Bovine viral diarrhea virus cyclically impairs long bone trabecular modeling in experimental persistently infected fetuses.

Persistent infection (PI) with bovine viral diarrhea virus (BVDV) has been associated with osteopetrosis and other long bone lesions, most commonly characterized as transverse zones of unmodeled metaphyseal trabeculae in fetuses and calves. This study was undertaken to characterize the morphogenesis of fetal long bone lesions. Forty-six BVDV-naïve pregnant Hereford heifers of approximately 18 months of age were inoculated with noncytopathic BVDV type 2 containing media or media alone on day 75 of gestation to produce PI and control fetuses, respectively, which were collected via cesarean section on days 82, 89, 97, 192, and 245 of gestation. Radiographic and histomorphometric abnormalities were first detected on day 192, at which age PI fetal long bone metaphyses contained focal densities (4 of 7 fetuses) and multiple alternating transverse radiodense bands (3 of 7 fetuses). Day 245 fetuses were similarly affected. Histomorphometric analysis of proximal tibial metaphyses from day 192 fetuses revealed transverse zones with increased calcified cartilage core (Cg.V/BV, %) and trabecular bone (BV/TV, %) volumes in regions corresponding to radiodense bands (P < .05). Numbers of tartrate resistant acid phosphatase positive osteoclasts (N.Oc/BS, #/mm(2)) and bone perimeter occupied (Oc.S/BS, %) were both decreased (P < .05). Mineralizing surface (MS/BS, %), a measure of tissue level bone formation activity, was reduced in PI fetuses (P < .05). It is concluded that PI with BVDV induces cyclic abnormal trabecular modeling, which is secondary to reduced numbers of osteoclasts. The factors responsible for these temporal changes are unknown but may be related to the time required for osteoclast differentiation from precursor cells.

Correlation of quantitative computed tomographic subchondral bone density and ash density in horses.

The purpose of this study was to compare subchondral bone density obtained using quantitative computed tomography with ash density values from intact equine joints, and to determine if there are measurable anatomic variations in mean subchondral bone density. Five adult equine metacarpophalangeal joints were scanned with computed tomography (CT), disarticulated, and four 1-cm(3) regions of interest (ROI) cut from the distal third metacarpal bone. Bone cubes were ashed, and percent mineralization and ash density were recorded. Three-dimensional models were created of the distal third metacarpal bone from CT images. Four ROIs were measured on the distal aspect of the third metacarpal bone at axial and abaxial sites of the medial and lateral condyles for correlation with ash samples. Overall correlations of mean quantitative CT (QCT) density with ash density (r=0.82) and percent mineralization (r=0.93) were strong. There were significant differences between abaxial and axial ROIs for mean QCT density, percent bone mineralization and ash density (p<0.05). QCT appears to be a good measure of bone density in equine subchondral bone. Additionally, differences existed between axial and abaxial subchondral bone density in the equine distal third metacarpal bone.

Subchondral bone failure in overload arthrosis: a scanning electron microscopic study in horses.

Mechanical overload leads to a common arthrosis in the metacarpal condyle of the fetlock joint of racehorses. This is usually asymptomatic but severe forms can cause lameness. Subchondral bone failure is often present and the predictability of the site provided an opportunity to study of the progression of bone failure from microcracks to actual collapse of subchondral bone. Twenty-five fetlock condyles from racehorses with various stages of disease were selected. Stages ranged from mild through severe subchondral bone sclerosis, to the collapse of bone and indentation or loss of cartilage known as 'traumatic osteochondrosis'. Parasagittal slices were radiographed and examined with scanning electron microscopy. Fine matrix cracks were seen in the subchondral bone layer above the calcified cartilage and suggested loss of water or other non-collagenous components. The earliest microcracks appeared to develop in the sclerotic bone within 1-3 mm of the calcified cartilage layer and extend parallel to it in irregular branching lines. Longer cracks or microfractures appeared to develop gaps as fragmentation occurred along the margins. Occasional osteoclastic resorption sites along the fracture lines indicated activated remodeling may have caused previous weakening. In one sample, smoothly ground fragments were found in a fracture gap. Bone collapse occurred when there was compaction of the fragmented matrix along the microfracture. Bone collapse and fracture lines through the calcified cartilage were associated with indentation of articular cartilage at the site.

Bacterial meningoencephalitis and ventriculitis due to migrating plant foreign bodies in three dogs.

Regional suppurative meningoencephalitis and ventriculitis of variable chronicity was diagnosed in three young dogs residing in Colorado. Grass awns were grossly identified in the right occipital cortex of one dog and in the right lateral ventricle of another. Intralesional plant material was microscopically evident in the dura mater overlying the right occipital cortex of the third dog. One grass awn was identified as a floret of Hordeum jabatum. In each case, aerobic culture of brain tissue identified multiple isolates of bacteria. The dogs presented with clinically variable, rapidly progressive neurologic dysfunction, including tetraplegia, depressed mentation, and episodic extensor rigidity, ataxia, circling, stupor, vocalization, and head-pressing. Encephalitis due to bacteria introduced from migrating plant foreign material is a potential sequela of intranasal, periocular, or pharyngeal foreign bodies.

Skeletal changes in hemochromatosis of Salers cattle.

Hemochromatosis is an inherited defect in Salers cattle, characterized by increased iron absorption and wasting in young animals. Loss of teeth and soft bones has been reported. This study details bone changes in a prospective study of an affected Salers heifer and an age-matched, half-sibling control. The heifer fell 2 weeks before euthanasia, developed non-weight bearing lameness, and then became recumbent. At necropsy, the heifer was smaller than the control and had fractures of the humerus, femur, and ribs. Distinctive circumferential laminations in the outer third of the cortex were seen radiographically as layers of variably decreased density. In midshaft cross sections, the cortex was wider in some long bones, and fluorescent labeling revealed irregular and intermittent mineralization in the outer cortical layers. Mineral apposition rates in osteons of the inner cortex were decreased as compared with the control, and longitudinal bone formation at the growth plate was markedly decreased. Histologically, there were buried layers of osteopenic, poorly mineralized plexiform bone in outer circumferential lamellae. There was stainable iron in woven bone cores of the matrix. Iron was found in occasional osteoclasts as well. The mandible was severely affected, with loss of cortical bone as well as trabecular bone around the teeth and resorption of dental roots. Bone analysis revealed iron levels in the affected calf that were 30-50 times greater than the control and decreased percent ash in the outer cortex. These results indicate that periosteal dysplasia and osteopenia are responsible for pathologic fractures and tooth loss.

Idiopathic pneumoperitoneum in a dog.

A 13-year-old, neutered male standard poodle with tachypnea and abdominal distension was diagnosed with pneumoperitoneum. Pneumoperitoneum can be due to a perforated gastrointestinal tract, penetrating abdominal wounds, gas-producing bacterial peritonitis, or it can be iatrogenically introduced during surgery. Idiopathic pneumoperitoneum is a condition diagnosed in humans after exclusion of perforated gastrointestinal tract and other known causes of free intra-abdominal gas. This report suggests that dogs may suffer from a similar syndrome.

Hepatic failure and hemochromatosis of Salers and Salers-cross cattle.

Hemochromatosis is rare in domestic mammals. Five clinical cases and one preclinical case of hemochromatosis were diagnosed in Salers and Salers-cross cattle. Clinical disease developed between 9 and 22 months of age. Animals were healthy until weaning but then lost weight, developed rough hair coats, and lost incisor teeth. In two animals, hemochromatosis was identified by liver biopsy, biochemical evidence of hepatic injury, and/or elevated transferrin saturation values. At necropsy, carcasses were thin, with firm dark brown livers and lymph nodes, soft bones, and brown-colored small bowel. The principal histologic changes were hepatocellular siderosis and periportal, bridging, and perivenular fibrosis. Siderocalcinosis involved collagen, elastin, reticulin, and basement membrane components in liver, lymph nodes, spleen, duodenum, and kidney. Hepatic iron concentrations in clinically affected cattle were 1,500-10,500 microg/g wet weight (reference range for cattle = <300 microg/ g). Ultrastructurally, the heaviest intrahepatic deposition was in hepatocytes, which contained large intracytoplasmic siderosomes. Iron deposition in bone was associated with osteopenia. Genetic analysis indicated a common ancestral bull in the pedigrees of five of six affected cattle; no pedigree was available for the remaining animal. Four dams of five affected animals were phenotypically normal and had histologically normal livers. Test mating of four cows to the ancestral bull resulted in a female calf that developed clinicopathologic and histologic evidence of preclinical hemochromatosis by 40 days of age. It was not possible to establish the pattern of inheritance because of the small number of pedigrees from affected cattle.

The role of subchondral bone in joint disease: a review.

Subchondral bone plays a role in the pathogenesis of osteochondral damage and osteoarthritis in horses and humans. Osteochondral fragmentation and fracture, subchondral bone necrosis and osteoarthritis are common diseases in athletic horses, and subchondral bone is now thought to play an integral role in the pathogenesis of these diseases. There have been numerous research efforts focused on articular cartilage damage and its pathogenesis, yet comparatively little effort focused on subchondral bone pathology or the coordinated disease states of the osteochondral tissues. The purpose of this report is to review the current understanding of osteochondral disease in all species and its application to equine research and practice. It can be concluded from this review that our current understanding of osteochondral disease is based on clinical and pathological sources; and that the lack of information about joint tissue adaptation and disease has hampered objective studies of osteochondral tissues.

Hip dysplasia in rabbits: association with nest box flooring.

PURPOSE: To study etiologic aspects of hip dysplasia in a colony of Dutch-belted rabbits. METHODS: Rabbits used in the study were part of a reproductive toxicologic study. Incidence of hip dysplasia among 296 Dutch-Belted rabbit kits raised on waxed cardboard, smooth Plexiglas, or Plexiglas covered with textured adhesive strips was recorded. All animals were examined at 2 to 4 weeks of age for inability to adduct one or more limbs, then were classified as normal or dysplastic. A subset of 16 juvenile male rabbits (4 normal, 12 affected) raised on Plexiglas flooring were given a physical examination at 12 weeks of age followed by complete necropsy. In four animals (one normal, three affected), pelvic radiography and neurologic examination were performed. RESULTS: Seven percent of the rabbits kits reared on waxed cardboard flooring and 22% of those reared on smooth Plexiglas flooring developed hip dysplasia. Animals reared on Plexiglas floor with traction strips did not have evidence of hip dysplasia. Among the animals selected for detailed analysis, body weight was similar between rabbits with or without splay leg. Affected animals had splaying of one or both hind limbs, various degrees of flattening and reduction of the size of the femoral head, subluxation of the hip, valgus deformity, and patellar luxation. Histologically, there was marked thickening of the hip joint capsule with fibrocartilage formation, mild trabecular bone loss, and bony sclerosis of the proximal portion of the femur and adductor muscle hypoplasia. CONCLUSIONS: Provision of non-slippery flooring during the postnatal period is critical in preventing development of hip dysplasia in rabbits. Hip dysplasia resulted in significant musculoskeletal changes, but not abnormal neurologic development.

Overload arthrosis: strain patterns in the equine metacarpal condyle.

An overload arthrosis occurs consistently in the palmar region of the metacarpal condyle of the equine fetlock (metacarpophalangeal) joint characterized by subchondral bone sclerosis, devitalization and mechanical failure leading to collapse of the overlying articular cartilage. Samples were selected of joints with mild, moderate, and severe subchondral sclerosis, in which cartilage collapse had not yet occurred. An additional group that had severe sclerosis with focal rarefaction suggesting impending collapse was also studied (n=5/group). Parasagittal slices were milled to 2.0 mm thickness and subjected to palmar forces 50 to 200% of those applied by the sesamoid bone at angles corresponding to early, mid and late stance support phases of the gait cycle. From contact radiographs in the loaded and unloaded samples, strains were determined by recognizing displacements in the trabecular patterns using texture correlation analysis. Failure did not occur in any of the samples. Strains were generally proportional to the forces applied and greatest at midstance. Strain patterns varied between samples and with the different loading positions. With increased subchondral bone sclerosis there was greater shear strain in overlying trabeculae. Strain patterns were not consistently different within the sclerotic bone at the site of failure. Focally higher strains at the surface were sometimes related to the edge of the platen which was molded to mimic the sesamoid bone in vivo. These results indicate that sclerotic thickening of subchondral bone transmits stresses to overlying trabeculae. No consistent strain pattern was recognized where devitalization and mechanical failure occurs. Focally higher strains related to the edge of the opposing sesamoid bone may play a role.

Clinical effects of exercise on subchondral bone of carpal and metacarpophalangeal joints in horses.

OBJECTIVE: To determine effects of treadmill exercise on subchondral bone of carpal and metacarpophalangeal joints of 2-year-old horses. ANIMALS: 12 healthy 2-year-old horses. PROCEDURE: Horses were randomly assigned to the control (n = 6) or exercised (6) groups. Horses in the exercised group ran on a high-speed treadmill 5 d/wk for 6 months. Horses in the control group were hand walked for the same amount of time. Results of clinical, radiographic, nuclear scintigraphic, and computed tomographic examinations, and serum and synovial concentrations of biochemical markers of bone metabolism were compared between groups. RESULTS: Exercised horses were significantly lamer at the end of the study than control horses. Radionuclide uptake in the metacarpal condyles, but not in the carpal joints, was greater in exercised horses, compared with control horses. Exercised horses also had a higher subchondral bone density in the metacarpal condyles than control horses, but such differences were not detected in the carpal bones. CONCLUSIONS AND CLINICAL RELEVANCE: None of the diagnostic techniques evaluated was sufficiently sensitive to detect all osteochondral damage. Computed tomography and computed tomographic osteoabsorptiometry were superior to conventional radiography for detecting small osteochondral fragments. Nuclear scintigraphy was a sensitive indicator of subchondral bone change but lacked specificity for describing lesions and discerning normal bone remodeling from damage. Newer techniques such as computed tomography may help clinicians better diagnose early and subtle joint lesions in horses prior to development of gross joint damage.

Calcified cartilage morphometry and its relation to subchondral bone remodeling in equine arthrosis.

The calcified layer of articular cartilage is known to be affected by age and mechanical factors that may play a role in the development of arthrosis. Because these factors are also related to subchondral remodeling and sclerosis, a morphometric study was carried out in fluorochrome-labeled animals to determine whether the level of subchondral remodeling affected the thickness of the calcified cartilage layer and its irregularity and vascularity at the interface with subchondral bone. These parameters were also studied at a site of increased mechanical stress. The area and thickness of the calcified cartilage layer was determined in basic fuchsin-stained ground sections (120 microm). The irregularity of the chondro-osseous interface was expressed as the ratio of its length to that of the relatively straight tidemark (Int/Tid) and the number of abutting vessels with and without fluochrome labels were counted (N.Ves/Tid,%L.Ves/Tid). These were compared with single-labeled surface (sLS/BS, %) in subchondral bone, which was used as an index of remodeling. In a group of 12 horses, in which one carpus had an osteochondral fragment surgically created 10 weeks earlier, there was activation of subchondral remodeling in the third carpal bone opposite the fragment. An increase in %L.Ves/Tid (p < 0.01) at the interface was correlated with the increase in %sLS/BS in subchondral bone (r=0.431, p=0.035). The number of abutting vessels and the interface irregularity were not significantly changed on the fragmented side. In the metacarpal condyles from the fetlock joints of the same horses there were no differences associated with the surgically created fragment in the carpus and no correlation of %L.Ves/Tid with subchondral %sLS/BS. At a site where mechanical overload and traumatic osteochondrosis is known to occur on the palmar surface, the calcified cartilage was thinner, and the interface irregularity tended to be greater. These findings indicate that activated subchondral remodeling extends to involve the calcified layer, but the thickness and irregularity of the calcified cartilage are not consistently related to current subchondral remodeling. At sites of mechanical overload the calcified cartilage was thinner and the interface tended to be more irregular, suggesting previous increased remodeling.

Subchondral bone failure in an equine model of overload arthrosis.

Gross examination of metacarpo-/metatarsophalangeal (fetlock) joints from racehorses revealed defects on the condylar surface that ranged from cartilage fibrillation and erosion to focal cartilage indentations and cavitation in subchondral bone characteristic of traumatic osteochondrosis. Because these lesions represented a spectrum of mechanically induced arthrosis in which microdamage is thought to play a role, a histologic study of sagittal sections was made to study the morphogenesis. Subchondral bone failure developed beneath a flattened section of the condyle where the margin of the sesamoid bone produces compression as well as shear on impact of the foot with the ground. Milder lesions had thickening of subchondral bone and underlying trabeculae. With advancing sclerosis an increased amount of osteocyte necrosis was present. Occasional vascular channels with plugs of matrix debris and cells were present just beneath the cartilage. There was increased prominence of subchondral vessels, and osteoclastic remodeling was seen in and around the sclerotic zone. Apparent fragmentation lines in the subchondral bone suggested increased matrix fragility. Irregular trabecular microfractures developed at a depth of a few millimeters. Increased vascularity with hemorrhage, fibrin, and fibroplasia could be seen in enlarged marrow spaces at this more advanced stage. The overlying articular cartilage was variably indented but remained largely viable with degeneration and erosion limited to the superficial layers. Focally, breaks in the calcified layer appeared to lead to collapse and cartilage infolding. In metacarpal condyles from experimental horses run on a treadmill, there were milder changes at the site. The subchondral bone was increased in volume and there was increased diffuse staining with basic fuchsin, but no increase in the number of microcracks was seen. The findings in the racehorses indicate that the equine fetlock condyle is a consistent site of overload arthrosis in which microfracture and failure in subchondral bone may occur. Controlled exercise in treadmill horses may provide a model in which to study the pathogenesis.

Effects of osteochondral fragmentation and intra-articular triamcinolone acetonide treatment on subchondral bone in the equine carpus.

To determine the effects of osteochondral fragmentation and intra-articular corticosteroid treatment on dynamics of bone remodelling and fragility, 12 horses each had a unilateral, 8 mm osteochondral fragment created in the distal aspect of one radiocarpal bone. Six of the horses were treated in the fragmented joint, and the other 6 were treated in the nonfragmented joint with 12 mg of triamcinolone acetonide (TA) 14 and 28 days after surgery. All horses were exercised on a high-speed treadmill starting 15 days, and ending 72 days after surgery. Horses treated with TA in the fragmented joints were significantly less lame than those treated in the nonfragmented joints. Third carpal bones from joints with fragments showed significantly more vascularity, single labelled surface, total labelled surface and mineralising surface in subchondral and subjacent trabecular bone. Trends were also seen towards higher vascular canal volume and osteochondral junction remodelling sites in third carpal bones from fragmented joints. No significant differences were seen in microdamage density or size between fragmented and nonfragmented joints. No significant influence of TA treatment was seen on any parameter measured. The results from this study show that osteochondral fragmentation induces significant changes in remodelling of opposing bones, and that the administration of corticosteroids into joints with fragmentation does not significantly alter bone remodelling or fragility.

Correlation of flexural structural properties with bone physical properties: a four species survey.

The present investigation explores the relationship between animal and bone physical traits and the mechanical properties of whole bone from four species. Mechanical testing was performed using three-point flexure on the femora and tibiae of mice, rats, rabbits and cats. Interspecies correlations of the physical traits to the mechanical properties were used to elucidate the most likely physical predictors of mechanical properties within a single species. Physical traits measured were total bone length (BL), mid-diaphyseal cortical area (CA), body mass (BM), body mass times bone length (BMBL) and bone dry mass (DM). Bone mechanical parameters determined by flexure testing to failure were the structural properties of stiffness (S), elastic strength (Pe), maximum strength (Pm), and the material properties of modulus of elasticity (E), elastic stress (sigma e), and elastic strain (epsilon e). Linear regressions were used to relate the physical trait to the mechanical properties. Interspecies regressions of physical traits to mechanical characteristics implied bone dry mass (DM) is a significant predictor of bone structural properties. Further evidence of this relationship was obtained by exploring the linear relationship for the femora of a single species (rabbit, N = 17) in which age and bone size were allowed to vary. Strength at the elastic limit (in N) within a single species was described by the equation, Pe = 42.9*DM + 42.9 +/- 42.0N, where DM is in grams.

Bone changes in mucopolysaccharidosis VI in cats and the effects of bone marrow transplantation: mechanical testing of long bones.

Mucopolysaccharidosis VI (MPS VI) is a genetic lysosomal storage disease in which a defect in aryl sulfatase B leads to accumulation of the glycosaminoglycan dermatan sulfate and abnormalities in the development of cartilage and bone. A feline model of this disease was used to evaluate the efficacy of bone marrow transplant (BMT) therapy. Long bones from MPS VI cats (N = 6) and MPS VI + BMT cats (N = 7) were compared with control cats (N = 11) and control + BMT cats (N = 5) in mechanical tests. Dissected femurs and tibias were subjected to three-point bending and a subgroup of tibias were tested with the mechanical response tissue analyzer (MRTA) in which vibration is used to measure tissue impedance. Cats with MPS VI had markedly decreased stiffness and strength in both bone (p < 0.01). There was no significant difference in the MPS VI + BMT group. In the tibias, there was also decreased stiffness and strength in the control + BMT group as compared to controls (p < 0.05). However, when cross-sectional area was used to normalize for bone size there was good correlation with strength in both femurs (r = 0.907, p < 0.01) and tibias (r = 0.915, p < 0.1), and there were no significant differences between groups in the modulus of elasticity. In the tibias, in which stiffness was measured by MRTA, there was significant correlation with three-point bending stiffness. These results indicate that, in cats with MPS VI, the decreases in stiffness and strength of long bones can be largely accounted for by the decrease in bone size (osteopenia) that is present.

Bone mineral density in feline mucopolysaccharidosis VI measured using dual-energy X-ray absorptiometry.

Dual-energy X-ray absorptiometry (DXA) was used to determine the in vivo bone mineral density (BMD) and bone mineral content (BMC) of lumbar vertebrae in six cats affected with the inherited lysosomal storage disease mucopolysaccharidosis VI (MPS VI). DXA was also performed on MPS cats that had a bone marrow transplant (BMT) and total body irradiation (TBI) (MPS + BMT; n = 7), normal cats that had a bone marrow transplant, and TBI (control + BMT; n = 8) and normal cats (control; n = 14). Following euthanasia, one of the lumbar vertebrae that had been scanned (L5) was harvested and bone volume (BV/TV%) was determined by histomorphometry. The in vivo BMD and BMD measurements were compared with the BV/TV%. There was a greater BMD and BMC in the MPS + BMT cats compared with the MPS cats but the difference was not statistically significant. However, there was a greater BV/TV% in the MPS + BMT cats compared with the MPS cats and the difference was significant (P = 0.0152). Correlation between the noninvasive in vivo DXA measurements of BMD and BMC and the BV/TV% was significant (r2 = 0.767, P < 0.0001; r2 = 0.504, P < 0.0001). Noninvasive in vivo DXA was a rapid and precise method for measuring the lumbar BMD and BMC in cats and it correlated well with histomorphometric determination of bone mass. Further, the response of inherited storage diseases such as MPS VI to therapy, such as BMT, could be monitored in a longitudinal fashion using DXA.

Characterization of osteopenia in feline mucopolysaccharidosis VI and evaluation of bone marrow transplantation therapy.

Studies on a feline model of MPS VI demonstrated a marked osteopenia in iliac crest bone samples from young adult animals with fewer, finer trabeculae. In the absence of significant differences in bone remodeling, this was considered due to defects in endochondral ossification and the formation of fewer trabeculae. Cell-level bone formation was normal despite the presence of vacuolated osteoblasts. Affected animals had vacuolated osteocytes in larger lacunae. Cats of the same age who had received a bone marrow transplant 12 months prior as young kittens, had significantly more trabecular bone with thicker trabeculae. The presence of smaller osteocyte lacunae in these animals as compared to their untreated MPS VI cats appeared to be a direct effect of bone marrow transplantation and a useful parameter to monitor its efficacy.

Anterior cruciate ligament fascia lata allograft reconstruction: progressive histologic changes toward maturity.

Biopsy samples were obtained arthroscopically from 21 patients who had undergone anterior cruciate ligament (ACL) reconstruction using rolled, freeze-dried fascia lata allograft in order to evaluate progressive histologic changes toward maturation. The study period was 3-20 months postoperation. The mean age (+/- SEM) was 31.9 +/- 10.3. Histomorphometry was used for quantitative evaluation. Arthroscopic examination showed fully synovialized allografts in all patients. Varying degrees of degenerative tissues were observed histologically. There was a significant, direct correlation between the percentage of polarized tissue and the maturity of the biopsy specimen (r = 0.9; p < 0.04). The mean area of polarization in the postrehabilitation period (10-20 months) was significantly higher (p < 0.01) than in the rehabilitation period (3-20 months). Overall, there was a progressive decrease in cellularity and vascularity as the allograft matured. Compared with the biopsy samples of normal ACLs, the allograft was still undergoing maturation 20 months postoperatively.

Effect of dietary phosphoric acid supplementation on acid-base balance and mineral and bone metabolism in adult cats.

Experimental evidence indicates that maintenance of urinary pH < or = 6.4 is the single most effective means of preventing feline struvite crystalluria or urolithiasis of noninfectious causes. This may be accomplished by dietary acidification, but must be moderated to avoid potential adverse effects of excessive acidification, including bone demineralization, negative calcium balance, potassium depletion, and renal disease. Effects of chronic dietary phosphoric acid supplementation on acid-base balance and on mineral and bone metabolism were investigated in adult, domestic cats. One group of 6 cats was fed a basal, naturally acidifying diet without added acidifiers, and another group of 6 cats was fed 1.7% dietary phosphoric acid. Changes observed during 12 months of study included development of noncompensated metabolic acidosis, increased urinary calcium excretion, and lower but positive calcium balance in cats of both groups. Urinary pH decreased in cats of both groups, but was significantly (P < 0.05) and consistently maintained < or = 6.4 in cats given dietary phosphoric acid. Urinary phosphorus excretion increased in cats of both groups, but was significantly (P < 0.05) greater in phosphoric acid-supplemented cats, leading to lower overall phosphorus balance as well. Potassium balance decreased in cats of both groups, but was only transiently negative in the phosphoric acid-supplemented cats midway through the study, and normalized at positive values thereafter. Plasma taurine concentration was not affected by dietary acidification, and remained well within the acceptable reference range for taurine metabolism. Double labeling of bone in vivo with fluorescent markers was followed by bone biopsy and histomorphometric measurement of several static and dynamic variables of bone formation. Overall indices of bone formation decreased in cats of both groups with age and confinement, but were not affected by dietary phosphoric acid supplementation. Dietary supplementation with phosphoric acid used as the principal inorganic P source to achieve moderate and stable degree of urinary acidification, did not appear over the course of 1 year, to have induced adverse effects on mineral, bone, or taurine balance in these adult domestic cats.