Regarding experimental data on the multi-factorial reduction of the thermostability of collagen, the following sequence of the mechanism of Dupuytren's contracture is discussed: 1. Hereditary or acquired weakness of fibres of the palmar fascia 2. Further disturbance of the physical property of collagen by the cumulative effects of mechanical, i.e. traumatic, influence. 3. By this means an induced stepwise shrinkage of released fascial fibres in body temperature. 4. Stabilisation of the shortening (contracture) by development of collagen. This hypothesis is supported by histological, polarizing-microscopic, electron-microscopic and chemical results.

Our understanding of the process of contracture of the fingers is based on extrinsic and intrinsic theories. Yet there has always been an inherent contradiction in these concepts. Additionally, nearly all of these theories proceed from the assumption of a contractio digitorum and this assumption is reflected in basic research as well. The author presents a concept, which describes the finger contracture more accurately as retention in the flexed position. This contraction-free concept, deduced from the function and structure of the palmar subcutaneous tissue, combines the different pathogenic aspects. Palmar fibromatosis primarily manifests itself in the palmar subcutaneous tissue. The function of this tissue was studied in the living hand; the anatomic structure of the subcutaneous fibrofatty tissue was studied for the first time in slice plastinates of adult hands. The palmar tissue exhibits varying tissue consistencies. It is compressed and expanded as the fingers move. In fibromatosis, fibrous nodules infiltrate the finger tissue in its shortened flexion configuration, which predominates both by day and by night. In the normal hand, the anchoring fibers allow nearly tension-free deformation of the skin tissue. In fibromatosis, this tissue loses its extensibility. Motion in the finger subjects the new formed tissue to tensile stress. This in turn provides the decisive stimulus for adaptive tissue transformation. This process does not require any active contraction. It plausibly explains the finger contracture as an extension block. In the contraction-free concept, the myofibroblast is understood to be a form of fibroblast that resists the tension arising in the tissue by isometric contraction. The contraction-free concept can explain all clinical pictures of fibromatosis as reactive remodeling of the specific local host tissue. It can also provide basic research with a conclusive anatomic pattern. Moreover, it implies a specific therapeutic paradigm: Treatment options that influence the formation of pathologic tissue and address the characteristic tensile stress will be able to control the root causes of the deformity.

Banded fibrous associates are described in the extracellular space of connective tissue from human endometrium, Ehlers-Danlos syndrome and of tendon rupture. In the cases of morbus Dupuytren these associates are also found as intracellular inclusions. The banded structures are interpreted as states of an enzymatically induced degradation of collagen in correlation with Type-III collagen.

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