The digital venous drainage in the human embryonic hand.

The histogenesis and morphology of the digital venous drainage in human embryonic and fetal hands, aged from 6 to 12 weeks, were studied by light microscopy in 18 fingers. In the sixth week, capillaries could be identified around the cartilaginous models of the phalanges. By the ninth week, the neurovascular bundles were identifiable in the palmar part of the finger. In 12 week fetuses, all of the superficial and deep vascular venous system could be seen easily in the palmar aspect of the finger in positions similar to those in the adult hand. However, the arch systems, present on the dorsum of the finger in the adult hand, were not yet differentiated.

In vivo regeneration of rat sciatic nerve in a double-halved stitch-less guide: a pilot-study.

It is about 20 years that tubular nerve guides have been introduced into clinical practice as a reliable alternative to autograft, in gaps not-longer-than 20 mm, bringing the advantage of avoiding donor site sacrifice and morbidity. There are limitations in the application of tubular guides. First, tubular structure in itself makes surgical implantation difficult; second, stitch sutures required to secure the guide may represent a site of unfavorable fibroblastic reaction; third, maximum length and diameter of the guide correlate with the occurrence of a poorer central vascularization of regenerated nerve. We report on the in vivo testing of a new concept of nerve-guide (named NeuroBox) which is double-halved, not-degradable, rigid, and does not require any stitch to be held in place, employing acrylate glue instead. Five male Wistar rats had the new guide implanted in a 4-mm sciatic nerve defect; two guides incorporated a surface constituted of microtrenches aligned longitudinally. Further five rats had the 4-mm gap left without repair. Contralateral intact nerves were used as controls. After 2 months, nerve regeneration occurred in all animals treated by the NeuroBox; fine blood vessels were well represented. There was no regeneration in the un-treated animals. Even if the limited number of animals does not allow to draw definitive conclusions, some result can be highlighted: an easy surgical technique was associated with the box-shaped guide and acrylate glue was easily applied; an adequate intraneural vascularization was found concurrently with the regeneration of the nerve and no adverse fibroblastic proliferation was present.

Histopathology of the A1 pulley in adult trigger fingers.

The histopathology of the central parts of 40 A1 pulleys from adult patients with primary trigger fingers was studied using light and transmission electron microscopes and the findings were compared with those in a control series of 10 normal A1 pulleys. The evaluation of the normal A1 pulley revealed a bi-laminar structure. The deepest layer was composed of dense normal connective tissue. The outermost layer was formed by loose connective tissue. In trigger digits, it was possible to identify a tri-laminar structure. The deepest layer was composed of irregular connective tissue, formed by small collagen fibres and abundant extracellular matrix. A considerable amount of chondroid-metaplasia was present in this layer. The middle layer contained dense, normal connective tissue with some fibrocytes. The outermost layer was formed of loose connective tissue. In conclusion, there was an additional layer in the A1 pulley in pathological cases which was not present in normal pulleys.

Scanning electron microscopic findings of the gliding surface of the A1 pulley in trigger fingers and thumbs.

The gliding surface of the A1 pulley was studied in 20 cases of primary trigger finger by scanning and transmission electron microscope. In 12 normal specimens, the whole deep surface was covered uniformly by an amorphous extracellular matrix. In the pathological samples, there was the same general surface appearance but, also, areas, varying in shape and dimension where loss of the extracellular matrix had exposed the collagen fibres and a few cells of the middle layer of the pulley. There were also changes typical of "chondroid-metaplasia". These data were confirmed by transmission electron microscopy. The fragmented areas are probably the result of altered forces of friction between the pulley and the flexor tendon and may be the "gate" through which the forces of friction cause chondroid-metaplasia in the underlying fibrous tissue, a phenomenon recognised to be one step in the pathogenesis of trigger finger.

Localization of collagen type IV, fibronectin and elastin in the flexor digitorum tendons and in the perichondrium during prenatal development of the human hand.

The distribution of collagen type IV, fibronectin and elastin in the flexor digitorum tendons and in the perichondrium of staged human embryos and fetal hand (from 6 to 12 weeks of gestation) has been studied to analyse the immunohistochemical features of the human hand during the first trimester of pregnancy. At 6 weeks in the transverse sections of the fingers there is no evidence of the presence of collagen type IV and elastin which remain absent even in the controls of 9, 11 and 12 weeks. On the contrary from 6 weeks of intrauterine life the fibronectin is widely distributed with thickening above all in the perichondrium and in the subjacent portion of the cartilaginous model of the bone. At 9 weeks a high positivity is detected not only along the perichondrium but even into the extra-cellular matrix of every mesenchymal cell. At 11 and 12 weeks the perichondrium is always positive but a high positivity is now present along the flexor tendons and their related sheaths that show a high grade of differentiation. To sum up, the absence of the collagen type IV into the flexor and extensor tendons is understandable because it isn't a fibrillar collagen. More difficult is to understand the absence of the elastin (component of the mature tendons) until the 12th week. On the contrary the presence of the fibronectin, a structural glycoprotein, proof of active morphogenesis of mesenchvmal cells, earlier in the perichondrium and cartilaginous sketch and later in the flexor tendons and their sheaths indicates that probably among the cells of mesenchymal origin the perichondrium with the cartilaginous model of the bone come before and perhaps orient the differentiation of the other components of the human hand.

Histogenesis and morphology of the flexor tendon pulley system in the human embryonic hand.

The number, position, structural and ultrastructural features of the flexor tendon pulley system in six human embryonic hands, aged from 6 to 12 weeks, were studied by light and electron microscope. The pulley system can be recognized from the ninth week; later, at 12 weeks, the structures are easily identified around the flexor tendon in positions closely correlated to those found during post-natal growth and in the adult hand. Structurally and ultrastructurally the pulleys are not simply thickened portions of the sheath. They are formed by three layers: an inner layer, one or two cells thick, probably representing a parietal synovial tendon sheath; a middle layer formed by collagen bundles and fibroblasts whose direction is mainly perpendicular to the underlying phalanx; and an outermost layer consisting of mesenchymal tissue with numerous vessels which extends dorsally in an identical layer, forming a ring that includes flexor and extensor tendons and the cartilaginous model of the phalanx. The pulley does not have a semicircular shape but a much more complicated one, owing to the middle layer which in part runs dorsally and in part ventrally, under the flexor tendons.