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Kienböck disease is an isolated disorder of the carpal lunate associated with characteristic, and often progressive, clinical and radiographic changes. Appropriate intervention at specific disease stages represents the best opportunity to achieve good outcomes. As understanding of the disease improves, new therapeutic and diagnostic innovations have surfaced that further augment existing treatment options. Biologic, not just traumatic, processes may explain the onset and progression through the disease continuum. In addition to observing the obvious osseous changes, there has been renewed interest in understanding the vascular and cartilaginous manifestations of the disorder. Recognition of these factors can permit focused areas of intervention, including gene and cell-based therapies in the earliest stages. New diagnostic techniques are also being investigated. Advanced imaging modalities can facilitate the earlier recognition of Kienböck disease and enhance the assessment of lunate vascularity. Moreover, diagnostic arthroscopy permits us to directly visualize and characterize affected structures, including cartilage. Finally, there has been much recent interest in the natural history of Kienböck disease. Infantile, juvenile, and geriatric forms have been described. It has been suggested that the disease pathway in these individuals may differ from the typical adult patient population. Integrating these contemporary findings with the classic information on Kienbock disease can permit a more sophisticated approach to stage-specific treatment. This article reexamines the current classification systems to account for these emerging concepts.

Background Reliable methods of fixation of soft tissue and bone are of utmost importance in reconstructive shoulder surgery and in many orthopaedic applications.

A man in his mid-80s presented with bilateral posterior fracture dislocations of the humerus after suffering a seizure. He had Parskinson’s disease and lived with his wife at home. His left shoulder was not felt to be reconstructable. The initial treatment plan was to perform reverse total shoulder arthroplasty (rTSA) on the left and non-operatively reduce his right shoulder. A left rTSA was performed, but his right shoulder was unstable due to a glenoid fracture and soft tissue instability. In order to preserve the patient’s quality of life, a right rTSA was performed 4 days later. In the follow-up period, the patient was able to regain enough pain-free range of motion on activities of daily living. The patient died from complications of Parkinson’s disease 10 months postoperatively.