Avascular necrosis of the femoral head in a cynomolgus macaque (Macaca fascicularis).

A cynomolgus macaque presented with right hindlimb lameness as well as crepitus and decreased passive range of motion of the right coxal joint. Radiography and histopathology were consistent with avascular necrosis of the femoral head. This case is the first published report of this condition in a cynomolgus macaque.

Upregulated genes in articular cartilage may help to counteract femoral head separation in broilers with 21 days of age.

Femoral head necrosis (FHN) is one of the most common conditions in fast growing broilers, being characterized by separation of articular cartilage from epiphysis and classified as femoral head separation (FHS) or FHS with laceration (FHSL) depending on severity. Although molecular mechanisms involved with this disorder have been observed, its etiology is still unclear. Therefore, the expression of 15 candidate genes, chosen based on previous transcriptomic studies, was evaluated in the articular cartilage (AC) of normal and FHS-affected broilers at 21 days of age. Samples were collected based on the absence or presence of FHS for physical-chemical and qPCR analysis. The AvBD2, RHAG, COL28A1, ADA and ANGPTL7 were upregulated in FHS-affected broilers compared to the healthy group. These genes are involved in immune response, defense against pathogens, inflammation, cellular migration and adhesion, indicating different molecular mechanisms to control FHS progression at early age. Our results can contribute to improve the knowledge on FHN etiology in chickens and other species, such as horse and pigs that are severely affected by bone disorders.

Endoplasmic reticulum stress, chondrocyte apoptosis and oxidative stress in cartilage of broilers affected by spontaneous femoral head necrosis.

With the promotion of the intensive breeding model, the incidence of leg diseases has risen in fast-growing commercial broilers with higher body weight, seriously affecting their feed efficiency and causing animal welfare problems. Femoral head necrosis (FHN) is the most common leg disease in broilers. Previous studies reported that hormone-induced FHN is related to endoplasmic reticulum (ER) stress, apoptosis, and oxidative stress, but no detailed study has been conducted in broilers with spontaneous FHN. In the study, the articular cartilage of 5-wk-old Ross 308 broilers with spontaneous FHN was used to investigate the pathogenesis of the disease. According to the degree of femoral head injury, the birds participating in the experiment were divided into 3 groups, namely a control group, femoral head separation group and femoral head separation with growth plate lacerations group. The morphological changes in articular cartilage were observed by hematoxylin and eosin, toluidine blue, alcian blue and safranine O-solid green staining, and the expressions of genes related to cartilage homeostasis, ER stress, autophagy, apoptosis and oxidative stress was detected using Real-Time Quantitative PCR. In the results, the expression of aggrecan and collagen-2 mRNA levels decreased in the articular cartilage of spontaneous FHN broilers, and the same changes were observed in the tissue staining results, indicating the disordered nature of articular cartilage homeostasis. At the same time, FHN in broilers causes ER stress in articular chondrocytes and regulates oxidative stress by activating the nuclear factor erythroid 2-related factor 2/antioxidant response element pathway through protein kinase RNA-like ER kinase. Autophagy can be activated through the protein kinase RNA-like ER kinase-activating transcription factor-4 pathway, and apoptosis can even be activated through CCAAT-enhancer-binding protein homologous protein. Therefore, the secretory activity of articular chondrocytes in spontaneous FHN broilers is negatively affected, which leads to the disorder of cartilage homeostasis and results in FHN due to ER-stress-mediated chondrocyte apoptosis and oxidative stress.

Changes of lipid and bone metabolism in broilers with spontaneous femoral head necrosis.

Blood biochemistry and bone metabolism were evaluated to investigate the etiology and mechanism of spontaneous femoral head necrosis (FHN) in broilers. According to the femoral head score of the fourth, fifth, and sixth week old FHN-affected broilers, they were divided into 3 groups, namely Normal group, femoral head separation group, and femoral head separation with growth plate lacerations group, and then carried out a comparative study. The results showed that the liver function (alanine aminotransferase and aspartate aminotransferase) and lipid metabolism (high-density lipoprotein and triglyceride) levels of broilers with spontaneous FHN were significant changed compared with the normal group. At the same time, accumulation of lipid droplets appeared in the liver, which illustrated that the occurrence of FHN may be related to lipid metabolism disorders. Tibia and femur parameters showed significant changes in bone mineral density and bone strength. The distribution of chondrocytes in the articular cartilage of broilers with FHN was irregular and vacuoles appeared, which indicated that cartilage homeostasis was destroyed. TUNEL staining showed that the apoptosis rate of articular chondrocytes in broilers with FHN in 6-week-old was significantly higher than that of normal broilers. Meanwhile, the bone markers (bone glaprotein and bone-specific alkaline phosphatase) changed significantly, indicating that the articular chondrocyte apoptosis and bone metabolism disorder may occur in FHN-affected birds. Therefore, FHN in broilers may be caused by dyslipidemia and abnormal bone metabolism.

A Field Study of Histologic and Bacteriologic Characterization of Femoral Head Separation and Femoral Head Necrosis.

Histologic and bacteriologic features for groups of average 31-day-old broilers displaying three gross categories of femoral head alterations were documented. Categories included simple femoral head separation (FHS), femoral head transitional changes (FHT), and femoral head necrosis (FHN). Groups with grossly normal (NORM) femoral heads and cull birds with FHN and having gross signs of sepsis (Cull-FHN) were also included in the study. There was a 10% occurrence of positive bacterial cultures for all birds tested. Most positive cultures (33%) were found in the Cull-FHN group, while only a 12% occurrence was seen in the FHS group, and no positives were present in the FHT or FHN groups. A 14% total occurrence of femoral bacterial chondronecrosis with osteomyelitis or simple osteomyelitis (BCO-O) was observed. A progressive increase in the prevalence of BCO-O was apparent between groups going from NORM (0%), FHS (4%), FHT (14%), FHN (13%), and reaching a maximum of 67% in the Cull-FHN group. Minimal to mild femoral head cartilage necrosis was present in 40% of NORM broilers and 100% of the FHS, FHT, and FHN groups, but at moderate severity in 20% of the Cull-FHN group. Thus, the majority of FHN cases were associated with aseptic cartilage necrosis rather than BCO-O. These findings suggest that aseptic cartilage necrosis may be as important as septic necrosis as a cause of gross femoral head disease. A 26% overall occurrence was seen for hip synovitis-arthritis, but group differences were not statistically significant. Synovitis was not seen in the NORM group and was present in some (12%) of the FHS group but was observed at a high rate in both the FHN (43%) and the Cull-FHN (50%) groups. Morphometric measurements demonstrated that the area size of femoral fibrous cortical defects or "cutback zones" were generally larger for all gross categories relative to NORM, with a significant difference between NORM and FHS groups. This study underscores the multifactorial etiology of FHN and the importance of conducting both histologic and bacteriologic evaluations in which gross evidence of FHN or BCO-O occurs.

Icariin Protects against Glucocorticoid-Induced Osteonecrosis of the Femoral Head in Rats.

BACKGROUND/AIMS: Glucocorticoid (GC)-related osteonecrosis of the femoral head (ONFH) is a common complication following administration of steroids to treat many diseases. Our previous study demonstrated that icariin (ICA) might have a beneficial effect on the bone marrow mesenchymal stem cells (BMSCs) of patients with steroid-associated osteonecrosis. In this study, we investigated the underlying mechanisms of ICA associated with the potential enhancement of osteogenesis and anti-adipogenesis in GC-related ONFH. METHODS: In vitro cell proliferation was evaluated by CCK-8 assay. Alizarin red S and alkaline phosphatase (ALP) activity were used to measure osteogenic differentiation, while adipogenic differentiation was revealed by oil red O staining and TG content assay. The expression level of osteogenesis-associated genes and PPARγ was evaluated by RT-qPCR, western blotting and immunofluorescence. A total of 30 female SD rats were randomly separated into three groups: a control group, a methylprednisolone (MPS) group and a MPS + ICA group. Serum ALP and TG (triglyceride), micro-CT scanning, histological and immunohistochemical analyses were performed in the animal model. RESULTS: In the in vitro study, ICA promoted proliferation, improved osteogenic differentiation and suppressed adipogenic differentiation of BMSCs treated with MPS. The group treated with MPS and 10-6 M ICA expressed higher levels of Runx2, ALP, bone morphogenetic protein (BMP) 2, and OC and lower expression of PPARγ than the MPS group. In the in vivo study, ICA prevented bone loss in a rat model of GC-related ONFH as shown by micro-CT scanning, histological and immunohistochemical analyses. CONCLUSIONS: ICA is an effective compound for promoting bone repair and preventing or delaying the progression of GC-associated ONFH in rats. This effect can be explained by its ability to improve the balance between adipogenesis and osteogenesis, indicating that ICA is an effective candidate for management of GC-associated ONFH.

Animal models of steroid-induced osteonecrosis of the femoral head-a comprehensive research review up to 2018.

Osteonecrosis of the femoral head (ONFH) is a significant cause of both pain and disability that often affects young adults during what ought to be their most productive age. Two broad categories of ONFH exist: traumatic and non-traumatic. Traumatic ONFH results from acute mechanical disruption of the femoral head's blood supply. Many factors that increase the risk of non-traumatic osteonecrosis have been identified. Steroid-induced osteonecrosis of the femoral head (SONFH) is the most common form of non-traumatic ONFH. Many hypotheses as to the pathogenesis of SONFH have been proposed, including intravascular thrombosis, abnormal fat metabolism, intramedullary adipocyte hypertrophy, and osteoporosis; however, the exact mechanism of SONFH is still not clearly understood. Animal models using rats, mice, rabbits, chickens, pigs, and emus have been used to study SONFH. Unfortunately, these models each have limitations. Therefore, it is necessary to establish a reproducible model that better simulates human disease. The present review is intended to summarize the currently available models, evaluative indicators, and application of current understanding to both the prevention and treatment of SONFH.

Salidroside inhibits steroid-induced avascular necrosis of the femoral head via the PI3K/Akt signaling pathway: In vitro and in vivo studies.

Dexamethasone (Dex) and other glucocorticoids are widely used to treat serious infections and immunological diseases, however they may cause steroid­induced avascular necrosis of the femoral head (SANFH). Salidroside (Sal) has demonstrated an anti­apoptotic effect on neurocytes by activating the phosphoinositide 3­kinase (PI3K)/protein kinase B (Akt) signaling pathway. In the present study, primary osteoblasts were used in vitro and in rats in vivo to determine the anti-apoptotic effect of Sal on SANFH. The result of the present study demonstrated that pretreatment with Sal increased the cell survival rate while decreasing the cell apoptosis and lactate dehydrogenase release rate. Additionally, Sal also caused the reduction of TUNEL positive cells in TUNEL staining assay. Sal decreased the expression of cleaved caspase-3, cleaved caspase­9, apoptosis regulator BAX and cytochrome C, while it increased the expression of B cell lymphoma­2 and phosphorylated­Akt in Dex­induced osteoblasts. In vivo Sal protected against SANFH in rats by decreasing the percentage of empty lacunae. The present study demonstrated that Sal alleviated Dex­induced osteoblast apoptosis by activating the PI3K/Akt signaling pathway and downregulating caspase­3 expression in osteoblasts. Sal also protected against SANFH in a rat model of SANFH by decreasing the percentage of empty lacunae. The inhibition of the mitochondrial apoptosis pathway was also involved. Further research is required to determine the full underlying mechanisms by which Sal has an effect.

Autologous Platelet Concentrates as Treatment for Avascular Necrosis of Femoral Head in a Dog.

Avascular necrosis of the femoral head is a developmental disturbance that generally affects young dogs of small breeds and produces ischemic necrosis of the femoral head resulting in an incongruous and malformed joint. The most common treatment is the excisional arthroplasty of the head and femoral neck. The aim of this study is to describe the treatment of avascular necrosis in a Yorkshire dog using intra-articular injections of autologous platelet concentrate. Evaluations were made at 0, 15, 30, 60, and 120 days of treatment, describing the following parameters: clinical gait analysis, perimetry, goniometry, and radiographic evaluations. The results obtained in this case suggest that the autologous platelet concentrate may be an alternative for the treatment of avascular necrosis of the femoral head in dogs.

Bone characteristics, histopathology, and chondrocyte apoptosis in femoral head necrosis induced by glucocorticoid in broilers.

Femoral head necrosis (FHN) is a common disorder in fast-growing broilers in the poultry industry, but the pathogenesis of FHN has not been clarified completely. In the present study, glucocorticoid (GC) administration was used to induce FHN in broilers. Compared with normal birds, histopathology showed that the length of the articular cartilage of GC-induced FHN broilers was thicker while the proliferative zone and prehypertrophic zone were obviously thinner. Moreover, hematoxylin and eosin (HE) staining showed the apoptotic chondrocyte in the growth plate of the femoral head in FHN-affected birds. Bone parameters also decreased significantly in GC-induced FHN broilers. In addition, as for the mRNA expression, GC-induced FHN broilers had an apparent reduction in Col-II, Col-X, and Bcl-2 but a significant promotion of Caspase-3, Caspase-9, ASK-1, and JNK-1 when compared with the normal birds. It showed glucocorticoid induced FHN in broilers by affecting the proliferation, differentiation, and apoptosis of chondrocytes accompanying the retarding of bone growth.

Comprehensive Genome-Wide Transcriptomic Analysis of Immature Articular Cartilage following Ischemic Osteonecrosis of the Femoral Head in Piglets.

OBJECTIVE: Ischemic osteonecrosis of the femoral head (ONFH) in piglets results in an ischemic injury to the immature articular cartilage. The molecular changes in the articular cartilage in response to ONFH have not been investigated using a transcriptomic approach. The purpose of this study was to perform a genome-wide transcriptomic analysis to identify genes that are upregulated in the immature articular cartilage following ONFH. METHODS: ONFH was induced in the right femoral head of 6-week old piglets. The unoperated femoral head was used as the normal control. At 24 hours (acute ischemic-hypoxic injury), 2 weeks (avascular necrosis in the femoral head) and 4 weeks (early repair) after surgery (n = 4 piglets/time point), RNA was isolated from the articular cartilage of the femoral head. A microarray analysis was performed using Affymetrix Porcine GeneChip Array. An enrichment analysis and functional clustering of the genes upregulated due to ONFH were performed using DAVID and STRING software, respectively. The increased expression of selected genes was confirmed by a real-time qRTPCR analysis. RESULTS: Induction of ONFH resulted in the upregulation of 383 genes at 24 hours, 122 genes at 2 weeks and 124 genes at 4 weeks compared to the normal controls. At 24 hours, the genes involved in oxidoreductive, cell-survival, and angiogenic responses were significantly enriched among the upregulated genes. These genes were involved in HIF-1, PI3K-Akt, and MAPK signaling pathways. At 2 weeks, secretory and signaling proteins involved in angiogenic and inflammatory responses, PI3K-Akt and matrix-remodeling pathways were significantly enriched. At 4 weeks, genes that represent inflammatory cytokines and chemokine signaling pathways were significantly enriched. Several index genes (genes that are upregulated at more than one time point following ONFH and are known to be important in various biological processes) including HIF-1A, VEGFA, IL-6, IL6R, IL-8, CCL2, FGF2, TGFB2, MMP1, MMP3, ITGA5, FN and Col6A1 were upregulated in the immature articular cartilage following ONFH. A qRTPCR analysis of selected genes confirmed the upregulated expression observed in the microarray analysis. CONCLUSION: Immature articular cartilage responds to ONFH by the upregulation of genes involved in hypoxic stress response, angiogenesis, matrix remodeling and inflammation. This study provides novel insights into the multi-faceted role of immature articular cartilage, with inflammation as a key component, following ONFH in piglets.

Poultry Femoral Head Separation and Necrosis: A Review.

Femoral head separation (FHS) is a degenerative skeletal problem in fast-growing poultry wherein the growth plate of the proximal femur separates from its articular cartilage. At its early phase, FHS may remain asymptomatic but lead to epiphyseal breakage, infection, and femoral head necrosis (FHN). Healthy femoral head is viewed as a positive trait for genetic selection. However, the etiology of FHS is poorly understood for use in noninvasive diagnosis and genetic selection. Focal cell death and atrophic changes are likely associated with separation of tissues and necrotic changes. Fibrotic thickening of the articular surface can also impair free movement of the proximal epiphysis in the acetabulum, leading to FHS, under strain. The major limitation to understanding the pathophysiology of FHN is the lack of suitable experimental models and biomarkers to diagnose the problem. In this review, we discuss the possible etiologic factors, anatomic features of the chicken femoral head, biomarkers, and molecular mechanisms relevant to FHN.

Downregulation of basic fibroblast growth factor is associated with femoral head necrosis in broilers.

Femoral head necrosis (FHN) is a metabolic cartilage disease of rapidly growing broilers. The aim of the present study was to investigate the role of basic fibroblast growth factor (bFGF) in the apoptotic processes associated with FHN. Broilers were selected and categorized based on clinical examination in 3 groups: healthy, femoral head separation, or femoral head separation with growth plate lacerations. Hematoxylin and eosin staining showed fewer chondrocytes in the resting zone of the growth plates when FHN occurred. Moreover, the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay revealed a significant increase in chondrocyte apoptosis. Furthermore, immunohistochemical assays and real-time quantitative PCR analysis demonstrated a decline in bFGF expression. In addition, reduced Bcl-2 mRNA expression was observed along with a corresponding increase in Bax and caspase-3 mRNA expression in FHN samples. There was a correlation between bFGF protein expression and the proportion of TUNEL-positive cells and a correlation between bFGF mRNA expression and expression of Bax, and caspase-3. The results of the study suggested that the expression of bFGF was reduced in the process of chondrocyte apoptosis, which could play an important role in the pathogenesis of FHN in chickens.

Nano total hip replacement in 12 dogs.

OBJECTIVE: To determine the short-term clinical outcome of nano total hip replacement (NanoTHR) in dogs. STUDY DESIGN: Retrospective case series. ANIMALS: Dogs (n = 12). METHODS: Medical records (2009-2011) of dogs that had nano-THR were reviewed for signalment, weight, clinical signs, side, age, prosthesis sizes, concurrent surgeries performed, complications, operative time, 3-month postoperative pelvic radiograph results, and lameness scores. RESULTS: Breeds were Yorkshire Terriers (n = 6), Toy Poodles (2), with 1 each of Maltese, Pomeranian, Cavalier King Charles Spaniel, and Shih-Tzu. Median body was 4.87 kg (range, 2.5-5.90 kg) and median age, 35.75 months (range, 12-144 months). Radiographs were taken in 4 dogs at 12 days (n = 2), 14 days (1), and 30 days (1) after surgery because of presentation for an acute grade 5 lameness. Three dogs had femoral fractures distal to the femoral implant tip and 1 dog displaced the acetabular implant medially. After revision surgery, all femoral fractures were assessed as healed with intact plate fixation. The dog with the medially displaced acetabular component responded to conservative management including strict confinement and analgesic administration. Eight dogs (58%) were assigned a grade 1 lameness and 4 dogs were grade 2 (33%) at 12-week examination. The 3 dogs with grade 5 lameness scores found to have femoral fractures within 1 month after surgery, subsequently improved to grade 1 (n = 1) and 2 (2) 12 weeks after revision surgery. The dog with medial acetabular displacement improved to a grade 2 lameness 12 weeks after conservative management. CONCLUSIONS: Although all 12 dogs had good-to-excellent outcomes, 33% experienced significant complications associated with the technique. As improvements in instrumentation and refinements in the technique are developed, NanoTHR can be considered an alternative to the femoral head and neck ostectomy (FHO) or medical management of coxofemoral disease for toy breed dogs. Further studies with a larger number of dogs and longer follow-up times are required.

Bone resorption markers and dual-energy x-ray absorptiometry in dogs with avascular necrosis, degenerative joint disease, and trauma of the coxofemoral joint.

OBJECTIVES: To compare the ability of N-terminal telopeptide (NTx) assays and dual-energy x-ray absorptiometry (DEXA) to detect bone resorption in dogs with nonneoplastic bone lysis and evaluate the correlation between these diagnostic tools. STUDY DESIGN: Prospective, cross-sectional clinical study. ANIMALS: Dogs (n = 35; 39 femoral heads) that had femoral head and neck ostectomy and 6 cadaver specimens from healthy immature small dogs. METHODS: Small dogs with avascular necrosis (n = 12), a reference group of small dogs (7), large dogs with degenerative joint disease (DJD; 10), and large dogs with trauma (10) were studied in addition to 6 femoral heads harvested from 6 small immature and healthy dogs euthanatized for reasons unrelated to this study. Densitometric measurements of femoral heads, urine NTx excretion, and serum NTx concentration were compared between groups. RESULTS: Avascular necrosis resulted in a decrease in bone mineral density (BMD) (0.18 ± 0.01 g/cm(2;) P < .01) of the femoral head and elevation of serum NTx (159.3 ± 59.4 nM; P = .03) compared to small dog controls (0.28 ± 0.02 g/cm(2) ; 18.7 ± 1.83 nM, respectively), but did not seem to affect urine NTx. DJD in large dogs did not seem to affect any of the densitometric parameters evaluated. BMD (P = .03) and serum NTx (P = .04) were lower in small compared to large dogs. Serum NTx and densitometric measurements correlate inversely with each other (P = .001) but neither test correlated with urine NTx (P = .8-.9). CONCLUSION: Serum NTx levels vary with dog size but seem to correlate better with BMD better than urine NTx excretion in dogs with nonneoplastic bone resorption.

Treatment of avascular necrosis of the femoral head in small dogs with micro total hip replacement.

OBJECTIVES: To evaluate clinical outcome of small dogs with avascular necrosis (AVN) of the femoral head treated with Micro total hip replacement (THR). STUDY DESIGN: Nonrandomized, retrospective efficacy case series. ANIMALS: Dogs (n = 7; 7 hips) that had Micro THR. METHODS: Medical records (December 2005-March 2009) of dogs affected with AVN treated with Micro THR were reviewed. Data analysis included age, sex, breed, body weight, and body condition. All dogs were evaluated at least 6 months after Micro THR was performed on the affected AVN limb. Physical, orthopedic, and radiographic examination, owner questionnaire, thigh girth, and ground reaction force were evaluated. RESULTS: Seven dogs (7 Micro THR) met the inclusion criteria. Mean age at time of onset of clinical signs was 7.7 months and mean age at time of Micro THR was 9.6 months. Mean body weight was 4.2 kg. Median body condition score was 5.0 (range, 4-6). Mean cumulative functional scores from client questionnaires before (19.5; range, 11-25) and after Micro THR (8.2; range, 7-14) were significantly different (P = .004). There was no significant difference between thigh girths of the Micro THR (17.8 ± 2.6 cm; range, 14.5-21.5 cm) limbs when compared with contralateral (17.5 ± 2.9 cm; range, 14.5-22.0 cm) limbs (P = .38). Peak vertical force (P = .20), vertical impulse (P = .81), peak braking force (P = .91), braking impulse (P = .19), peak propulsion force (P = .32), and propulsion impulse (P = .19) were not significantly different in Micro THR limbs compared with contralateral limbs. CONCLUSION: There was no relationship between age, sex, and breed for development of AVN in this study. Dogs that received Micro THR for the treatment of AVN had no significant differences in thigh girth and ground reaction forces when Micro THR limb was compared with the contralateral limb.

Enterococcus cecorum infections in broiler breeders and their offspring: molecular epidemiology.

Increased mortality and problems with lameness were reported in Dutch broiler flocks from the year 2008 onwards. Therefore, a field inventory, including 10 affected broiler flocks, nine corresponding broiler breeder flocks and five hatcheries, was carried out. The onset of clinical signs (lameness and increased mortality) started at about 2 weeks of age. The flock mortality varied from 3.1 to 8.1% at slaughter. Post-mortem lesions of broiler flocks were characterized by the occurrence of pericarditis/hydropericardium, arthritis and femoral head necrosis. Enterococcus cecorum was isolated from approximately 30% of the lesions. In the broiler breeders, E. cecorum was not isolated from any of the lesions. However, it was isolated from 31 out of 65 (47%) cloacal swabs, from two out of 65 (3%) oviduct samples, from one out 65 (1.5%) bone marrow samples and from two out of 25 (8%) blood samples. E. cecorum was not isolated from the air samples or dead-in-shell originating from the hatcheries involved. In total, 78 isolates were subjected to further typing by means of tRNA intergenic spacer PCR and confirmed as E. cecorum. The genetic relatedness of these cocci was subsequently studied using pulsed-field gel electrophoresis. The banding patterns of approximately 68% of E. cecorum isolates originating from parent stock flocks were clonal to one or more isolates of the same or other parent flocks. In contrast, isolates originating from their diseased offspring showed much greater genetic variation. Therefore, the vertical transmission of E. cecorum could not be demonstrated.

Biochemical and physiological weaknesses associated with the pathogenesis of femoral bone degeneration in broiler chickens.

Femoral bone degeneration has been recognized as an important cause of lameness in broiler chickens for many years, but the pathogenesis of this condition has not been completely elucidated. The current work presents comprehensive analyses of changes associated with femoral bone degeneration based on findings from gross pathology, histopathology, biochemistry, and synchrotron-based imaging techniques. Gross lesions were predominantly seen in epiphysis and metaphysis of the proximal femur, and infrequently in distal femur, but we did not observe gross lesions in the diaphysis. Bone fractures were observed occasionally, but the most common lesions involved separation of articular cartilage of the femoral bone head, with progressive erosions of the subchondral bone. In advanced cases, on histopathological examination, changes in femoral bone were indicative of chondronecrosis and osteonecrosis. Computed tomography revealed that the degenerative process involves loss of trabecular bone. The course of the lesion development in the mineralized matrix appears to be coupled with increased bone resorption associated with excessive proliferation of pathologically altered osteoclasts. Light microscopy, Fourier transform infrared spectroscopy, and biochemical analysis provided consistent evidence that lowered protein content of the bone organic matrix is an integral component of femoral bone pathology, but these changes do not appear to be associated with excessive activity of matrix metalloproteinases. Taken together, our findings indicate that femoral bone degeneration is associated with structural changes occurring in both inorganic and organic matrix of the bone, but insufficiency in protein metabolism is most probably a primary aetiological factor in the natural history of femoral bone degeneration. However, it is important to stress that our findings do not negate the importance of bacterial infection in the evolution of this condition. Pathogens play a critical role in the progressive pathogenesis of this condition, which ultimately is manifested, in most instances, as femoral head necrosis.

Necrosis avascular de la cabeza femoral: estudio experimental en corderos / Avascular necrosis of the femoral head: experimental study in lambs

Objetivo: Establecer un modelo experimental reproducible, en el cordero, para provocar una necrosis avascular de la cabeza del fémur. Material y metodología: Utilizamos 21 corderos, con edades comprendidas entre los 6 y 22 semanas. En el primer grupo (13 corderos) se seccionó la musculatura ilio-inguinal, inyectando una sustancia esclerosante y ligando los vasos pericapsulares en el cuello femoral, mediante cerclaje de alambre. En el segundo grupo (9 corderos) se ligó el cuello femoral mediante brida de plástico y sección del ligamento redondo. No se utilizó ningún tipo de inmovilización. El sacrificio de los animales se realizó, según el grupo, entre las 15 y 34 semanas. Efectuamos estudios radiográficos, macroscópicos e histológicos. Resultados: Las cabezas femorales mostraron un centro secundario de osificación y un adelgazamiento del cartílago fisario, más intenso en los animales con evolución superior a 7 semanas tras el insulto vascular. Se observó un aumento de la densidad ósea de la cabeza femoral, con aplanamiento cefálico, disposición irregular de la fisis e hipercrecimiento del trocánter mayor. Hallamos necrosis del cartílago articular sin apreciar una invasión vascular de la zona hipertrófica del cartílago de crecimiento. En la metáfisis hallamos áreas fibróticas. Conclusión: La lesión vascular experimental en la cadera de corderos inmaduros produce cambios apreciables en el cartílago articular, el centro secundario de osificación, la fisis de crecimiento y la metafisis (AU)

Objective: To establish a reproducible experimental model in lambs to cause avascular necrosis of the femoral head. Material and Methods: We used 21 lambs, aged between 6 and 22 weeks. In the first group (13 lambs), the ilioinguinal musculature was sectioned, injecting a sclerosing substance and ligating the pericapsular vessels in the femoral neck by wire cerclage. In the second group (9 lambs), the femoral neck was ligated using a plastic loop and sectioning of the round ligament. No type of immobilization was used. The animals were sacrificed, depending on the group, between 15 and 34 weeks. We conducted radiographic, gross, and histological studies. Results: The femoral heads showed a secondary site of ossification and thinning of growth plate cartilage, more severe in the animals with course longer than 7 weeks after vascular injury. Increased bone density in the femoral head, with cephalic flattening, irregular arrangement of the physis and hypergrowth of the greater trochanter was observed. We found necrosis of joint cartilage without evidence of vascular invasion. of the hypertrophic area of cartilage growth. We found fibrotic areas in the metaphysis. Conclusion: Experimental vascular injury in the hip of immature lambs causes substantial changes in joint cartilage, the secondary site of ossification, the growth physis and metaphysis (AU)