The menisci and their insertions into bone (entheses) represent a functional unit. Thanks to their firm entheses, the menisci are able to distribute loads and therefore reduce the stresses on the tibia, a function which is regarded essential for cartilage protection and prevention of osteoarthrosis. The tissue of the hypocellular meniscal body consists mainly of water and a dense elaborate type I collagen network with a predominantly circumferential alignment. The content of different collagens, proteoglycans and nonproteoglycan proteins shows significant regional variations probably reflecting functional adaptation. The meniscal horns are attached via meniscal insertional ligaments mainly to tibial bone. At the enthesis, the fibres of the insertional ligaments attach to bone via uncalcified and calcified fibrocartilages. This anatomical configuration of gradual transition from soft to hard tissue, which is identical to other ligament entheses, is certainly essential for normal mechanical function and probably protects this vulnerable transition between 2 biomechanically different tissues from failure. Clinical treatment of meniscal tears needs to be based on these special anatomical and functional characteristics. Partial meniscectomy will preserve some of the load distribution function of the meniscus only when the meniscal body enthesis entity is preserved. Repair of peripheral longitudinal tears will heal and probably preserve the load distribution function of the meniscus, whereas radial tears through the whole meniscal periphery or more central and complex tears may be induced to heal, but probably do not preserve the load distribution function. There is no proof that replacement of the meniscus with an allograft can reestablish some of the important meniscal functions, and thereby prevent or reduce the development of osteoarthrosis which is common after meniscectomy. After implantation, major problems are the remodelling of the graft to inferior structural, biochemical and mechanical properties and its insufficient fixation to bone which fails to duplicate a normal anatomical configuration and therefore a functional meniscal enthesis.

En bloc staining with basic fuchsin is an established method for demonstrating microdamage in bone. Using transmitted light microscopy, variations in light intensity, depth of focus and magnification are necessary to distinguish fully-stained microcracks generated in vivo, from partially-stained or unstained artefactual cracks due to cutting and machining. This process is both difficult and time-consuming. In this study, 2 methods were used to examine fuchsin-stained microcracks in human rib sections, transmitted light and epifluorescence microscopy. No differences were found in crack number, density or length between the 2 methods indicating comparable accuracy. Using green epifluorescence, only microcracks containing fuchsin fluoresced orange against the darkfield background, enabling unstained, artefactual cracks to be screened out. Under UV epifluorescence, microcracks stained through the full 100 μm depth of the section fluoresced purple. Partially-stained artefactual cracks failed to fluoresce and were screened out. Epifluorescence is a simple, rapid and accurate screening method for differentiating fully-stained from artefactual microcracks in bone.

The aim of this study was to determine the degree to which the epidermis and oral epithelium of species other than man express cytokeratin (CK) intermediate filaments, which are markers of epithelial differentiation. Fixed, wax-embedded samples of skin, buccal mucosa and gingiva from rhesus monkey, marmoset, cow, sheep, pig, ferret, hamster, axolotl and trout were tested for CK expression using a panel of antihuman CK antibodies and an immunoperoxidase procedure. Human skin and oral mucosa were also stained to act as positive control. The results showed that antihuman CK antibodies stained animal tissues, but the patterns of staining were not always identical to the established human CK profile. Of particular interest was the expression of CK18, typically only detected in ‘simple’ epithelium in man, in bovine, ferret and hamster stratified epithelium from different sites. However, there was evidence of variable anti-CK antibody cross-reactivity, both as a result of intrinsic variations in CK polypeptide structure and as artifacts of fixation. We conclude that some CK are conserved between species, but that biological variables, for example local functional requirements, and technical factors affect the results. These considerations need to be borne in mind in animal studies of epithelial differentiation employing CK immunohistochemistry. Biochemical characterisation is ultimately necessary to determine specific differences between human and animal CK.

The axon determines whether or not it is myelinated by the Schwann cell. At maturity there is a positive correlation between sheath thickness and axon calibre. This correlation is initially very low or absent, but gradually strengthens during development. This increase could come about because the axon continuously controls Schwann cell myelinating activity, so that a given axon calibre is associated with a particular myelin sheath thickness, an interaction which would entail the Schwann cell continuously monitoring and responding to axon size. This seems unnecessarily complex. This theoretical study shows that the strong correlation between the 2 parameters within a given myelinated fibre population may come about in a much simpler way than outlined above. This is demonstrated by modelling the growth and myelination of a hypothetical population, utilising data from earlier studies on cervical ventral motoneuron axon development. The hypothesis tested shows that the only instructive interactions by the axon on the Schwann cell necessary for the strong correlation between the 2 parameters to emerge are for the initiation of myelination, its continuation and its termination. These could result from a single stimulus being switched on, persisting for a time and being switched off. Under this influence, the Schwann cell is assumed to proceed to form the myelin sheath at a constant rate which it itself inherently determines, in the absence of any quantitative influence exerted by the axon. This continues until the stimulus for myelination ceases to emanate from the axon. The validity of the hypothesis is demonstrated, because the resulting myelin-axon relationships correspond closely to those observed during development.

The objective of this study was to investigate the normal distribution of cartilage thickness in the major joints of the lower limb in elderly individuals. A 12.5 MHz ultrasound transducer was used to measure the cartilage thickness in the right and left hip, knee and ankle joint of 10 individuals aged between 62 and 99 y. Distribution patterns of cartilage thickness were derived by b-spline interpolation and the average distribution computed in each surface. The maximum cartilage thickness in the hip joint was 2.6 (±0.36) mm and the mean thickness 1.3 (±0.17) mm. The CV% (a measure of thickness inhomogeneity within the joint surface) was 32%. In the knee, the maximal and mean values were 3.8 (±0.46) mm and 1.9 mm (±0.24) mm, respectively (CV%=34%), and in the ankle 1.7 (±0.25) mm and 1.0 (±0.16) mm (CV%=32%). Systematic differences existed between both sides in the knee, the distal femur showing a significantly greater thickness on the right. While the mean and maximal thicknesses were systematically higher in the knee than in the hip, and in the hip higher than in the ankle (P<0.05), there were no systematic differences in the thickness inhomogeneity of the 3 joints. Only the malleolus showed a somewhat more uniform thickness than the other joint surfaces. The variablity between individuals was similar for all joints for mean thickness, but the interindividual variability of the maximal thickness values was highest in the knee and lowest in the ankle. Whereas the cartilage thickness distributions in the joints of the lower limb have been suggested to reflect the pressure distribution within the articular surface, the absolute thickness is proposed to be a function of dynamic loading (range of motion) during gait, rather than being a reflection of the static articular pressure.

Tendon cells have complex shapes, with many cell processes and an intimate association with collagen fibre bundles in their extracellular matrix. Where cells and their processes contact one another, they form gap junctions. In the present study, we have examined the distribution of gap junction components in phenotypically different regions of rat Achilles tendon. This tendon contains a prominent enthesial fibrocartilage at its calcaneal attachment and a sesamoid fibrocartilage where it is pressed against the calcaneus just proximal to the attachment. Studies using DiI staining demonstrated typical stellate cell shape in transverse sections of pure tendon, with cells withdrawing their cell processes and rounding up in the fibrocartilaginous zones. Coincident with change in shape, cells stopped expressing the gap junction proteins connexins 32 and 43, with connexin 43 disappearing earlier in the transition than connexin 32. Thus, there are major differences in the ability of cells to communicate with one another in the phenotypically distinct regions of tendon. Individual fibrocartilage cells must sense alterations in the extracellular matrix by cell/matrix interactions, but can only coordinate their behaviour via indirect cytokine and growth factor signalling. The tendon cells have additional possibilities — in addition to the above, they have the potential to communicate direct cytoplasmic signals via gap junctions. The formation of fibrocartilage in tendons occurs because of the presence of compressive as well as tensile forces. It may be that different systems are used to sense and respond to such forces in fibrous and cartilaginous tissues.

In a previous study, an antigen consisting of proteins secreted by retinal pigment epithelial (RPE) cells was injected into a sheep and the specificity of the resulting antiserum was shown by Western blotting and its effects on retinal development were determined in vitro and in vivo. In the present study, the distribution of these secreted proteins was determined by light microscopy immunocytochemistry in cultured neonatal rat RPE cells and retinas of normal and Royal College of Surgeons (RCS) dystrophic rats and cerebrum of normal adult rats. Immunolabelling for these RPE-secreted proteins was detected in cytoplasmic vesicles surrounding nuclei and within processes of cultured normal and transformed rat RPE. In retinas of late postnatal and adult rats, dense immunostaining was found in the cytoplasm of RPE cells and ganglion cell bodies. In addition to RPE and ganglion cells, scattered photoreceptors within the thin outer nuclear layer and small structures within the debris zone were also densely immunoreactive in retinas of 2-mo-old RCS dystrophic rats. The numbers of immunostained ganglion cells appeared to decrease in retinas of older RCS rats, although the immunoreactivity within the RPE appeared to increase in density. No other neuron within the retina, i.e. bipolar, amacrine or horizontal, was immunoreactive for RPE-secreted proteins. In the cerebral cortex of adult rats, immunoreactivity for RPE-secreted proteins was primarily detected within large perikarya of pyramidal neurons and smaller granule neurons. In conclusion, we report an immunocytochemical analysis of an antiserum raised against secreted proteins of rat RPE. This antiserum recognised proteins within secretory-like vesicles of cultured neonatal normal and transformed rat RPE and showed a specificity for RPE and ganglion cells in normal rat retinas, that appeared to be developmentally regulated, and neuron perikarya in adult rat cerebrum.

The proliferation sites and cellular kinetics of villous epithelial cells and M cells in the intestine of the adult chicken have never been clarified. In this study, we determined the proliferation sites in the chicken caecum using colchicine treatment and detection of proliferative cell nuclear antigen (PCNA). The cellular kinetics of these cells were also studied using bromodeoxyuridine (BrdU) as a tracer. Enterocytes in their mitotic period were observed along the entire length of the intestinal crypt of the caecum, with a denser distribution in the middle portion of the crypt, except for the caecal tonsil. The centres of distributions were at 49% of the distance from the bottom of the crypt in the base and 41% in the apex of the caecum. In the caecal tonsil, the centres of distributions were at 64% in the long type of crypt from the bottom of the crypt and at 44% in the short type of crypt. On the other hand, the PCNA-positive enterocytes were distributed more densely at the bottom of the crypt, except for the caecal tonsil. The centres of distributions were at 36% in the base from the bottom of the crypt, 37% in the body, and 34% in the apex. In the caecal tonsil, they were at 54% in the long type of crypt and 44% in the short type. The BrdU-labelled enterocytes reached to the basement of the intestinal villi in all caecal portions at 1 d after the BrdU administration. The leading edge of the labelled enterocytes disappeared from the villous tips at 4 d in the base and the body and 3 d in the apex. In the caecal tonsil, the BrdU-labelled microvillous epithelial cells and the M cells appeared near the orifice of the crypt at 1 d, and BrdU-labelled M cells were not observed in the crypt. Thereafter, almost all of these cells disappeared at 5 d from the follicle associated epithelium (FAE). These results suggest that M cells are transformed from their precursors within 1 d, and the turnover time for M cells occurs within 4 d after the cell division of the precursors.

We have explored the innervation of the rainbow trout (O. mykiss) liver using immunohistochemical procedures and light microscopy to detect in situ protein gene product 9.5 and neuronal nitric oxide synthase immunoreactivities (PGP-IR and NOS-IR). The results showed PGP-IR nerve fibres running with the extralobular biliary duct (EBD), hepatic artery (EHA) and portal vein (EPV) that form the hepatic hilum, as well as following the spatial distribution of the intrahepatic blood vessel and biliary channels. These nerve fibres appear as single varicose processes, thin bundles, or thick bundles depending on their diameter and location in the wall of the blood vessel or biliary duct. No PGP-IR fibres were detected in the liver parenchyma. NOS-IR nerve fibres were located only in the vessels and ducts that form the hepatic hilum (EBD, EHA, EPV); in addition, NOS-IR nerve cell bodies were found isolated or forming ganglionated plexuses in the peribiliary fibromuscular tissue of the EBD. No PGP-IR ganglionated plexuses were detected in the EBD. The location of the general (PGP-IR) and nitrergic (nNOS-IR) intrinsic nerves of the trout liver suggest a conserved evolutionary role of the nervous control of hepatic blood flow and hepatobiliary activity.

This paper presents a study of 3-dimensional growth in the facial skeleton of the mangabey, Cercocebus torquatus. The pattern of facial cortical remodelling in this species is already well mapped from an earlier study. In this paper we consider the extent to which these remodelling maps relate to ontogenetic changes in size and shape of the face. This study is based on 31 facial landmarks taken from 49 adult and subadult faces. Our analysis draws on some of the tools of geometric morphometrics and we take this opportunity to describe our implementation of these tools for 3D data. The geometric analysis permits the known remodelling maps to be interpreted in the context of the general pattern of facial growth in this species. We are also able to examine sexual dimorphism in the face of this species and consider the extent to which males and females share similar ontogenetic allometries. Our findings indicate that the general pattern of size-related shape variation during facial growth is more or less identical for males and females up to eruption of the third permanent maxillary molar (M3). After this, ontogenetic allometries appear to diverge. The finding of a common growth allometry that is well approximated for younger specimens by a simple linear model is consistent with the earlier findings of a consistent pattern of facial remodelling up to M3 eruption. We consider the implications of these findings in terms of the potential for these approaches in the study of comparative growth in related species.

Peripheral nerve transection induces significant changes in neuropeptide expression and content in injured primary sensory neurons, possibly due to loss of target derived neurotrophic support. This study shows that neurotrophin-3 (NT-3) delivery to the injured nerve influences neuropeptide Y (NPY) expression within dorsal root ganglia (DRG) neurons. NT-3 was delivered by grafting impregnated fibronectin (500 ng/ml; NT group) in the axotomised sciatic nerve. Animals grafted with plain fibronectin mats (FN) or nerve grafts (NG) were used as controls. L4 and L5 DRG from operated and contralateral sides were harvested between 5 and 240 d. Using immunohistochemistry and computerised image analysis the percentage, diameter and optical density of neurons expressing calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP) and NPY were quantified. Sciatic nerve axotomy resulted in significant reduction in expression of CGRP and SP, and significant upregulation of VIP and NPY (P<0.05 for ipsilateral vs contralateral DRG). By d 30, exogenous NT-3 and nerve graft attenuated the upregulation of NPY (P<0.05 for NT and NG vs FN). However, NT-3 administration did not influence the expression of CGRP, SP or VIP. The mean cell diameter of NPY immunoreactive neurons was significantly smaller in the NT-3 group (P<0.05 for NT vs FN and NG) suggesting a differential influence of NT-3 on larger neurons. The optical densities of NPY immunoreactive neurons of equal size were the same in each group at any time point, indicating that the neurons responding to NT-3 downregulate NPY expression to levels not detectable by immunohistochemistry. These results demonstrate that targeted administration of NT-3 regulates the phenotype of a NPY-immunoreactive neuronal subpopulation in the dorsal root ganglia, a further evidence of the trophic role of neurotrophins on primary sensory neurons.

The vertebral artery, in its course from the subclavian artery to the basilar artery, is vulnerable to damage or distortion from external factors such as bony, ligamentous or muscular structures (Mehalic & Farhat, 1974; Parkin et al. 1978; Schellhas et al. 1980; Braun et al. 1983; Dunne et al. 1987; Fast et al. 1987). In the atlas vertebra, the retroarticular canal and the lateral bridge are examples of bony outgrowth or exostosis which may cause external pressure on the vertebral artery as it passes from the foramen transversarium of the vertebra to the foramen magnum of the skull. If this pressure is severe enough, as may occur during the extreme rotatory movements carried out during therapeutic manipulation of the cervical spine, the vertebral artery may be compressed (Lamberty & Zivanovich, 1973), reducing its cross-sectional area, and compromising its blood flow (Taitz & Nathan, 1986). Vertebrobasilar ischaemia from compression of the vertebral arteries by osteophytes is an uncommon occurrence under normal circumstances (Warlow, 1996).

There are few studies of the lateral bridge of the atlas reported in the literature (MacAlister, 1869, 1893; Lamberty & Zivanovic, 1973; Saunders & Popovich, 1978; Taitz & Nathan, 1986). The lateral bridge was first described by MacAlister (1869, 1893) as a variety of the ‘posterior glenoid process’ (the retroarticular canal), which he termed the ‘gleno-transverse bony arch’. As its name implies, it is a lateral outgrowth of bone from the superior articular facet or lateral mass to the posterior root of the transverse process of the atlas (MacAlister, 1869, 1893; Lamberty & Zivanovic, 1973; Saunders & Popovich, 1978; Taitz & Nathan, 1986). The retroarticular canal is formed by an exostosis passing from the posterior surface of the lateral mass to the posterior margin of the vertebral artery groove of the atlas. Thus the lateral bridge forms another arch, secondary to the retroarticular canal, through which the vertebral artery must pass (MacAlister, 1869).

The sternalis muscle is an uncommon anatomical variant. It is located on the human anterior pectoral wall, superficial to pectoralis major. This muscle has been reported both in males and females, and in whites, blacks and Asians (Barlow, 1934; Kida & Kudoh, 1991; Shen et al. 1992; Bradley et al. 1996).

Although the importance of this muscle is still a mystery, various different interpretations have been made. Clemente (1985) considered sternalis to be a misplaced pectoralis major, although some embryologists have viewed it as part of a ventral longitudinal column muscle layer arising at the ventral tip of the hypomeres (Sadler, 1995). Sadler claimed that this muscle is represented by rectus abdominis in the abdominal region and by the infrahyoid musculature in the cervical region; in the thorax, this layer usually disappears but occasionally remains as a sternalis muscle. Kitamura et al. (1985) reported a case of congenital partial deficiency of pectoralis major accompanied by an enormous sternalis. Barlow (1934), on the other hand, claimed that sternalis represents the remains of a panniculus carnosus.

The importance of continuing to record and discuss anatomical anomalies was addressed recently by Hicks & Newell (1997) in the light of technical advances and interventional methods of diagnosis and treatment. Two recent radiological reports (Bradley et al. 1996; Murphy & Nokes, 1996) highlighted the diagnostic dilemma posed by a sternalis muscle in the detection of breast cancer.

A joint meeting of the Anatomical Society of Great Britain and Ireland, the Nederlandse Anatomen Vereniging and the Anatomical Society of Southern Africa was held from 15 to 17 April 1998 at Rolduc, Limburg, The Netherlands. It included symposia on ‘Recent advances in human evolution research’ on Wednesday 15 April and on ‘Adaptation of cells and tissues to mechanical stimuli’ on Thursday 16 April. The first EFEM Lecture was given by Professor J. Voogd of Erasmus University Rotterdam on ‘Transformations and interactions of cerebellar maps’ on Friday 17 April. The following are abstracts of communications and demonstrations presented at the meeting.

Anatomical Society of Great Britain and Ireland

Future meetings

26–27 November 1998. Symposium on the morphogenetic and genetic analysis of vertebrate development, hosted by the Spanish Anatomical Society in Madrid, Spain, with the participation of the ASGBI.

5–7 January 1999. Winter meeting hosted by the Centre for Human Biology, University of Leeds.

13–15 July 1999. Summer meeting hosted by the Laboratory of Human Anatomy, University of Glasgow.

Anatomical Society Research Studentships. Grant funding is available for Research Studentships in the anatomical sciences, commencing October 1999. The closing date for applications is 9 October 1998.

The International Society for the Study of the Lumbar Spine (ISSLS). The 26th annual meeting of the ISSLS will be held in Hawaii on 21–25 June 1999. The deadline for submission of abstracts is 15 November 1998.

ISSLS International Fellowship Fund. Appropriate individuals from developing countries are eligible for this Fellowship to enable them to attend the 1999 meeting in Hawaii. The applicants should have a demonstrated interest in clinical or nonclinical spinal research and should send a letter outlining their work together with 2 letters of sponsorship from their superiors and the abstract of a paper or poster to Dr Hanley at the above address by 1 January 1999.

Surgical Dynamics Travelling Fellowship Fund. The ISSL has received an educational grant from Surgical Dynamics for a Travelling Fellowship for US $5000. The deadline for applications is 1 March 1999. The committee will announce its selection at the annual meeting of the Society in Hawaii, 21–25 June 1999.