Developmental stage and lower quadriceps flexibilities and decreased gastrocnemius flexibilities are predictive risk factors for developing Osgood-Schlatter disease in adolescent male soccer players.

PURPOSE: This study aimed to elucidate the influential predictive risk factors of Osgood-Schlatter disease (OSD) on the support (non-kicking) leg among adolescent soccer players considering peak height velocity (PHV) age and investigate the cut-off values of the predictive variables. METHODS: A cohort of 302 Japanese adolescent male soccer players aged 12-13 years were followed over 6 months. All players underwent physical examination, tibial tubercle ultrasonography, anthropometric and whole-body composition measurements, and muscle flexibility test of the support leg at the baseline. The developmental stage was evaluated from the PHV age. The OSD of the support leg was diagnosed 6 months later; players were divided into the OSD and control (CON) groups. The predictive risk factors were analyzed by multivariate logistic regression analysis. RESULTS: There were 42 players who had developed OSD at baseline and they were excluded from the study. Among the 209 players, 43 and 166 belonged to the OSD and CON groups, respectively. The predictive risk factors of OSD development were PHV age ± 6 months at baseline (p = 0.046), apophyseal stage of tibial tuberosity maturity at baseline (p < 0.001), quadriceps flexibility ≥ 35° at baseline (p = 0.017), and decrease in gastrocnemius flexibility in 6 months (p = 0.009). CONCLUSION: PHV age ± 6 months at baseline, apophyseal stage of the tibial tuberosity at baseline, quadriceps flexibility ≥ 35° at baseline, and decrease in gastrocnemius flexibility in 6 months are predictive risk factors of OSD development in the support leg among adolescent male soccer players. It is crucial to know the PHV age of each player, and not only the flexibility of quadriceps muscle but also the gastrocnemius should be monitored to predict OSD. LEVEL OF EVIDENCE: II.

Angular limb deformities due to distal radial physeal osteochondrosis in farmed deer stags in New Zealand.

CASE HISTORY: Three different farms reported cases of angular limb deformities (ALD) in rising 2-year-old velvet, mostly red deer (Cervus elaphus), stags with the earliest recorded cases occurring in 2010. Farm 1 reported a prevalence of 10-35%, farm 2, 5-11.5%, and farm 3, 2-5%. Farms 1, 2, and 3 are located in South Canterbury, northern Southland, and the Waikato, respectively. CLINICAL FINDINGS: Affected animals developed ALD, with predominantly varus forelimb (bowed) deformities. On all farms serum calcium and phosphorus concentrations in affected animals were normal. Serum and liver copper concentrations were variable across the period of the study and between farms. Although some measurements were below the reference ranges, there was no evidence for a statistical association with the prevalence of abnormalities. PATHOLOGICAL FINDINGS: The distal radius from 25 affected and four control red and red-wapiti (Cervus canadensis) cross deer from Farm 1 in 2010/2011, two affected red deer from Farm 2 in 2016, and one affected red deer from Farm 3 in 2021, were examined. The most consistent lesions were present in the distal radial physis, most commonly the lateral edge. There was mild-to-severe segmental thickening of the physis and, in some animals, physeal cartilage was duplicated with both sections of physis varying in thickness. Microscopically, in severely affected animals there was massive segmental thickening of physeal cartilage which often contained large cystic cavities. The cartilage matrix was eosinophilic and showed a loss of metachromatic staining with toluidine blue. In less severe cases, necrotic physeal vessels were present, consistent with vascular failure. In more chronic cases, there was duplication of the physis, the two layers being separated by a combination of normal trabecular bone and dense fibrous connective tissue. DIAGNOSIS: Physeal osteochondrosis. CLINICAL RELEVANCE: Osteochondrosis has a multifactorial aetiology and we propose that an increased requirement for nutrients for velvet production and increased weight-bearing stress (behaviour and rapid weight gain) may lead to progression of osteochondrosis and ALD in these deer. The involvement of periods of copper deficiency is unclear at this time.

Influence of osteochondrosis on the longevity and racing performance of standardbred trotters and pacers.

OBJECTIVE: To determine the influence of clinical osteochondrosis (OC) on the short-term (2, 3, and 4-year-old) and long-term racing performance and longevity of standardbred racehorses. STUDY DESIGN: Retrospective case-control study. SAMPLE POPULATION: Standardbred racehorses from a single breeding farm born between 2009 and 2017 that survived to racing age (n = 2711). Three hundred eighty-two (14%) horses were OC-affected (829 lesions confirmed arthroscopically during surgical treatment), and 2329 (86%) horses were nonaffected. METHODS: Racing performance data were obtained from an online database and evaluated with multiple linear regression models. RESULTS: Trotters were more likely than pacers to be affected by OC (odds ratio [OR] = 1.4, 95% CI = 1.1-1.9, P = .006). Compared with nonaffected horses, long-term OC-affected horses had 8.8 fewer starts (95% CI = -14.4 to -3.2, P = .002), 1.0 fewer wins (95% CI = -1.9 to -0.1, P = .030), and 3.8 fewer total number of first through third place finishes (95% CI = -6.2 to -1.4, P < .0001). Nonaffected horses had longer careers compared with OC-affected horses, racing 0.32 years longer (95% CI = -0.52 to -0.12, P = .002). Osteochondrosis had no impact on short-term racing performance. Horses with lesions at the distal intermediate ridge of the tibia or lateral trochlear ridge of the talus had decreased performance compared with horses without these lesions. CONCLUSION: Pacers were less likely than trotters to be affected by OC. Affected horses had fewer starts and shorter careers, despite early surgical intervention. CLINICAL SIGNIFICANCE: Osteochondrosis decreases long-term racing performance in racing standardbreds.

Insight into the possible aetiologies of Blount's disease: a systematic review of the literature.

Blount's disease or bowed leg deformity, is a unilateral or bilateral growth deformity of the medial proximal tibia that leads to a tibial varus deformity. A distinction can be made in an early and late onset type. The disease seems to have a predisposition for certain descends. Since the first publication of Blount's disease, different hypotheses on the aetiology are proposed but no consensus exists. The objective of this study is to provide an overview of the available hypotheses on the aetiology of Blount's disease since its first description and assessment of the available level of evidence, the quality of evidence and the occurrence of bias supporting these individual hypotheses. A systematic search according to the PRISMA statement was conducted using PubMed, MEDLINE, EMBASE and the Cochrane Library using a broad combination of terminology to ascertain a complete selection. Proper MESH search criteria were formulated and the bibliographic search was limited to English and Dutch language articles. Articles with no mention of aetiology or a disease related to Blount's were excluded. Level of evidence and types of bias were assessed. Thirty-two articles that discuss the aetiology of Blount's disease were selected. A variety of hypotheses was postulated in these articles with most research in the field of increased mechanical pressure (obesity, early walking age) and race (descend). Blount's disease most likely has a multifactorial origin with influence of genetic and racial predisposition, increased mechanical pressure on the growth plate as a consequence of obesity or early walking age and possibly also nutrition. However, the exact aetiology remains unclear, the probable explanation is that multifactorial factors are all contributing to the development of Blount's disease. Histological research has shown that a disorganization of bone and cartilage structures on the medial side of the proximal tibial physis is present in patients with Blount's disease. Based on the available evidence on the aetiology of Blount's disease, we conclude that it is multifactorial. Most papers focus only on one hypotheses of Blount's disease occurrence and all are characterized as low level of evidence. There seems to be a preference for certain descends. Further research on especially genetic predisposition is needed to provide more insight in this factor of Blount's disease.

Is There a Relationship between Patellofemoral Alignment and Osgood-Schlatter Disease? A Case-Control Study.

This study was aimed to investigate the role of anatomic variations in patellofemoral alignment in patients with or without Osgood-Schlatter disease (OSD) and to determine the potential anatomic risk factors that may play role in the etiology. This prospective observational case-control study was conducted on two groups of adolescent patients. Group 1 comprised patients who were diagnosed as having OSD and group 2 consisted of an equal number of age-matched patients who presented to the outpatient clinic with traumatic knee injury and underwent knee radiographic examination but without a diagnosis of OSD. Age, height, weight, body mass index (BMI), dominant side, and level of sporting activity were recorded. Quadriceps (Q) angles were measured using a long-arm goniometer with patients lying in the supine position with their knees in full extension and contracting the Q muscles. On anteroposterior, lateral knee, and tangential patella (Merchant and Laurin views) radiographs, the following measurements were performed: Insall-Salvati (IS), Caton-Deschamps (CD), and Blackburne-Peel (BP) indexes, congruence angles, lateral patellofemoral angles, sulcus angles, and patella type according to Grelsamer's morphology classification. Both groups were similar in respect of age (p = 0.160), sex (p = 0.311), height (p = 0.326), weight (p = 0.596), BMI (p = 0.153), and dominancy (p = 0.500). The rate of patients engaged in sports activities was significantly greater in the OSD group (p = 0.003). No significant difference was determined between the groups in respect to IS index, CD index, BP index, sulcus angle, lateral patellofemoral angle, and congruence angle (p-values: 0.358, 0.995, 0.912, 0.802, 1.000, and 0.907, respectively). The mean Q angle was measured as 15.6 ± 2.2 degrees in the OSD group and 14.3 ± 2.5 degrees in the control group (p = 0.014). Despite the difference being statistically significant, it was clinically insignificant because the difference was only 1.3 degrees. The principle etiologic factor seems to be increased physical activity rather than subtle variations is patellofemoral anatomy and alignment of extensor mechanism.

Slipped capital femoral epiphysis and Blount disease as indicators for early metabolic surgical intervention.

BACKGROUND: Slipped capital femoral epiphysis (SCFE) and Blount disease are strongly associated with pediatric obesity, yet they have only recently been identified as indications for consideration of metabolic and bariatric surgery (MBS). OBJECTIVES: To describe the relationships between pediatric obesity, MBS, SCFE, and Blount disease. SETTING: Nationwide database. METHODS: The national inpatient sample was used to identify patients ≤20 years old with obesity who underwent MBS from 2007 to 2016. Presence of SCFE and Blount disease was similarly extracted. RESULTS: The overall prevalence of SCFE and Blount disease among patients ≤20 years old is .02% for both (14,976, 11,238 patients, respectively) with no statistically significant change over the study period (P = .68, .07, respectively). The rates of SCFE and Blount disease in children with and without obesity are .46% versus .02% and .36% versus .01%, respectively (P < .001 for both). The mean age of patients with SCFE and obesity was 12 years old, while the mean age of those without obesity was 12.2 years old (P = .03). None of the children with obesity and SCFE underwent MBS. Similarly, the mean age of patients with Blount disease and obesity was 12.6 years old, while the mean age of those without obesity was 13.1 years old. Moreover, the mean age of children with Blount disease and obesity who underwent MBS was 16 years old (P < .001). CONCLUSIONS: Orthopedic complications remain a persistent problem in the pediatric population who suffer from obesity. Despite being diagnosed at a young age, patients with SCFE and/or Blount disease are not undergoing MBS until their later adolescent years, potentially leading to unnecessary disease progression or recurrence of disease after orthopedic interventions. Therefore, SCFE and Blount disease should be considered indications for early consideration of MBS in this pediatric population.

Double-Stranded RNA Is a Novel Molecular Target in Osteomyelitis Pathogenesis: A Translational Avian Model for Human Bacterial Chondronecrosis with Osteomyelitis.

Osteomyelitis remains a serious inflammatory bone disease that affects millions of individuals worldwide and for which there is no effective treatment. Despite scientific evidence that Staphylococcus bacteria are the most common causative species for human bacterial chondronecrosis with osteomyelitis (BCO), much remains to be understood about the underlying virulence mechanisms. Herein, we show increased levels of double-stranded RNA (dsRNA) in infected bone in a Staphylococcus-induced chicken BCO model and in human osteomyelitis samples. Administration of synthetic [poly(I:C)] or genetic (Alu) dsRNA induces human osteoblast cell death. Similarly, infection with Staphylococcus isolated from chicken BCO induces dsRNA accumulation and cell death in human osteoblast cell cultures. Both dsRNA administration and Staphylococcus infection activate NACHT, LRR and PYD domains-containing protein (NLRP)3 inflammasome and increase IL18 and IL1B gene expression in human osteoblasts. Pharmacologic inhibition with Ac-YVAD-cmk of caspase 1, a critical component of the NLRP3 inflammasome, prevents DICER1 dysregulation- and dsRNA-induced osteoblast cell death. NLRP3 inflammasome and its components are also activated in bone from BCO chickens and humans with osteomyelitis, compared with their healthy counterparts. These findings provide a rationale for the use of chicken BCO as a human-relevant spontaneous animal model for osteomyelitis and identify dsRNA as a new treatment target for this debilitating bone pathogenesis.

Prevalence of osteochondral lesions in the fetlock and hock joints of Standardbred horses that survived bacterial infection before 6 months of age.

BACKGROUND: Young Standardbred horses frequently develop fragments in joints. Some fragments represent osteochondrosis; others are considered developmental, but it is uncertain whether they result from preceding osteochondrosis. Osteochondrosis occurs as a consequence of failure of the cartilage canal blood supply and ischaemic chondronecrosis. In heritably predisposed foals, failure was associated with incorporation of vessels into bone. However, bacterial vascular failure was also recently documented in foals suffering spontaneous infections, proving that bacteria can cause osteochondral lesions in foals up to 150 days old. The aim was to determine prevalence of fetlock and hock lesions at screening age in Standardbred horses that survived infections before 6 months of age, and compare this to prevalence reported in the literature. METHODS: The material consisted of 28 Standardbred horses; 17 males and 11 females that presented and were diagnosed clinically with bacterial infections from 1 to 150 days of age (average: 41.3 days). A screening set of 8 radiographic projections was available from all 28 horses at 7-85 months of age (average: 23.6 months). Lesion prevalence was compared to three previously reported Standardbred cohorts. RESULTS: Osteochondral lesions were detected in one or more joints of 19/28 horses (67.9%); in the fetlock joint of 14/28 horses (50%) and the hock joint of 11/28 horses (39.3%). These prevalences were ≥ 2 x higher than the corresponding prevalences in the comparison cohorts, and statistically significantly so in 5:6 comparisons (p-values from < 0.00001 to 0.01). In the sepsis cohort, there were an average of 2.3 affected joints and 2.5 lesions per affected horse, whereas there in the one comparable literature cohort were an average of 1.5 affected joints and 1.7 lesions per affected horse. CONCLUSIONS: Standardbred horses that survived bacterial infections before 6 months of age had more osteochondral lesions than literature comparison cohorts at screening age. The implication was that some of the lesions in this group were caused by bacteria. It may become necessary to develop methods for differentiating between acquired, septic and aseptic, heritably predisposed lesions.

Septic Arthritis/Osteomyelitis May Lead to Osteochondrosis-Like Lesions in Foals.

Failure of the cartilage canal blood supply leads to ischemic chondronecrosis which causes osteochondrosis, and osteochondral lesions. Osteochondrosis is a disease with a heritable component and usually occurs under aseptic conditions. Because bacteria can bind to growth cartilage and disrupt the blood supply in pigs and chickens, we considered whether this might play a role in development of equine osteochondrosis. The aim of this study was to examine whether bacteria are present in canals in the growth cartilage of foals with septic arthritis/osteomyelitis, and whether this is associated with osteochondrosis. The material consisted of 7 foals aged 9-117 days euthanized because of septic arthritis/osteomyelitis. The 7 cases had 16 lesions in growth cartilage that were evaluated histologically. Bacteria were present in cartilage canals in foals with septic arthritis/osteomyelitis. Portions of necrotic canals adjacent to bacteria frequently contained neutrophils, termed acute septic canals; or granulation tissue with neutrophils, termed chronic septic canals. Acute and chronic septic canals were associated with ischemic chondronecrosis in the articular-epiphyseal cartilage complex (AECC) of 5 cases and in the physis of 2 cases, and ossification was focally delayed in 5 of those 7 cases. Lesions occurred with and without adjacent osteomyelitis. Bacteria were present in cartilage canals and were associated with focal chondronecrosis in both the AECC and the physis. This establishes sepsis as a plausible cause of some osteochondral lesions in horses. It is recommended that horses with sepsis-related osteochondral lesions may be used for breeding without increasing the prevalence of OCD-predisposing genes in the population.

Update on treatment of adolescent Blount disease.

PURPOSE OF REVIEW: Treatments available to correct adolescent Blount disease deformities differ in terms of features, advantages, and disadvantages. Each is indicated, therefore, for different scenarios of severity, physeal condition, and maturity. The purpose of this review is to update basic concepts, surgical treatments, and controversies concerning this disorder. RECENT FINDINGS: The cause of Blount disease is unknown although etiologic factors as morbid obesity and hypovitaminosis D are thought to be associated with it. Recently, semiinvasive techniques (guided growth) have been proposed for mild deformities but remain controversial. Osteotomies with external fixation (hexapodes) are still the most recommended corrective treatment in this condition. SUMMARY: Little is known about the origin and natural history of Blount disease. Treatment is always surgical and, given their complexity, should be preceded by a thorough analysis and planning regarding all deformities. Treatment principles are to correct the three-dimensional deformity and avoid recurrence. The choice of technique mainly depends on patient maturity and severity. Guided growth is a good choice for more immature patients with moderate deformities. Progressive correction using osteotomy or physeal distraction is indicated for patients with severe deformities and low remaining growth. The Taylor spatial frame is currently the most popular progressive correction device.

Arthroscopic Treatment of Osteochondral Lesions of the Talus Using Juvenile Articular Cartilage Allograft and Autologous Bone Marrow Aspirate Concentration.

Juvenile allogenic chondrocyte implantation (JACI; DeNovo NT Natural Tissue Graft®; Zimmer, Warsaw, IN) with autologous bone marrow aspirate concentrate (BMAC) is a relatively new all-arthroscopic procedure for treating critical-size osteochondral lesions (OCLs) of the talus. Few studies have investigated the clinical and radiographic outcomes of this procedure. We collected the clinical and radiographic outcomes of patients who had undergone JACI-BMAC for talar OCLs to assess treatment efficacy and cartilage repair tissue quality using magnetic resonance imaging (MRI). Forty-six patients with critical-size OCLs (≥6 mm widest diameter) received JACI-BMAC from 2012 to 2014. We performed a retrospective medical record review and assessed the functional outcomes pre- and postoperatively using the Foot and Ankle Outcome Score (FAOS) and Short-Form 12-item general health questionnaire. MRI was performed preoperatively and at 12 and 24 months postoperatively. Cartilage morphology was evaluated on postoperative MRI scans using the magnetic resonance observation of cartilage tissue (MOCART) score. The pre- to postoperative changes and relationships between outcomes and lesion size, bone grafting, lesion location, instability, hypertrophy, and MOCART scores were analyzed. Overall, the mean questionnaire scores improved significantly, with almost every FAOS subscale showing significant improvement postoperatively. Concurrent instability resulted in more changes that were statistically significant. The use of bone grafting and the presence of hypertrophy did not result in statistically significant changes in the outcomes. Factors associated with outcomes were lesion size and hypertrophy. Increasing lesion size was associated with decreased FAOS quality of life subscale and hypertrophy correlating with changes in the pain subscale. Of the 46 patients, 22 had undergone postoperative MRI scans that were scored. The average MOCART score was 46.8. Most patients demonstrated a persistent bone marrow edema pattern and hypertrophy of the reparative cartilage. Juvenile articular cartilage implantation of the DeNovo NT allograft and BMAC resulted in improved functional outcome scores; however, the reparative tissue still exhibited fibrocartilage composition radiographically. Further studies are needed to investigate the long-term outcomes and determine the superiority of the arthroscopic DeNovo procedure compared with microfracture and other cartilage resurfacing procedures.

Maternal obesity increases insulin resistance, low-grade inflammation and osteochondrosis lesions in foals and yearlings until 18 months of age.

INTRODUCTION: Obesity is a growing concern in horses. The effects of maternal obesity on maternal metabolism and low-grade inflammation during pregnancy, as well as offspring growth, metabolism, low-grade inflammation, testicular maturation and osteochondrotic lesions until 18 months of age were investigated. MATERIAL AND METHODS: Twenty-four mares were used and separated into two groups at insemination according to body condition score (BCS): Normal (N, n = 10, BCS ≤4) and Obese (O, n = 14, BCS ≥4.25). BCS and plasma glucose, insulin, triglyceride, urea, non-esterified fatty acid, serum amyloid A (SAA), leptin and adiponectin concentrations were monitored throughout gestation. At 300 days of gestation, a Frequently Sampled Intravenous Glucose Tolerance Test (FSIGT) was performed. After parturition, foals' weight and size were monitored until 18 months of age with plasma SAA, leptin, adiponectin, triiodothyronine (T3), thyroxine (T4) and cortisol concentrations measured at regular intervals. At 6, 12 and 18 months of age, FSIGT and osteoarticular examinations were performed. Males were gelded at one year and expression of genes involved in testicular maturation analysed by RT-qPCR. RESULTS: Throughout the experiment, maternal BCS was higher in O versus N mares. During gestation, plasma urea and adiponectin were decreased and SAA and leptin increased in O versus N mares. O mares were also more insulin resistant than N mares with a higher glucose effectiveness. Postnatally, there was no difference in offspring growth between groups. Nevertheless, plasma SAA concentrations were increased in O versus N foals until 6 months, with O foals being consistently more insulin resistant with a higher glucose effectiveness. At 12 months of age, O foals were significantly more affected by osteochondrosis than N foals. All other parameters were not different between groups. CONCLUSION: In conclusion, maternal obesity altered metabolism and increased low-grade inflammation in both dams and foals. The risk of developing osteochondrosis at 12 months of age was also higher in foals born to obese dams.

Chronic lateral epiphyseal separation of the proximal tibia causes late-onset tibia vara.

An adolescent obese boy showed late-onset unilateral tibia vara associated with physeal separation (slipped epiphysis) of the lateral proximal tibia and physeal widening of the lateral distal femur. These affected physes showed normal signal intensities by MRI. He was treated with lateral hemiepiphysiodesis of the left proximal tibia and the distal femur using two parallel eight-Plates, and varus deformity rapidly improved postoperatively without recurrence. This is the first case of late-onset tibia vara caused by lateral physeal separation of the proximal tibia. Normal growth of the medial physes around the knee would contribute toward significant correction after surgery.

Surgical Management of Osteochondrosis in Foals.

Osteochondrosis is common in young, athletic horses. Some lesions respond to conservative therapy. Surgical management is the mainstay of treatment. Arthroscopic debridement is useful in the femoropatellar joint, tarsocrural joint, fetlock joint, and shoulder joint. Debridement is associated with good outcomes, except in the shoulder joint. Osteochondrosis lesions in the elbow may be difficult to access arthroscopically, thereby transosseous debridement. Surgical management of subchondral cystic lesions of the medial femoral condyle consists of debridement, debridement with grafting, transcondylar screws, and intralesional corticosteroid injection. Surgical management is indicated with lameness and persistent effusion, and in many horses intended for athletic use.

Femoral epiphyseal cartilage matrix changes at predilection sites of equine osteochondrosis: Quantitative MRI, second-harmonic microscopy, and histological findings.

Osteochondrosis is an ischemic chondronecrosis of epiphyseal growth cartilage that results in focal failure of endochondral ossification and osteochondritis dissecans at specific sites in the epiphyses of humans and animals, including horses. The upstream events leading to the focal ischemia remain unknown. The epiphyseal growth cartilage matrix is composed of proteoglycan and collagen macromolecules and encases its vascular tree in canals. The matrix undergoes major dynamic changes in early life that could weaken it biomechanically and predispose it to focal trauma and vascular failure. Subregions in neonatal foal femoral epiphyses (n = 10 osteochondrosis predisposed; n = 6 control) were assessed for proteoglycan and collagen structure/content employing 3T quantitative MRI (3T qMRI: T1ρ and T2 maps). Site-matched validations were made with histology, immunohistochemistry, and second-harmonic microscopy. Growth cartilage T1ρ and T2 relaxation times were significantly increased (p < 0.002) within the proximal third of the trochlea, a site predisposed to osteochondrosis, when compared with other regions. However, this was observed in both control and osteochondrosis predisposed specimens. Microscopic evaluation of this region revealed an expansive area with low proteoglycan content and a hypertrophic-like appearance on second-harmonic microscopy. We speculate that this matrix structure and composition, though physiological, may weaken the epiphyseal growth cartilage biomechanically in focal regions and could enhance the risk of vascular failure with trauma leading to osteochondrosis. However, additional investigations are now required to confirm this. 3T qMRI will be useful for future non-invasive longitudinal studies to track the osteochondrosis disease trajectory in animals and humans. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:1743-1752, 2016.

The aetiology of rickets-like lower limb deformities in Malawian children.

UNLABELLED: Debilitating rickets-like lower limb deformities are common in children throughout the world, particularly in Malawi, Africa where the causes are unknown. We have identified that Blount disease and calcium deficiency rickets are the likely causes of these deformities and propose calcium supplementation as a potential treatment of Malawian rickets. INTRODUCTION: Surgical correction of rickets-like lower limb deformities is the most common paediatric operation performed at Beit Cure Orthopaedic Hospital, Malawi. The aim of this study was to investigate the aetiology of these deformities. METHODS: Children with a tibio-femoral angle of deformity >20° were enrolled (n = 42, 3.0-15.0 years). Anthropometric and early life and well-being data were collected. Early morning serum and urine samples were collected on the morning of the operation for markers of calcium and phosphate homeostasis. Knee radiographs were obtained, and the children were diagnosed with either Blount (BD, n = 22) or evidence of rickets disease (RD, n = 20). As BD is a mechanical rather than metabolic disease, BD were assumed to be biochemically representative of the local population and thus used as a local reference for RD. RESULTS: There were no differences in anthropometry or early life experiences between BD and RD. Parathyroid hormone (PTH), 1,25-dihydroxyvitamin D, total alkaline phosphatase and urinary phosphate were significantly higher and serum phosphate, 25-hydroxyvitamin D (25OHD) and tubular maximal reabsorption of phosphate significantly lower in RD than BD. There was no difference in serum calcium, fibroblast growth factor 23 or markers of iron status between groups. All children had 25OHD > 25 nmol/L. CONCLUSIONS: Vitamin D deficiency is not implicated in the aetiology of RD or BD in Malawian children. The cause of RD in Malawi is likely to be dietary calcium deficiency leading to elevated PTH resulting in increased losses of phosphate from the bone and glomerular filtrate. The causes of BD remain unclear; there was no evidence in support of previously suggested risk factors such as being overweight or starting to walk early. Prior to surgical intervention, supplementation with calcium should be considered for children with RD.

Impact of feeding and housing on the development of osteochondrosis in foals-A longitudinal study.

Osteochondrosis dissecans (OCD) is a developmental orthopedic disease caused by a failure of the endochondral ossification in epiphyseal plates and joint cartilage. This trouble may induce the presence of osteochondral fragments in the articulation, fissures or subchondral bone cysts in the growth cartilage. Occurrence of osteochondrosis is influenced by a complex interaction of different factors. Among these, the effect of the housing and the feeding of the foals during their first months of life, have been described as risk factors for the development of osteochondrosis. The aim of this study was to investigate the evolution of OCD lesions with a longitudinal study in 204 young foals from 6 to 18 months in comparison to the type of feeding and the type of housing conditions. These factors and OCD status were obtained by a questionnaire and radiological examination, respectively. This allowed dividing the foals into four groups according to the initial OCD status and the evolution of the condition. As a result, we found that foals fed with concentrates show a higher probability to develop OCD lesions (p=0.06), while foals not receiving concentrates, had a higher probability to heal from existing OCD lesions (p=0.001). This study supports the theory that management factors such as feeding or housing may influence the evolution of the osteochondrosis disease.

Differences in the vascular tree of the femoral trochlear growth cartilage at osteochondrosis-susceptible sites in foals revealed by SWI 3T MRI.

Focal ischemic chondronecrosis of epiphyseal growth cartilage (EGC) during endochondral ossification is believed to be a key early event on the pathway to osteochondrosis (OC) in both animals and humans. The lateral ridge of the equine trochlea is a site where severe osteochondritis dissecans lesions frequently arise and is a model for the study of naturally occurring disease. Non-invasive imaging to investigate EGC vascularity may help elucidate why focal ischemia occurs. 3T MRI susceptibility-weighted imaging (SWI) of femoral trochlea of OC predisposed (n = 10) and control (n = 6) day-old foals, with minimal joint loading after birth, was performed. SWI and 3D images revealed the EGC vascular architecture without a contrast agent, and matched histologic observations. No vascular lesions were identified. There was no difference in the vascular density and architecture between control and OC specimens, but a striking difference in vascular pattern was seen at the OC-predilected site in the lateral ridge of the trochlea in all specimens, when compared to the medial ridge of the trochlea, where OC lesions are rarely observed. This site was less ossified with more perichondrial vessels not yet bridging with the subchondral bone. Furthermore, the mean vascular density of all specimens was significantly higher at this site. We speculate that joint morphology and focal internal trauma on this site with a unique vascular architecture may trigger ischemic events at this site. SWI permitted visualization of EGC in young foals with a clinical 3T MRI and paves the way for non-destructive longitudinal studies to improve understanding of OC in all species. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:1539-1546, 2016.