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.

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.

Trabecular bone remodeling and bone mineral density in the adult cat during chronic dietary acidification with ammonium chloride.

Ammonium chloride (NH4Cl) is used as a urinary acidifier in the treatment and prevention of feline urologic syndrome. It is reported to cause alterations in calcium and bone metabolism in humans, dogs, and rats. Adult cats with normal renal function were fed 1.5% NH4Cl for 6 months to study the effects of chronic dietary acidification on trabecular bone remodeling of the iliac crest and bone mineral density (BMD) of lumbar vertebral trabecular bone and femoral cortex. Histomorphometric analyses of iliac crest biopsies were performed before and after treatment. Static and dynamic parameters of bone resorption and formation were determined. Single-energy quantitative computed tomography (SEQCT) was used to measure lumbar trabecular and femoral cortical BMD. There were no significant treatment effects in iliac crest trabecular bone remodeling or BMD of the vertebrae and femora. Bone remodeling activity decreased with time in both acidotic and control cats. Vertebral BMD increased with time in both groups of cats, whereas no change was seen in the femora. Thus, chronic dietary acidification for 6 months with therapeutic levels of NH4Cl produced no significant changes in trabecular bone remodeling or bone mineral density in adult cats.

Humoral hypercalcemia of malignancy in canine lymphosarcoma.

Studies on the pathogenesis of hypercalcemia in canine lymphosarcoma have led to conflicting results. The biochemical and bone histomorphometric findings in canine lymphosarcoma were examined in 19 hypercalcemic and 17 nonhypercalcemic dogs with lymphosarcoma. Compared to the nonhypercalcemic group, the hypercalcemic dogs demonstrated an increase in fasting and 24-h calcium excretion, an increase in fractional phosphorus excretion, and a significant increase in nephrogenous AMP excretion. Plasma 1,25-dihydroxyvitamin D and immunoreactive PTH levels were equivalent in the two groups. Quantitative bone histomorphometry performed on iliac crest biopsies revealed increased parameters of bone resorption in those hypercalcemic dogs with no evidence of tumor at the biopsy site, without a compensatory increase in bone formation. Acid-urea tumor tissue extracts from eight hypercalcemic and six nonhypercalcemic dogs were examined for adenylate cyclase-stimulating activity (ACSA). All tumors from hypercalcemic dogs contained ACSA, whereas none of the tumors from nonhypercalcemic dogs had ACSA. Further purification of one tumor extract yielded an adenylate cyclase-stimulating protein which appeared to interact specifically with the PTH receptor. We conclude that in some cases, hypercalcemia in canine lymphosarcoma is mediated by a tumor-derived circulating bone-resorbing factor which is distinct from PTH. ACSA detected in tumor tissue appears to be a reliable marker for the syndrome in vivo. The role of this activity in the pathogenesis of the syndrome remains to be determined.

Effect of prostaglandin E1 on regional haversian remodeling in beagles with fractured ribs: a histomorphometric study.

A histomorphometric study was carried out on healing defects in the ribs of beagles. A transverse fracture was made surgically in the midshaft of the left 9th and 10th ribs. Ten beagles received injections of either a buffer vehicle (n = 4) or prostaglandin E1 (PGE1) at a dose of 0.4 mg/day locally (n = 6) into the fracture sites for a 10-day period and were killed 30 days after the surgery. Double-pulsed fluorescent labels were given with each of two fluochrome markers, calcein before surgical treatment and oxytetracycline hydrochloride before killing. The objectives were to determine manifestations of the regional acceleratory phenomenon (RAP) as changes in regional remodeling in the haversian envelope induced by fracture, effects of PGE1 on modification of the RAP in the haversian envelope, and systemic effects of PGE1 on remodeling changes of the contralateral matching sites. The differences in haversian remodeling between the injured and uninjured ribs of the experimental dogs indicated an increase in activation frequency, that is, regional acceleratory phenomenon. The significant effect of PGE1 on enhancing fracture-induced acceleration of haversian remodeling was doubtful, because of the preexistent biologic differences found in the two experimental groups. Nevertheless, the two groups shared a similar pattern of remodeling activity. The posttraumatic mineralization that declined at the sampled sites need further investigation.

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.

A sequential study of bone lesions caused by isolates of an avian osteopetrosis virus, MAV-2(0).

The pathogenesis of avian osteopetrosis caused by rapid and slow-onset isolates of myeloblastosis associated virus, MAV-2(0), was studied by inoculation of 10-day-old chick embryos with virus. Femur and calvarium were examined at 15, 17 and 19 days in ovo and 7 and 25 days after hatching by histologic and immunoperoxidase techniques. Femur and calvarium were also examined by electron microscopy at 17 and 19 days in ovo and at 7 days after hatching. Avian osteopetrotic bone lesions were characterized by exuberant periosteal proliferation; the time of onset varied with different virus isolates. In the femur virus was first associated with osteoprogenitor cells, then with osteoblasts and finally with osteocytes as the cells progressed through normal sequences of differentiation. The amount of virus produced by these cells did not correlate with onset of periosteal proliferation. Slow onset isolates provoked early virus production, but proliferative lesions did not develop until later. Conversely, the rapid onset isolate induced little early virus production, although lesions were present. Periosteal proliferation was associated with and preceded by perivascular edema and perivascular cell necrosis within the bone cortex following infection by all isolates. However, the rapid onset isolate caused more severe lesions than other isolates. These lesions included vascular thrombosis, capillary necrosis and focal bone necrosis. The relationship between early vascular lesions and late periosteal proliferation seen with the slow onset isolates is not as clear as with the rapid onset isolate. Calvarial bone, a representative flat bone, was found to have virus present, but at a level less than the femur. Vascular lesions were rarely seen in the calvarium and bone proliferation did not occur at this site.

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.

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.

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.

The role of prostaglandins in bone in vivo.

Prostaglandins of the E series, primarily E2 and E1, have the greatest activity in bone. Following discovery of their potent ability to stimulate bone resorption in vitro, clinical investigations have placed prostaglandins at sites of localized bone resorption associated with inflammatory or space occupying lesions in vivo. These studies have shown that prostaglandin production at such sites may be increased by cytokines such as interleukin-1 but the mechanisms by which prostaglandins stimulate bone resorption are not yet known. Observation of periosteal bone formation in patients given, pharmacological doses of prostaglandin has led to investigation of its bone forming activity. Young, growing rats have increased metaphyseal bone formation and this is accompanied by increased periosteal and endocortical bone formation in older animals. In the mature animals there is a generalized activation of remodelling with increased formation in the remodeling cycle. This is also seen in oophorectomized rats and results in repletion of the lost bone in this model of osteoporosis. In animal models of localized disuse osteopenia, prostaglandins are found to be elevated at the site of bone loss and prostaglandin inhibitors at least partially protect against the exaggerated resorption that occurs. This is also seen in models of orthodontic tooth movement, periodontitis and osteomyelitis. Prostaglandin synthesis inhibitors have been shown to delay healing of bone and this has led to limitations on their use clinically in some situations. Exogenously administered prostaglandins have been found to enhance periosteal callus formation, but healing is not uniformly enhanced. Prostaglandins have also been associated with hypercalcemia in certain animal tumors that model human hypercalcemia of malignancy but are probably most important in this condition as mediators in the localized resorption of bone at tumor sites. These in vivo studies have shown that prostaglandins are involved with increases in both bone formation and bone resorption. In vitro studies have shown that prostaglandins stimulate osteoblasts as well as osteoclastic bone resorption but understanding these effects under in vivo conditions will require further investigation.

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.

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.

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.

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.

Comparison of carbon fibre and nylon suture for repair of transected flexor tendons in the horse.

Carbon fibre-polylactic acid composites and monofilament non-absorbable suture material were compared for the repair of surgically transected superficial digital flexor tendons in 10 horses. All surgical wounds healed by first intention. The repaired tendons were enlarged, the carbon implanted tendons being larger than those sutured. The horses were killed at six, eight, 12,20 or 24 weeks. Greater fibrous thickening occurred in tendons repaired with carbon fibre, especially at 12 weeks postoperatively. Carbon fibre incited a greater histological response with macrophages, lymphocytes, plasma cells, eosinophils and fibroblasts. The fibrous tissue in the repair sites appeared to mature and the collagen to align at a similar rate irrespective of the method of repair. Only that tissue within and immediately surrounding the carbon bundles was immature at six months. There was minimal tendency for carbon filaments to separate and those that did were often surrounded by epithelioid macrophages forming a granuloma. Massive eosinophil concentrations were present between each granuloma. With each sequential test period the sutured tendons became increasingly stronger than the carbon implanted tendons. This may have been because of the immature core of tissue associated with the carbon bundles. No carbon particles were detected in draining lymph nodes.

Effects of intramuscular polysulfated glycosaminoglycan on chemical and physical defects in equine articular cartilage.

The effect of intramuscular polysulfated glycosaminoglycan (PSG) on repair of cartilage injury was evaluated in eight horses. In each horse, one middle carpal joint had both a partial-thickness and a full-thickness articular cartilage defect created. In the contralateral middle carpal joint, chemical articular cartilage injury was created by intra-articular injection of 50 mg sodium monoiodoacetate (MIA). Horses were divided into two groups for treatment. Group 1 horses (control) received an intramuscular injection of normal saline every four days for a total of seven injections starting seven days after cartilage injury. Group 2 horses received 500 mg of PSG intramuscularly every four days for seven treatments starting seven days after cartilage injury. Horses were maintained for 12 weeks. Horses were evaluated clinically, and their middle carpal joints were evaluated radiographically and arthroscopically at the end of the study. Joint tissues were also collected and examined microscopically. The only significant difference between groups was slightly greater matrix staining intensity for glycosaminoglycans in the radiate articular cartilage layer in MIA injected and PSG treated joints. Partial-thickness defects had not healed and the predominant repair tissue in full-thickness defects was fibrous tissue. It was concluded that using this joint injury model, 500 mg PSG administered intramuscularly had no effect on the healing of articular cartilage lesions, and minimal chondroprotective effect from chemically induced articular cartilage degeneration.

Effect of prostaglandin E1 on the periosteal regional acceleratory phenomenon in fractured ribs: histomorphometric study in beagles.

Transverse fractures were made surgically in the midshaft of the left 9th and 10th ribs in adult Beagles. A buffer vehicle (n = 4) or 0.2 mg of prostaglandin (PG) E1/day (n = 6) was injected into the fracture sites twice a day for 10 days, and dogs were euthanatized on day 30. Double-pulsed fluorescent labels were given with each of 2 fluorochrome markers--calcein before surgical treatment and oxytetracycline HCl before euthanasia. Histomorphometric analysis was carried out on specimens collected in adjacent regions of the healing defects. The surface extent and width of the osteoid on fractured (P less than 0.01, P less than 0.05, respectively) and nonfractured (P less than 0.05) sites in the treated group were greater than those in the nontreated group. The net loss of mineralizing surfaces was noticed on both ribs of both groups. Of 11 samples on the fractured side in the treated group, 4 contained periosteal new bone proliferation. There was increased osteoid formation and decreased mineralizing surfaces in the PGE1-treated group. Seemingly, administration of PGE1 induced bone matrix formation on periosteal envelope adjacent to a fracture site and its contralateral matching site.

Effect of prostaglandin E2 on rib fracture healing in beagles: histomorphometric study on periosteum adjacent to the fracture site.

A histomorphometric study was done on healing defects in the ribs of Beagles. A transverse fracture was made in the left 9th and 10th ribs. Beagles were given either ethanol vehicle (n = 6) or prostaglandin (PG) E2 orally (n = 5) for the 30-day period after surgical manipulation to time of necropsy. Double fluorescent labels to measure bone matrix mineralization were given with each of 2 fluorochrome markers--calcein before dogs were surgically manipulated and oxytetracycline hydrochloride before they were euthanatized. The objectives were to determine the effects of fracture on regional remodeling in the periosteum, the effects of PGE2 on the regional remodeling changes in the periosteum induced by the fracture, and the systemic effect of PGE2 on remodeling changes of the contralateral matching sites. The fracture in the nontreated dogs (ethanol only) stimulated remodeling activity in the periosteum with increased resorption (P less than 0.01). However, after surgical manipulation (necropsy) was done, the extent of mineralization on the bone surface was decreased and was decreased more on the nonfractured ribs (right side) than on the fractured (healing) ribs (left side) (P less than 0.05). In the treated dogs, the administration of PGE2 increased the extent of mineralization on the bone surface on the healing ribs. However, as in the nontreated dogs, the administration of PGE2 did not alter the decreasing pattern of mineralization when comparing the bone surfaces at necropsy with the bone surfaces before surgical manipulation was done.(ABSTRACT TRUNCATED AT 250 WORDS)

Histomorphometric comparison of measurements of trabecular bone remodeling in iliac crest biopsy sites and lumbar vertebrae in cats.

Trabecular bone remodeling values of the right and left iliac crest and lumbar vertebrae in cats were quantitated histomorphometrically and were compared. Healthy cats were given calcein (n = 2) or oxytetracycline (n = 2) twice for double-labeling of bone. Static and dynamic variables of bone resorption and formation were determined. Bone remodeling variables between right and left iliac crest were not significantly different (P less than 0.05). Significant differences (P less than or equal to 0.05) were not detected between values of iliac crest and lumbar vertebrae except in the percentage of osteoid surface. Percentage of osteoid surface was significantly (P less than or equal to 0.05) increased in the iliac crest compared with that in the vertebral body. Although not significantly different, values for bone formation were generally greater in the iliac crest than in the vertebral body. In healthy cats, values of trabecular bone remodeling were comparable between right and left iliac crest, and also were comparable between iliac crests and lumbar vertebrae.