Anatomical and clinical literature describes the arrangement of collagen fibrils in the human meniscus as being "arcade-like". The "arcade-like" orientation, mainly running in a radial direction in the internal circumference and in a circular direction in the external circumference, was found in polarization light microscopic studies. This, however, does not provide a mechanical explanation for the direction of meniscus tears. In view of this contradiction collagen fibrils in the menisci of adults aged from 18 to 85 years were exposed layer-by-layer to study their arrangement by scanning electron microscopy. The results obtained by this procedure were compared to the path of the split lines. Scanning electron microscopy reveals three distinct layers in the meniscus cross section: (1) The tibial and femoral sides of the meniscus surfaces are covered by a meshwork of thin fibrils with a diameter of approximately 30 nm. (2) Beneath the superficial network there is a layer of lamellalike collagen fibril bundles on the tibial and femoral surface. In the area of the external circumference of the anterior and posterior segments the bundles of collagen fibrils are arranged in a radial direction. In all other parts the collagen fibril bundles intersect at various angles. (3) The main portion of the meniscus collagen fibrils are located in the central region between the femoral and the tibial surface layers. Everywhere in the central main portion of the meniscus the bundles of collagen fibrils are orientated in a circular manner. The split lines in the region of the internal circumference of the menisci are arranged in a circular manner, generally running in a radial direction in the portions adjacent to the base. Scanning electron microscopy reveals that the direction of the split lines depends on the orientation of the collagen fibrils in the superficial lamellar layer. The arcade-like path of the collagen fibrils described in the literature can not be confirmed either by scanning electron microscopy or by the course of the split lines. The circular arrangement of collagen fibrils in the central portion of the meniscus provides a functional explanation for the longitudinal orientation of the majority of tears in the meniscus tissue.

Variations of the course of the internal carotid artery in the parapharyngeal space and their frequency were studied in order to determine possible risks for acute haemorrhage during pharyngeal surgery and traumatic events, as well as their possible relevance to cerebrovascular disease. The course of the internal carotid artery showed no curvature in 191 cases, but in 74 cases it had a medial, lateral or ventrocaudal curve, and 17 preparations showed kinking (12) or coiling (5) out of a total of 265 dissected carotid sheaths and 17 corrosion vascular casts. In 6 cases of kinking and 2 of coiling, the internal carotid artery was located in direct contact with the tonsillar fossa. No significant sex differences were found.Variations of the internal carotid artery leading to direct contact with the pharyngeal wall are likely to be of great clinical relevance in view of the large number of routine procedures performed. Whereas coiling is ascribed to embryological causes, curving is related to ageing and kinking is thought to be exacerbated by arteriosclerosis or fibromuscular dysplasia with advancing age and may therefore be of significance in relation to the occurrence of cerebrovascular symptoms.

More than 100 years ago Wilhelm Roux (1895) introduced the term "functional adaptation to anatomy and physiology". Compared with other organ systems the functional adaptation processes are best identifiable in the locomotor system, like for example in the two types of tendons: traction and gliding tendons. Traction tendons are tendons where the direction of pull is in line with the direction of the muscle (e.g. Achilles tendon). Gliding tendons (e.g. tibialis posterior tendon) change direction by turning around a bony or fibrous hypomochlion. In this region the tendon is subjected to intermittent compressive and shear forces and the extracellular matrix consists of avascular fibrocartilage. Avascularity is considered to be a key factor for the etiology of degenerative tendon disease. The repair capability after repetitive microtrauma is strongly compromised in avascular tissue of gliding tendons. Reduced vascularity is not a specific feature of gliding tendons; several studies have shown that the number and size of blood vessels are largely shortened in the waist of the Achilles tendon. However, histological biopsies from degenerated Achilles tendons and Doppler flow examinations revealed a high blood vessel density in patients with degenerative tendon disease. Angiogenesis is mediated by angiogenic factors and recent studies have shown that the vascular endothelial growth factor (VEGF) is highly expressed in degenerative Achilles tendons, whereas VEGF expression is nearly completely downregulated in healthy tendons. Several factors are able to upregulate VEGF expression in tenocytes: hypoxia, inflammatory cytokines and mechanical load. Since VEGF has the potential to stimulate the expression of matrix metalloproteinases and inhibit the expression of tissue inhibitors of matrix metalloproteinases tissue inhibitor of metalloproteinases (TIMP) in various cell types (e.g. endothelial cells, fibroblasts, chondrocytes), this cytokine might play a significant role for the pathogenetic processes during degenerative tendon disease. An animal experiment in the rabbit has shown that local injection of VEGF reduced the material properties of the Achilles tendon. These experimental findings are in accordance with clinical results that a locally administered (in the area with neovascularization) sclerosing drug (Polidocanol) has a beneficial effect on chronic mid-portion Achilles tendinosis. In conclusion, decreased and increased vascularity might be involved in the pathogenesis of degenerative Achilles tendon disease.

The structure and vascularization of the human anterior and posterior cruciate ligament were investigated by light microscopy, transmission electron microscopy,, injection techniques and by immunohistochemistry. The major part of the anterior and posterior cruciate ligament is composed of bundles of type I collagen. Type III collagen-positive fibrils separate the bundles. The major cell type is the elongated fibroblast, lying solitarily between the parallel collagen fibrils. The histologic structure of the cruciate ligaments is not homogeneous. In both ligaments there is a zone where the tissue resembles fibrocartilage. In the anterior cruciate ligament the fibrocartilaginous zone is located 5-10 mm proximal of the tibial ligament insertion in the anterior portion of the ligament. In the posterior cruciate ligament the fibrocartilage is located in the central part of the middle third. Within those zones the cells are arranged in columns and the cell shape is round to ovoid. Transmission electron microscopy reveals typical features of chondrocytes. The chondrocytes are surrounded by a felt-like pericellular matrix, a high content of cellular organelles and short processes on the cell surface. The pericellular collagen is positive for type II collagen. The major blood supply of the cruciate ligaments arises from the middle geniculate artery. The distal part of both cruciate ligaments is vascularized by branches of the lateral and medial inferior geniculate artery. Both ligaments are surrounded by a synovial fold where the terminal branches of the middle and inferior arteries form a periligamentous network. From the synovial sheath blood vessels penetrate the ligament in a horizontal direction and anastomose with a longitudinally orientated intraligamentous vascular network. The density of blood vessels within the ligaments is not homogeneous. In the anterior cruciate ligament an avascular zone is located within the fibrocartilage of the anterior part where the ligament faces the anterior rim of the intercondylar fossa. The fibrocartilaginous zone of the middle third of the posterior cruciate ligament is also avascular. According to Pauwel's theory of the "causal histogenesis" (1960) the stimulus for the development of fibrocartilage within dense connective tissue is shearing and compressive stress. In the anterior cruciate ligament this biomechanical situation may occur when the ligament impinges on the anterior rim of the intercondylar fossa when the knee is fully extended. Compressive and shearing stress in the center of the middle third of the posterior cruciate ligament may result from twisting of the fiber bundles.