Spontaneous recovery of experimental valgus deformity in lambs.

INTRODUCTION: Angular deformity in the growing skeleton of animals, especially in the radius and ulna, is occasionally seen in clinical practice. The mechanism of spontaneous correction of these angular deformities however remains to be elucidated. The purpose of our experiment was to explore the ability of a growth plate to correct an induced valgus deformity, and to study the mechanism of correction. METHODS: Before beginning the study, valgus deformity of the distal radius had been induced in lambs by the application of a device that causes asymmetrical compression of the growth plate. The study began after removal of the device and spontaneous correction of the induced deformity was observed weekly for 20 weeks. The angles of the deformity and longitudinal growth on the medial and lateral portions of the growth plate were respectively measured on craniocaudal and mediolateral radiographs. RESULTS AND CONCLUSIONS: Spontaneous correction of the valgus deformity occurred during the first 16 weeks. It resulted from asymmetrical growth characterised by restricted activity of the medial portion of the growth plate (14.8%) in comparison to the lateral portion of the experimental radius, and also in comparison to the medial portion of the control radius.

A case of dorso-medial luxation of the radial carpal bone in a dog.

Luxation of the radial carpal bone is an uncommon injury in the dog and cat. Previous clinical cases have reported palmaro-medial luxation with injury to the short radial collateral ligament. In this study a case of dorsomedial luxation of the radial carpal bone in a 10-year-old female Gordon Setter is described. A closed reduction of the luxation was performed and a conservative treatment was carried out. Thirteen months after the reduction, the dog had a satisfactory limb function, despite the presence of degenerative joint disease of the carpus. A pathogenic hypothesis for this dorso-medial luxation of the radial carpal bone is proposed reproducing the luxation on canine cadavers.

Reduced psychostimulant effects on dopamine dynamics in the nucleus accumbens of mu-opioid receptor knockout mice.

Dopamine neurotransmission in the nucleus accumbens plays a pivotal role in the reinforcing properties of drugs of abuse. Two interacting processes regulate nucleus accumbens dopamine overflow: release of dopamine from presynaptic terminals and the subsequent reuptake by dopamine transporters. Opioid neurotransmission, primarily through mu-opioid receptors has also been strongly implicated in drug reward. We have previously shown that mice lacking the mu-opioid receptor display decreased cocaine self-administration. In addition, we found decreased impulse activity of midbrain dopaminergic neurons and an increased GABAergic input to these neurons in mu-opioid receptor knockout mice. In the present study we investigated whether these changes in dopaminergic cell bodies are accompanied by altered dopamine dynamics at the terminal level. To that aim, we measured nucleus accumbens dopamine overflow using fast scan cyclic voltammetry. Our data demonstrate that in mu-opioid receptor knockout mice 1) the reuptake of dopamine in the nucleus accumbens is slower, and 2) the relative effect of cocaine and amphetamine on the reuptake of dopamine is smaller compared with wild type mice. These data provide a mechanism for the decreased reinforcing properties of cocaine observed in mu-opioid receptor knockout mice.

Increased gabaergic input to ventral tegmental area dopaminergic neurons associated with decreased cocaine reinforcement in mu-opioid receptor knockout mice.

There is general agreement that dopaminergic neurons projecting from the ventral tegmental area (VTA) to the nucleus accumbens and prefrontal cortex play a key role in drug reinforcement. The activity of these neurons is strongly modulated by the inhibitory and excitatory input they receive. Activation of mu-opioid receptors, located on GABAergic neurons in the VTA, causes hyperpolarization of these GABAergic neurons, thereby causing a disinhibition of VTA dopaminergic neurons. This effect of mu-opioid receptors upon GABA neurotransmission is a likely mechanism for mu-opioid receptor modulation of drug reinforcement. We studied mu-opioid receptor signaling in relation to cocaine reinforcement in wild-type and mu-opioid receptor knockout mice using a cocaine self-administration paradigm and in vitro electrophysiology. Cocaine self-administration was reduced in mu-opioid receptor knockout mice, suggesting a critical role of mu-opioid receptors in cocaine reinforcement. The frequency of spontaneous inhibitory post-synaptic currents onto dopaminergic neurons in the ventral tegmental area was increased in mu-opioid receptor knockout mice compared with wild-type controls, while the frequency of spontaneous excitatory post-synaptic currents was unaltered. The reduced cocaine self-administration and increased GABAergic input to VTA dopaminergic neurons in mu-opioid receptor knockout mice supports the notion that suppression of GABAergic input onto dopaminergic neurons in the VTA contributes to mu-opioid receptor modulation of cocaine reinforcement.

Osseointegration of composite calcium phosphate bioceramics.

The resistance of macroporous calcium phosphate ceramics to compressive strength generally is low and depends on, among other factors, porosity percentage and pore size. A compromise always is adopted between high porosity, required for a good integration, and mechanical strength, which increases with material density. We improved the strength of macroporous calcium phosphate ceramics of interconnected porosity by filling the pores with a highly soluble, self-setting calcium phosphate cement made of TCP and DCPD. Cylinders of the resulting material were implanted in sheep condyles and subjected to histological analysis after 20, 60, and 120 days. Microradiographs were made of the histological sections. The control material consisted of ceramic that had not been loaded with cement. Progressive ingrowth of bone into the ceramic pores occurred as the cement was degraded during the first implantation period. Marked degradation of the cement was apparent after 2 months, with fragmentation of the cement in most of the pores and the presence of bone tissue between the fragments. All the cement had been replaced by bone after 4 months. Some fragments of cement still were embedded in the newly formed bone. There was no significant difference between the integration of loaded and nonloaded ceramics. Filling the macroporous ceramic pores with a calcium phosphate cement significantly improved the mechanical strength of these ceramics without modifying their integration in the healing bone.

Histological integration of allogeneic cancellous bone tissue treated by supercritical CO2 implanted in sheep bones.

UNLABELLED: Different chemical or physical methods of bone processing have been developed to decrease the antigenicity of allogeneic bone which may delay or prevent graft integration. We have developed a method based on delipidation and deproteination of the bone with a supercritical fluid and hydrogen peroxide. Cylinders of cancellous allogeneic bone treated in this way were implanted for four weeks, four months or eight months in holes drilled in sheep condyles or tibial plateau. Histological sections were then processed and analysed qualitatively and quantitatively using an image analysis software coupled to a light microscope. Measurements were made of the trabecular bone surface (BS/TS), the relative osteoid surface (OS/BS), the active osteoid surface (OS/BS), active resorption surface (Oc.S/BS) and the relative surface of newly formed bone. After four weeks, the control cylinders (non-treated allogeneic bone) had been invaded by cellular tissue composed of lymphocytes and plasmocytes surrounding remnants of the donor bone marrow tissue. The processed cylinders showed osteoid apposition at the surface of their external trabeculae. The trabecular bone and osteoid surfaces were significantly higher in the processed bone sections than in the control bone sections. After four months, most of the control material had been osteolysed and replaced by connective tissue containing lymphocyte islets, while the processed materials showed a large amount of bone synthesized at the surface of implant trabeculae which appeared fragmented and disseminated within the newly formed bone. All the histomorphometric parameters measured were significantly different from those of the control. By eight months, most of the control material had been totally osteolysed with very little bone ingrown in the implantation site. Only one control implant had been integrated. The processed cylinders were difficult to discern from the bone in which they were implanted. The parameters measured on the processed cylinders were significantly higher than those measured on the control sections. IN CONCLUSION: the treatment applied to the bone enhanced allogeneic bone integration and could provide a new kind of tissue treatment for bone banking.