The relationship between microstructure, stiffness and compressive fatigue life of equine subchondral bone.

Subchondral bone injuries often precede articular cartilage damage in osteoarthritis and are common in thoroughbred racehorses due to the accumulation of fatigue damage from high speed racing and training. Thus, racehorses provide a model to investigate the role of subchondral bone in joint disease. We assessed the association of horse and racing related factors and micro-CT based micromorphology of three separate subchondral bone layers with the initial stiffness and compressive fatigue life of bone plugs. Furthermore, we investigated three different definitions of fatigue failure of subchondral bone during compressive fatigue testing. Initial stiffness was 2,362 ±â€¯443 MPa (mean ±â€¯standard deviation). Median compressive fatigue life during cyclic loading to -78 MPa was 16,879 (range 210 to 57,064). Subchondral bone stiffness increased over a median of 24% (range 3%-42%) of fatigue life to a maximum of 3,614 ±â€¯635 MPa. Compressive fatigue life was positively associated with bone volume fraction in the deeper layers of subchondral bone, maximal stiffness, and the number of cycles to maximal stiffness. Initial stiffness was positively associated with tissue mineral density in the deeper layers and bone volume fraction in the superficial layer. Most specimens with a fatigue life of less than 5,500 cycles fractured grossly before reaching 30% reduction of maximal stiffness. Cycles to 10% reduction of maximal stiffness correlated strongly with cycles to lowest recorded stiffness at gross fracture and thus is a valid alternative failure definition for compressive fatigue testing of subchondral bone. Our results show that subchondral bone sclerosis as a result of high speed exercise and measured as bone volume fraction is positively associated with compressive fatigue life and thus has a protective effect on subchondral bone. Further research is required to reconcile this finding with the common collocation of fatigue damage in sclerotic subchondral bone of racehorses.

Subchondral bone morphology in the metacarpus of racehorses in training changes with distance from the articular surface but not with age.

The repetitive large loads generated during high-speed training and racing commonly cause subchondral bone injuries in the metacarpal condyles of racehorses. Adaptive bone modelling leads to focal sclerosis at the site of highest loading in the palmar aspect of the metacarpal condyles. Information on whether and how adaptive modelling of subchondral bone changes during the career of a racehorse is sparse. The aim of this cross-sectional study was to describe the changes in subchondral bone micromorphology in the area of highest loading in the palmar aspect of the metacarpal condyle in thoroughbred racehorses as a function of age and training. Bone morphology parameters derived from micro-CT images were evaluated using principal component analysis and mixed-effects linear regression models. The largest differences in micromorphology were observed in untrained horses between the age of 16 and 20 months. Age and duration of a training period had no influence on tissue mineral density, bone volume fraction or number and area of closed pores to a depth of 5.1 mm from the articular surface in 2- to 4-year-old racehorses in training. Horses with subchondral bone injuries had more pores in cross-section compared with horses without subchondral bone injuries. Differences in bone volume fraction were due to the volume of less mineralised bone. Tissue mineral density increased and bone volume fraction decreased with increasing distance from the articular surface up to 5.1 mm from the articular surface. Further research is required to elucidate the biomechanical and pathophysiological consequences of these gradients of micromorphological parameters in the subchondral bone.

Compressive fatigue life of subchondral bone of the metacarpal condyle in thoroughbred racehorses.

In racehorses, fatigue related subchondral bone injury leads to overt fracture or articular surface collapse and subsequent articular cartilage degeneration. We hypothesised that the fatigue behaviour of equine subchondral bone in compression follows a power law function similar to that observed in cortical and trabecular bone. We determined the fatigue life of equine metacarpal subchondral bone in-vitro and investigated the factors influencing initial bone stiffness. Subchondral bone specimens were loaded cyclically in compression [54MPa (n=6), 66MPa (n=6), 78MPa (n=5), and 90MPa (n=6)] until failure. The fatigue life curve was determined by linear regression from log transformed number of cycles to failure and load. A general linear model was used to investigate the influence of the following variables on initial Young's Modulus: age (4-8years), specimen storage time (31-864days), time in training since most recent rest period (6-32weeks), limb, actual density (1.6873-1.8684g/cm(3)), subchondral bone injury grade (0-3), and cause of death (fatigue injury vs. other). Number of cycles to failure was (median, range) 223,603, 78,316-806,792 at 54MPa; 69,908, 146-149,855 at 66MPa; 13204, 614-16,425 at 78MPa (n=3); and 4001, 152-11,568 at 90MPa. The fatigue life curve was σ=112.2-9.6 log10Nf, (R(2)=0.52, P<0.001), where Nf is number of cycles to failure and σ is load. Removal of the three horses with the highest SCBI grade resulted in: σ=134.2-14.1 log10Nf, (R(2)=0.72, P<0.001). Initial Young's Modulus (mean±SD) was 2500±494MPa (n=22). Actual density (ρ) was the only variable retained in the model to describe initial Young's Modulus (E): E=-8196.7+5880.6ρ, (R(2)=0.34, P=0.0044). The fatigue behaviour of equine subchondral bone in compression is similar to that of cortical and trabecular bone. These data can be used to model the development of SCBI to optimize training regimes.

Another case of canine amoebic meningoencephalitis--the challenges of reaching a rapid diagnosis.

A case of granulomatous amoebic meningoencephalitis in a previously healthy, mature, apparently immunocompetent dog, with a history of exposure to stagnant water, is reported. The case presented with ataxia and a tendency to fall to the left side. A computed tomography (CT) showed a ring-enhancing lesion within the cerebellum; an examination of cerebrospinal fluid (CSF) revealed nonspecific mixed-cell pleocytosis. Despite antibiotic and anti-inflammatory therapy, clinical signs progressed rapidly to decerebellate rigidity over 4 days, and the dog was euthanased. Significant post-mortem findings were restricted to the brain, with a localised lytic lesion in the deep cerebellar white matter. Histopathological examination of the brain showed focally extensive cavitation of the white matter and communication of the lesion with the fourth ventricle. The affected area contained structures consistent with amoebae and was infiltrated by neutrophils mixed with lower numbers of macrophages, plasma cells and lymphocytes. The amoebae were identified as Balamuthia mandrillaris, based on specific immunofluorescence detection. Amoebic meningoencephalitis should be considered in dogs with evidence of focal cavitary lesions in the brain, particularly in cases with a history of swimming in stagnant water.

Gastrointestinal obstruction caused by a radiolucent foreign body in a green iguana (Iguana Iguana).

This report describes an intestinal obstruction in a green iguana (Iguana iguana). The patient was presented with vomiting and subtle signs of abdominal pain. Radiographs and ultrasound imaging did not reveal any abnormalities. A coeliotomy was performed and a 30-cm piece of absorbent cotton was removed surgically from the large intestine.

MRI characteristics and histology of bone marrow lesions in dogs with experimentally induced osteoarthritis.

Signal changes within the bone marrow adjacent to osteoarthritic joints are commonly seen on magnetic resonance (MR) images in humans and in dogs. The histological nature of these lesions is poorly known. In this study, we describe the MR imaging of bone marrow lesions adjacent to the stifle joints of dogs with experimental osteoarthritis over 13 months. Histology of the proximal tibia at the end of the study was compared with the last MR imaging findings. In five adult dogs, the left cranial cruciate ligament was transected. Post-operatively, MR imaging was performed at 1, 2, 3, 4, 6, 8, and 13 months. Dogs were euthanised after 13 months and histological specimen of the proximal tibia were evaluated. Bone marrow edema like MR imaging signal changes were seen in every MR examination of all dogs in one or more locations of the proximal tibia and the distal femur. Lesions varied in size and location throughout the whole study with the exception of constantly seen lesions in the epiphyseal and metaphyseal region at the level of the tibial eminence. On histology, hematopoiesis and myxomatous transformation of the bone marrow and/or intertrabecular fibrosis without signs of bone marrow edema were consistent findings in the areas corresponding to the MR imaging signal changes. We conclude that within the bone marrow, zones of increased signal intensity on fat suppressed MR images do not necessarily represent edema but can be due to cellular infiltration. Contrary to humans, hematopoiesis is seen in bone marrow edema-like lesions in this canine model of osteoarthritis.

Low-field Mri and arthroscopy of meniscal lesions in ten dogs with experimentally induced cranial cruciate ligament insufficiency.

Little is known about the magnetic resonance imaging (MRI) appearance of canine meniscal lesions. The aim of this study is to describe the MR appearance of meniscal lesions in dogs with experimentally induced cranial cruciate ligament (CCL) deficiency. The pilot study revealed dogs weighing approximately 10 kg to be too small for meniscal evaluation on low-field MRI. In the main study, dogs weighing approximately 35 kg were used. The left CCL was transected and low-field MRI was performed regularly until 13 months post-surgery. Normal menisci were defined as grade 0. Intrameniscal lesions not reaching any surface corresponded to grade 1 if focal and to grade 2 if linear or diffuse. Grade 3 lesions consisted in linear tears penetrating a meniscal surface. Grade 4 lesions included complex signal changes or meniscal distortion. Between 2 and 13 months post-surgery, all dogs developed grade 4 lesions in the medial meniscus. Most of them corresponded to longitudinal or bucket handle tears on arthroscopy and necropsy. Two dogs showed grade 3 lesions reaching the tibial surface of the lateral meniscus on MRI but not in arthroscopy. Such tears are difficult to evaluate arthroscopically; MRI provides more accurate information about the tibial meniscal surface. Grades 1 and 2 lesions could not be differentiated from presumably normal menisci with our imaging technique. An MRI grading system better adapted to canine lesions has yet to be developed. MRI is a helpful tool for the diagnosis of complete tears in the canine meniscus, especially in larger dogs.

Antigenic and genetic characterisation of lipoprotein lppC from Mycoplasma mycoides subsp. mycoides SC.

Lipoprotein lppC, an immunodominant antigen, and its corresponding gene lppC were characterised in Mycoplasma mycoides subspecies mycoides small colony (SC) type, the etiological agent of contagious bovine pleuropneumonia (CBPP). The lppC gene was found in the type strain of M. mycoides subsp. mycoides SC and in field strains isolated in Europe, Africa, and Australia, as well as in vaccine strains. Southern blot analysis indicated the presence of at least four copies of lppC in the genome of M. mycoides subsp. mycoides SC, of which only one seems to be functional. Genes homologous to lppC have also been detected in closely related mycoplasmas such as M. mycoides subsp. mycoides large colony (LC) type and in M. sp. bovine group 7. lppC is encoded as a precursor with a consensus sequence for a prokaryotic signal peptidase II. The amino acid sequence of lppC and its precursor showed similarity to both LppB (at the N-terminal domain) and LppQ (at the C-terminal domain), two lipoproteins described previously in M. mycoides subsp. mycoides SC. The N-terminal domain of the mature lppC seems to be surface exposed. The C-terminal domain presented an integral membrane structure made up of five repeated units, rich in hydrophobic and aromatic amino acids, which may have pore forming potential in the mycoplasmal membrane. A recombinant peptide representing the N-terminal half of lppC was obtained following cloning in vector pETHIS-1 and expression in Escherichia coli hosts. The recombinant protein was used on immunoblots for serological analysis of sera from cattle that were naturally or experimentally infected with M. mycoides subsp. mycoides SC.