Contraction Versus Contracture: Considerations on the Pathogenesis of Dupuytren Disease

Fig. 9.1

Normal palmar aponeurosis. (a) Transverse section palmar aponeurosis. The skin is on the left side. Collagen fiber bundles ascend to the skin between fat lobules forming a three-dimensional network to permit soft gripping and distribute pressure. These fiber bundles emerge from the palmar aponeurosis, which fills the right upper quarter of the picture. The fiber bundles are cut transversely. In the right upper angle, one sees longitudinally cut collagen fibers, which belong to the deep transverse ligament of the palm. Hematoxylin–eosin, 1:28. (b) Center: Two collagen fiber bundles with collagen fibers showing the crimp structure of the collagen fibers and very few tiny elastic fibers between. This corresponds to a tension-bearing fiber bundle of a tendon. Left side: A fiber bundle with few collagen fibers and relatively more elastic fibers. This corresponds to gliding tissue. Prantner’s elastic stain, 1:250

Fig. 9.2

Dermis–aponeurosis connections. An ascending collagen fiber bundle from the palmar aponeurosis merges into the dermis. This figure demonstrates the formation of a functional unit between the dermis, the ascending collagen fibers, the palmar aponeurosis, and the whole tension transmitting system of the palmar side of the hand. It is impossible to define a border between collagen fibers of the ascending segment of the palmar aponeurosis and the ones of the dermis. Hematoxylin–eosin 1:100

One common feature of the connective tissues composing the dense connective tissue body of the palmar side of the hand is that they contain a high amount of elastic fibers and consequently have a high degree of elasticity. Another common feature is their involvement in Dupuytren Disease. In contrast, tendons are force-transmitting structures with a low elastic component and do not develop Dupuytren contracture. Figure 9.3 shows the difference in response to load bearing between normal flexor tendons and palmar aponeurosis (Millesi 2012).

Fig. 9.3

Stress–strain test of flexor tendon and of palmar aponeurosis. Comparing the stress–strain test of fiber bundles of flexor tendon (green) and fiber bundles of palmar aponeurosis (red). The flexor tendon tissues are more stiff, and the palmar aponeurosis tissues are more elastic (Millesi 2012)

Figure 9.3 shows that each tissue type lengthens (strain) moderately under low tensile load (stress). This is referred to as the toe-in region of the stress–strain curve. The toe-in region of connective tissues represents tissue lengthening under tension accommodated by the elastic capacity of the tissue. However, beyond this elastic capacity, tissue lengthens less for a given increase in load, and the slope of the stress–strain curve rises abruptly. This segment, between elastic tissue deformation and mechanical tissue failure, is referred to as the linear region of the stress–strain curve. The slope of the linear region reflects tissue stiffness. Figure 9.3 shows that palmar aponeurosis tissue is less stiff than flexor tendon tissue.

Elastic fibers are present in all dense connective tissue, including tendons and ligaments. These elastic fibers have two functions. The first is to recoil collagen fibers back into their resting crimp conformation when stress subsides. The second is mechanical energy storage and release through which tissue stretch and recoil supplement the force of intermittent muscle action. Compared to tendon tissue, the palmar aponeurosis tissue contains more elastic fibers in different arrangement, which may be a reason why the palmar aponeurosis may develop Dupuytren contracture, while tendons do not.

The majority of the body’s elastic fibers are created early in life and normally have a low rate of degradation and turnover during one’s life span (Sherratt 2009). Their life span may be shorter in the elastic connective tissue and due to genetic factors. Various other conditions may influence the properties of elastic fibers (alcohol, smoking, diabetes mellitus, etc.). Loss or weakness of elastic fibers causes loss of crimp structure, changing the mechanical characteristics of collagen fiber bundles. With loss of recoil and crimp, residual elongation increases (Table 9.1). This mechanical role of elastin is demonstrated by significant increase of the residual elongation of specimens of normal palmar aponeurosis treated with elastase to remove elastin (Reihsner et al. 1991).

Table 9.1

Residual elongation

Elongation of 2.5 % (blue), 5 % (orange), and 10 % (gray)

I. Palmar aponeurosis

II. Apparently normal palmar aponeuroses of a patient with DC

III. Thickening of collagen fiber bundles

IV. Contracture bands

V. Advanced contracture bands

9.3 How Does Dupuytren Contracture Start?

The cellular nodule, described by Langhans (1887), is the first stage of Dupuytren contracture (Luck 1959). On average, at least 2.5 years pass from the earliest diagnosis to the earliest surgery (DiBenedetti et al. 2011).

The author performed a unique series of cadaver dissections to define the earliest stages of the onset of Dupuytren contracture. All palmar aponeuroses of all cadavers dissected during one semester at the Department of Anatomy of the University of Vienna were studied by the author for signs of Dupuytren Disease. Specimens with very early, subclinical changes and their gradual transition into the full picture of DC could be studied. These results were compared with surgical specimens after complete fasciectomy containing apart from the contracture bands all stages of beginning DC and also apparently normal segments. The result was that the cellular proliferation is preceded by significant changes of collagen fibers and collagen fiber bundles (Millesi 1959). The most impressive change identified was the loss of the crimp structure (Fig. 9.4). The collagen fiber bundles thicken and fuse partially to form major units, but the original structure can still be recognized (Fig. 9.5). The elastic fibers disappear between the thickened fiber bundles exposed to traction. They survive in transverse fiber bundles of the deep transverse palmar ligament, which never is involved by DC (Fig. 9.6). Elastic fibers of the gliding tissue between the bundles lose their function and can be viewed as collections of deformed remnants of elastic fibers (Fig. 9.7; Millesi 1965).

Fig. 9.4

Normal crimp structure. Palmar aponeurosis showing the crimp structure of the normal collagen fiber bundles in relaxed state. Note the rather transparent parallel running fiber bundles. The “cross striation” is caused by the undulated fiber bundles in relaxed state. The light illuminates the height of the waves and causes shadow in between. View by loupe with oblique light, 1: 20

Fig. 9.5

Loss of normal crimp structure in DC. Palmar aponeurosis with initial changes of Dupuytren contracture. The collagen fiber bundles are thicker than in Fig. 9.4. They have lost their transparent appearance and the crimp structure. There is a tendency to fuse with neighboring bundles. View by loupe with oblique light, 1: 20

Fig. 9.6

Palmar aponeurosis with early DC. Longitudinal section at the level of the deep transverse ligament. Prantner’s elastic stain. At the upper right part of Fig. 9.6, a thickened fiber bundle of the palmar aponeurosis is sectioned longitudinally. The thickening, corresponding to an early stage of DC, can clearly be seen. There is no cellular proliferation. There are no elastic fibers. In the lower left part of Fig. 9.6, the transversely running collagen fiber bundles of the deep transverse palmar ligament are cut transversely. This ligament is never involved in DC. Here the elastic fibers appear normal and are normally distributed. This supports the concept that the function of the elastic fibers plays a role in the early phase of DC

Only gold members can continue reading. Log In or Register to continue