The Frozen Shoulder syndrome plus other evidence and the Utah Paradigm suggest the syndrome's pathogenesis and new targets for collagenous tissue research.

Sometimes naturally occurring disorders combined with other evidence can provide a "virtual laboratory" exercise that answers old questions and reveals new problems and questions that need appropriately "targeted" research. This article provides an example that involves the frozen shoulder syndrome, for which varied evidence and insights of the still-evolving Utah paradigm of skeletal physiology suggest a plausible pathogenesis. It involves organ- and tissue-level vital-biomechanical features of collagenous tissues that need systematic study. The features include diametric modeling, irreversible creep, a creep compensation mechanism, the regional acceleratory phenomenon, and the signals and thresholds that can help to determine how and where those things act in anatomical space. Such features participate in many extraskeletal as well as skeletal disorders, so the frozen shoulder syndrome can provide an instructive model of them. As an aside, in over 120 consecutive cases managed by me since 1956 this syndrome resolved completely in six or less months without treatment. That shows this untreated syndrome is usually if not always self limited. While I respect the doubts of colleagues who do not agree yet, that experience shows the conclusion is correct.