthopaedic Surgeon

loss of terminal tufts of digits; found in
* scleroderma / connective-tissue disease
* psoriatic arthritis
* Reiter disease
* frostbite(thumbs spared)/burns
* leprosy
* polyvinylchloride exposure
* hyperparathyroidism
* Lesch-Nyhan syndrome (they bite 'em off)
* cleidocranial dysostosis
* progeria
* pyknodysostosis (aplasia/hypoplasia of distal digits)
* sarcoidosis
* epidermolysis bullosa

Distal clavicle osteolysis was first described in 1936 as a condition secondary to acute shoulder trauma. Today, distal clavicle osteolysis is described as a sequela of trauma associated with contact sports, falls, and motor vehicle accidents. In 1959, this condition was reported in an air-hammer operator without evidence of acute trauma. In 1982, Cahill reported on 45 male athletes with distal clavicle osteolysis, confirming repetitive microtrauma as an etiology. Forty-four of Cahill's patients were weight lifters.
Distal clavicle osteolysis is a pathologic process involving resorption of subchondral bone in the distal clavicle. The condition usually presents as pain localized to the acromioclavicular (AC) joint.
Synonyms and related keywords: clavicle osteolysis, shoulder pain, overuse injury, shoulder trauma, shoulder microtrauma, chronic shoulder pain, collar bone pain, broken collar bone, collar bone microtrauma
Author: Brett D Owens, MD 2006

The most common skeletal manifestation of malignancy is focal osteolysis in association with metastases. In order for tumor cells to grow and invade mineralized bone, osteolysis must occur. Osteoclasts appear uniquely adapted to produce the microenvironment and the biochemical milieu that are needed to resorb bone. Although previous reports have indicated that some tumor cells appear capable of assuming an osteoclast phenotype and directly resorbing bone (3), the bulk of the evidence suggests that most tumor cells act indirectly by co-opting the physiologic mechanisms that normally favor bone resorption. Thus, they release agents such as hormones, eicosanoids, growth factors, and cytokines into the bone microenvironment, which act on osteoblastic stromal cells to enhance the production of osteoclast activating factors.
Full text. David Goltzman J Clin Invest. 2001 May 15; 107(10): 1219–1220.