Orthopaedic Diagnoses in the Black Pediatric Population : JAAOS - Journal of the American Academy of Orthopaedic Surgeons

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Reviews: Review Article

Orthopaedic Diagnoses in the Black Pediatric Population

Bridges, Carla M. MD; Agarwal, Rashmi MD; Raney, Ellen M. MD

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Journal of the American Academy of Orthopaedic Surgeons 31(6):p 274-282, March 15, 2023. | DOI: 10.5435/JAAOS-D-22-00535
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Dr. Martin Luther King Jr. stated that “of all forms of inequity, injustice in health care is the most shocking and inhumane.”1 Differences in care exist at all levels of the healthcare delivery system based on socioeconomic status and race. Access to primary care, treatment in the emergency department, and hospital treatment have all been found to have racial discrepancies, with Black children most commonly ending up with less care and poorer quality of care.2 In the emergency department, patient race can affect analgesia, triage scores, wait times, treatments, diagnostic procedure utilization, rates of patients leaving without being seen, and patient experiences.3

One particularly problematic area is in the treatment of pain. Opioid treatment of pain in adolescents has been found to favor treating non-Hispanic White patients over minorities. A study by Phan et al2 demonstrated variability in treating pain based on race for the same diagnoses. These trends persist into adulthood, with pain in the Black population being ignored or undertreated across fields and through the end of life. Extensive work has been done in the past 5 years looking at persistent racial disparities in pediatric surgical outcomes and anesthesia.4 Variability in surgical outcome has previously been attributed to baseline preoperative characteristics. Recent studies demonstrate that even when controlling for American Society of Anesthesiologists (ASA) scores, Black children have markedly poorer outcomes than White children, including higher rates of complications and death.4,5

Recent health research has looked at the effect of social deprivation as a surrogate for socioeconomic status, factoring in education level, economic security, housing quality, and neighborhood quality. Black children are disproportionately represented in the most socially deprived quartiles (45% to 47% Black and 50% to 53% White) versus the least deprived quartiles (4% to 6% Black and 88% to 92% White).6 The Black pediatric population carries a higher risk of certain pathologies than children of other races, of which the practicing orthopaedic surgeon must be aware. These increased prevalences have been established through demographic studies.7–9 They may have atypical presentations, possibly presenting at lower ages, requiring a greater degree of scrutiny by the treating physician to accurately diagnose and intervene.

Bone Age Assessment

Treatment of many pediatric conditions requires assessment of skeletal maturity. Skeletal maturity assessment is essential for accurate management of leg length discrepancy, angular limb deformity, and scoliosis and consideration of risk of contralateral slipped capital femoral epiphysis (SCFE). The Greulich and Pyle Atlas (GPA) remains the most common method of assessing skeletal maturity.10 The index population for the atlas was White children nearly 100 years ago. GPA skeletal age standards may not be universally applicable. Mora et al reviewed hand and wrist radiographs of 534 children born after 1980. Half of the children were Black, and half were of European-American descent. The bone age per the GPA for 10% of all prepubertal Black children was assessed as two standard deviations more than their chronologic age. Postpubertal Black male patients had delayed bone age compared with postpubertal European-American male patients.11 A recent meta-analysis of 49 articles reviewing the bone age per GPA standards versus chronologic age noted three studies that included Black female patients, four studies including Black male patients, and one study limited to South African male patients. The meta-analyses found that Black female patients' bone ages were advanced by a mean of 0.37 years.12

Alternative strategies are being developed. Many, such as the calcaneal apophysis ossification staging system, are still based on the same historic patient population used to create the GPA and require adjustments for Black children. The Sanders method of assessing skeletal maturity is more recent and is commonly being used for the treatment of scoliosis, but the original article contains no indication of the race of the study population.13

Slipped Capital Femoral Epiphysis

SCFE involves dissociation of the femoral head epiphysis from the remainder of the bone, resulting in a “slip” usually posterior and inferior of the epiphysis relative to the neck (Figure 1, A and B). In 1996, Loder et al looked at the demographics of SCFE. Specifically, 1,630 children who had a SCFE were reviewed: 47.5% were White, 24.8% were Black, 16.9% were American Indian, 7.4% were Indonesian-Malay (East and Southeast Asian), 2.1% were native Australian/Pacific Islander, and 1.3% were Indo-Mediterranean (Near East, North African, Indian subcontinent). The age of SCFE was noted to be slightly younger in Black girls than White girls, with Black boys presenting at a similar or slightly older age to White boys. An additional finding was that Black children with SCFE in the study were the heaviest.7 An update on the epidemiology of SCFE was published by Lemann et al in 2006, noting the relative incidence of SCFE to be 3.94 times higher in Black children than White children. Hispanics were 2.53 times more likely and Asian/Pacific Islanders had 1.62 times the rate of SCFE compared with White children, with Native Americans having a lower relative risk of 0.66. They also noted younger ages of presentation than previously, which they attributed to earlier maturation.14 There is a strong association between obesity and SCFE, with reported rates of obesity being 51% to 77% in patients with SCFE.7

Figure 1:
A, AP radiograph of the pelvis with bilateral SCFE, which is not readily appreciated. B, Lateral radiograph of the hips in the same patient: SCFE is much more apparent. AP = anteroposterior, SCFE = slipped capital femoral epiphysis

Several studies have reported that 5% to 8% of SCFE cases are related to an endocrinopathy and that SCFEs are 6 times more common in a patient who has an endocrinopathy.15 The most common endocrinopathies seen with SCFE are hypothyroidism, panhypopituitarism, growth hormone deficiency, and hypogonadism; hyperparathyroidism and hypoparathyroidism have also been reported.15,16 Basic endocrine laboratory test results (Table 1) should be obtained if children are younger than 10 years or older than 15 years and/or are of short stature at presentation of SCFE, with a referral to endocrinology if findings are abnormal.

Table 1 - Endocrine Workup in the Setting of SCFE
Laboratory Tests to Order
Hemoglobin A1c
TSH and T4 levels
Complete metabolic panel
GH levels
Vitamin D
PTH level
TSH = thyroid stimulating hormone, GH = growth hormone, PTH = parathyroid hormone, SCFE = slipped capital femoral epiphysis

The most common presenting symptom of a patient with SCFE is pain in the groin, hip, thigh, or knee for days to months. Hip pain may be absent in as many as 50% of cases, and 8% of patients may present with a painless limp.16 The pain may be isolated to the knee or distal thigh. Patients may present with external foot progression angles and obligate external rotation with flexion. Inaccurate evaluation leads to a delay in diagnosis, with worsening of the underlying condition. Misdiagnosis has resulted in unnecessary knee radiographs and even knee surgery.

SCFE requires urgent surgical stabilization to prevent potentially catastrophic worsening. Many children with one SCFE will experience a contralateral SCFE leading to a debate as to whether the contralateral side should undergo concomitant stabilization. A recent large cohort study, with 49% Black patients, noted a 73% risk of contralateral SCFE in the presence of three risk factors: chronologic age ±11 years, modified Oxford score of maturity based on patency of physes ±20 points, and difference in the epiphyseal-diaphyseal angle of ±21°.17

Blount Disease

Blount disease is a pathologic varus deformity of the proximal medial tibia. There are two primary forms: Infantile Blount disease is usually noted between the ages of 2 to 5 years and is typically bilateral, whereas children with adolescent Blount disease are older at presentation and often have unilateral presentation. Pirpiris et al8 reported that more than 90% of the reported cases in North America are in Black male patients who are obese demonstrating strong racial, gender, and size associations. Montgomery et al found a notable association with an increased body mass index (BMI) and likelihood of developing Blount disease. Each whole number increase in BMI increased the likelihood of Blount disease by 3%.18

Sabharwal et al found a notable relationship between the magnitude of obesity and biplanar radiographic deformities in children with the early-onset form of Blount disease and in those with a body mass index of ≥40. They also conducted a subgroup analysis that confirmed Black race to be a predisposing factor common to both forms of the disease, but that the risk was greater in those with the late-onset Blount disease.19 Other factors that have been identified as predisposing to Blount disease are large stature, early walking age, vitamin D deficiency, or a combination of these.

For those patients who are older than 18 months with continued clinical bowing, infantile Blount disease should be ruled out. Full-length radiographs should be obtained with the patient standing and their patella pointing forward. The source of the malalignment in a young child with bowed legs may be the femur, tibia, or both. In children with Blount disease, most of the deformity is in the tibia (Figure 2, A and B). Management is more likely to be successful in the early stages before changes in the growth potential of the medial tibia become irreversible.

Figure 2:
A, Photograph of a 4-year-old boy with bilateral infantile Blount disease. B, Upright AP radiograph of bilateral lower extremities demonstrating bilateral infantile Blount disease with beaking of the medial tibial metaphysis and depression of the medial epiphysis. AP = anteroposterior

Adolescent Blount disease is again a varus deformity of the proximal medial tibia, which may also involve deformity of the distal femur, occurring later in childhood or early adolescence (Figure 3). The incidence of Blount disease continues to increase corresponding to the development of earlier and more severe adolescent obesity. These patients may present with deformity, knee pain, and instability with lateral collateral ligament laxity.

Figure 3:
Clinical photograph of a teenage boy with unilateral adolescent Blount disease.

Postaxial Polydactyly

Postaxial polydactyly is a duplication of the small finger or little toe. Type A postaxial polydactyly denotes a well-formed duplicate digit that articulates with a metacarpal. Type B is a small floppy duplicate digit without articulation. Type A is less common than type B and occurs at approximately equivalent rates in Black children and White children, whereas Type B has a variable racial incidence. The incidence of hand postaxial polydactyly is reported to be one in 100 to 300 live births among Black children and one in 1,500 to 3,000 live births among White children. Polydactyly is the most congenital anomaly of the hand in Black infants.9

Postaxial polydactyly in Black children usually exhibits an autosomal dominant inheritance pattern and is not typically associated with other syndromes, whereas the opposite has been found for children of other races. In White children, a genetic workup should be conducted to evaluate for chondroectodermal dysplasia or Ellis-van Creveld syndrome. Ellis-van Creveld syndrome is an autosomal recessive skeletal dysplasia characterized by short limbs, postaxial polydactyly, congenital cardiac defects, and dysplastic nails and teeth.

Postaxial polydactyly in Black children is almost always an isolated malformation, is often bilateral, and often involves soft tissue alone. The duplicate finger or toe may be entirely separate distally, or there may be simple (soft tissue only) or complex (bone involved) syndactyly. To help with surgical planning, an anteroposterior radiograph should be obtained (Figure 4).

Figure 4:
AP radiograph of the foot demonstrating complex postaxial polydactyly with discrete ossification centers due to young age. AP = anteroposterior

Sickle Cell Disease

Sickle cell disease (SCD) is an autosomal recessive disorder of hemoglobin synthesis involving the beta-globin gene, resulting in hemolytic anemia due to abnormal hemoglobin and erythrocyte levels. A retrospective review by Cusano et al20 of 96 patients found that 90.3% of the people referred to orthopaedics for SCD were Black and 60.4% were women. SCD can have multiple orthopaedic manifestations.


Dactylitis is painful swelling of fingers or toes. It often occurs in early childhood and may be the first clinical manifestation of SCD. Miller reported that the onset of dactylitis before the age of 1 year is predictive of a more severe case of SCD. Radiographs are initially normal but progress to demonstrate periosteal elevation and osteolysis, mimicking osteomyelitis.21

Pain Crises

Acute vaso-occlusion causing painful microinfarction is the most common reason for admission to the hospital for children, adolescents, and young adults with SCD. A study from 2010 looked at the timing of administration of opioids between patients presenting with an SCD-associated vaso-occlusive episode versus isolated long bone fracture. Patients with SCD had higher triage pain scores, spent less time in the waiting room, and were given higher initial doses of opiates. However, time from triage to analgesic intervention did not differ.22 Unfortunately, a more recent study of emergency department visits did find that there were longer wait times for patients with SCD than long bone fracture, even when controlling for race.23 Pain crises commonly occur in the humerus, tibia, and femur. They may have variable findings, including swelling, local warmth, erythema, fever, and loss of joint motion.24 The differentiation of acute osteomyelitis from bone infarction can be challenging. The clinical response to early interventions is important for differentiation. In a pain crisis, symptoms should subside within 24 to 48 hours with hydration and analgesics. Radiographic changes of sclerosis may be seen in regions of infarcts25Figure 5, A and B.

Figure 5:
AP and lateral radiographs A and B of the knee demonstrating an irregular area of intramedullary sclerosis involving the distal tibia related to changes of prior infarct (arrows). The figure reproduced with permission from Kosaraju et al.25 AP = anteroposterior


Osteomyelitis is less common than bone infarction as a cause of pain in youth with SCD but more common than that in the general population secondary to impaired osseous circulation from sickled erythrocytes. Osteomyelitis is more likely than infarction to have a fever and pain for 24 hours or more. Osteomyelitis is more likely to involve a single area, although multifocal involvement is a possibility. Laboratory inflammatory markers are increased, and initial radiographs may be normal in both conditions. Fluid collection on ultrasonography of greater than 4 mm is consistent with osteomyelitis with abscess. MRI with gadolinium contrast is beneficial for evaluating edema, periosteal reaction, fluid collection, cortical involvement, or cellulitis24,25Figure 6, A–C. Septic arthritis is less common than osteomyelitis but still does have a reported incidence rate of up to 5% of children with SCD.

Figure 6:
Coronal T1 (A), coronal T1 post-contrast, (B) and coronal short tau inversion recovery (C) images of the femur demonstrating extensive marrow edema with associated serpiginous and tubular marrow enhancement in the distal femoral metaphysis/diaphysis (solid arrows) with extensive associated periosteal reaction (arrowhead), adjacent soft-tissue swelling, and edema (dashed arrows). These findings are characteristic of osteomyelitis. The figure reproduced with permission from Kosaraju et al.25


Infarction of a large area, also termed as osteonecrosis, is a common finding in patients with SCD, with the most common locations being the femoral head, followed by the humeral head and distal femur and proximal tibia. Milner reported that by the age of 45 years, nearly one-third of patients have femoral head osteonecrosis and nearly one-fourth have humeral head osteonecrosis. Femoral head osteonecrosis is bilateral in 54% of patients, and humeral head osteonecrosis is bilateral in 67% of patients.26

The prognosis is worse in osteonecrosis due to SCD than other causes. The hips are less likely to respond to hip preservation strategies, such as strut grafting, core decompression, or osteotomies. Arthroplasty is frequently required. A literature review of hip arthroplasty in SCD noted a mean age of 36 years, much younger than that in the general population. Total hip arthroplasty in SCD was associated with longer lengths of stay and higher rates of readmission and medical complications. The mean revision rate was 16% at 10 years for all causes. The implant survival rate inclusive of aseptic loosening but not infection was comparable with that of the general population.27

Perioperative Considerations

Cusano reported that surgical management of patients with SCD poses a unique challenge to orthopaedic surgeons associated with increased surgical and perioperative risk. Patients with SCD require close monitoring in the perioperative period because of the risk of vaso-occlusive crisis and acute chest syndrome.20 Any surgery in patients with SCD should be accompanied by adequate hydration, maintenance of blood volume, oxygenation, and prevention of hypothermia. Transfusions are typically given perioperatively to keep the total hemoglobin around 10 g/dL, which may be hampered by alloimmunization and the presence of antibodies in this population.

Vitamin D Deficiency

It is well-known that vitamin D is an important component in bone health, yet the rates of hypovitaminosis D are shockingly high. It has been estimated that as many as 70% of American children have inadequate vitamin D levels (<30 ng/mL). Levels have been found to be lower in Hispanics and Blacks compared with Whites. Melanin impedes the penetration of sunlight to the deep epidermal layers to produce vitamin D. Additional risk factors of vitamin D deficiency include lack of safe outdoor play areas, obesity, and breastfeeding disparities.

Vitamin D levels in the setting of extremity fractures have also been studied. Ryan et al looked at vitamin D levels in Black children with forearm fractures and found that 59% of subjects had an insufficient level (mean level of 20 ng/mL). The radiograph appearance of bone mineralization was found to be normal on all cases of this study.28 James et al reported that hypovitaminosis D is common among children with upper extremity fractures. They looked at 181 patients with upper extremity fractures and found that 24% had deficient vitamin D levels; 41% had insufficient levels; and 35% had normal levels. Black children were more likely to have insufficient or deficient levels of vitamin D.29 Obtaining adequate 25-vitamin D levels during childhood and treatment of hypovitaminosis are important for maintaining good bone health.


While adolescent idiopathic scoliosis (AIS) can affect teens of all races, Black teens present with larger curves at the first visit, more often requiring surgery as the first line of treatment.30 Sensitivity is required when counseling these patients about surgical correction of AIS because priorities regarding body image vary by race. The rates of blood transfusions after posterior spinal fusion for AIS have been found to be markedly higher in the Black population, although no clear etiology has been identified.31 A study looking at early postoperative complications after posterior spine fusion for AIS noted slightly increased rates of venous thromboembolism in Black patients, after controlling for baseline factors, including higher BMI, more female patients, higher ASA scores, preoperative diagnosis of asthma or cardiac risk factors, and prior use of steroids.32

Prenatal Care

It has been well established that Black mothers have decreased access to and poorer quality of prenatal care. While the full scope of the problem is beyond this article, this discrepancy can lead to long-term orthopaedic consequences for the children they bear. A meta-analysis of access to care by da Silva et al in 2022 concluded that Black women had lower access to prenatal care, varying from 8.1% to 74.81%, whereas among White women, access varied from 44.9% to 94.0%. They also noted that Black mothers were less likely to start prenatal care in the first trimester, with only 60.7% of Black women starting care versus 72.9% of White women.33 Early intervention with folate supplementation and screening procedures might help identify and/or prevent myelodysplasia, maternal diabetes, and gestational hypertension and provide for early intervention for mothers at risk of premature delivery. Prematurity, gestational hypertension, premature rupture of membranes, and emergency cesarean section are all risk factors of cerebral palsy (CP).34

Population-based studies have shown an increase in CP prevalence in Black children. A study by Durkin et al35 showed that Black children have a 50% higher risk of spastic CP compared with their White counterparts. This higher risk remains after controlling for socioeconomic factors but is mitigated after controlling for preterm birth and size for gestational age. Severe CP is more prevalent in Black children as well, with Black children having a 70% higher risk of being a Gross Motor Function Classification System (GMFCS) four or five. This may be multifactorial including differences in risk factors, access to interventions, and underidentification of mild CP in Black children.

Nonaccidental Trauma

No caregiver should miss nonaccidental trauma (NAT), but we need to be mindful that intrinsic biases may alter a clinician's response to a given injury. Rib fractures, head trauma, and fractures of different stages of healing correlate with nonaccidental trauma, but no true benchmark for this diagnosis exists. A study published in 2020 used the KIDS database to create a “probability score” that a patient's particular constellation of injuries were due to NAT—factors that increased the score included Black race, rib fractures, intracranial injuries, and burns.36 A limitation of this study was that the determination of a diagnosis of NAT was based on a provider's suspicion, coding, and referral to protective services, all of which may be influenced by unconscious biases. Care should be taken when assigning socially constructed diagnoses.

A review of the data from the National Incidence Study noted a selection bias for increased reporting to child protective services for Black children but no difference in rates of abuse between Black and White children.37 Standardization of care practices has been shown to lead to more equitable evaluation for possible abuse, avoiding a possible bias of increased scrutiny for Black children and parents. The disparity in the rate of referral for evaluation for nonaccidental trauma in children less than 36 months was reduced from 43% for non-White versus 19% for White children to 43% for non-White versus 47% for White children after implementing the use of the American Academy of Orthopaedic Surgeons clinical practice guideline on the treatment of pediatric diaphyseal femur fractures.38


Although the entities described previously are distinct in their presentation and pathology, there are factors that overlap between them. One intersection is that of obesity and advanced skeletal age. Earlier puberty has been attributed to obesity, which may explain some of the difference seen in bone age between Black children and White children. While obesity prevalence is trending upward in all populations in the United States, there is a disproportionate rise occurring in Black children. However, McCormack et al found that healthy, nonobese children of Black ancestry had relatively advanced skeletal maturation independent of growth, body composition, and puberty.39

A link has been drawn between infantile Blount disease, obesity, and vitamin D deficiency.19 However, there is a paucity of literature regarding the degree to which each of these overlapping factors may contribute to the development of these diagnoses.


While the root causes of each of these diagnoses deserve additional investigation, treatment of the Black pediatric population as a whole deserves specific attention. Race is frequently ignored in the literature. A study by Somerson et al in 2014 looked at reporting of race in orthopaedic research studies. Only 1/3 of studies reported race, and those that did demonstrated notable underrepresentation of minorities in their study populations. This brings into question the overall generalizability of these studies to the US population.40


Enhanced understanding of pediatric orthopaedic conditions prevalent in the Black population facilitates prompt diagnosis and appropriate intervention. We can use information on modifiable risk factors to improve anticipatory guidance. Practitioners should vigilantly avoid disparate provision of care.


1. King LutherM Jr: Presentation at the second national convention of the medical committee for human rights. Chicago, March 25, 1966.
2. Phan MT, Tomaszewski DM, Arbuckle C, et al.: Racial and ethnic disparities in opioid use for adolescents at US emergency departments. BMC Pediatr 2021;21:252.
3. Owens A, Holroyd BR, McLane P: Patient race, ethnicity, and care in the emergency department: A scoping review. CJEM 2020;22:245-253.
4. Nafiu OO, Mpody C, Kim SS, Uffman JC, Tobias JD: Race, postoperative complications, and death in apparently healthy children. Pediatrics 2020;146:e20194113.
5. Chen C, Mpody C, Sivak E, Tobias JD, Nafiu OO: Racial disparities in postoperative morbidity and mortality among high-risk pediatric surgical patients. J Clin Anesth 2022;81:110905.
6. Okoroafor UC, Gerull W, Wright M, Guattery J, Sandvall B, Calfee RP: The impact of social deprivation on pediatric promis health scores after upper extremity fracture. J Hand Surg 2018;43:897-902.
7. Loder RT: The demographics of slipped capital femoral epiphysis an international multicenter study. Clin Orthop Relat Res 1996;322:8-27.
8. Pirpiris M, Jackson KR, Farng E, Bowen RE, Otsuka NY: Body mass index and Blount disease. J Pediatr Orthop2006;26:659-663.
9. Comer GC, Potter M, Ladd AL: Polydactyly of the hand. J Am Acad Orthop Surgeons 2018;26:75-82.
10. Gruelich WW, Pyle SI: Radiographic Atlas of Skeletal Development of the Hand and Wrist, ed 2. Stanford, CA, Stanford University Press, 1959.
11. Mora S, Boechat MI, Pietka E, Huang HK, Gilsanz V: Skeletal age determinations in children of European and African descent: Applicability of the Greulich and Pyle standards. Pediatr Res 2001;50:624-628.
12. Alshamrani K, Messina F, Offiah AC: Is the greulich and Pyle atlas applicable to all ethnicities?: A systematic review and meta-analysis. Eur Radiol 2019;29:2910-2923.
13. Sanders JO, Browne RH, McConnell SJ, Margraf SA, Cooney TE, Finegold DN: Maturity assessment and curve progression in girls with idiopathic scoliosis. J Bone Joint Surg 2007;89:64-73.
14. Lehmann CL, Arons RR, Loder RT, Vitale MG: The epidemiology of slipped capital femoral epiphysis: An update. J Pediatr Orthop 2006;26:286-290.
15. Shaw KA, Shiver AL, Oakes T, Fletcher ND: Slipped capital femoral epiphysis associated with endocrinopathy: A narrative review. JBJS Rev 2022;10.
16. Cowell HR: The significance of early diagnosis and treatment of slipping of the capital femoral epiphysis. Clin Orthop Relat Res 1966;48:89-94.
17. Swarup I, Shah R, Gohel S, Baldwin K, Sankar WN: Predicting subsequent contralateral slipped capital femoral epiphysis: An evidence-based approach. J Children's Orthop 2020;14:91-97.
18. Montgomery CO, Young KL, Austen M, Jo CH, Blasier RD, Ilyas M: Increased risk of Blount disease in obese children and adolescents with vitamin D deficiency. J Pediatr Orthop 2010;30:879-882.
19. Sabharwal S, Zhao C, McClemens E: Correlation of body mass index and radiographic deformities in children with Blount disease. J Bone Joint Surg 2007;89:1275-1283.
20. Cusano J, Curry EJ, Kingston KA, Klings E, Li X: Epidemiology and perioperative complications in patients with sickle cell disease after orthopaedic surgery: 26 years' experience at a major academic center. J Am Acad Orthop Surgeons 2019;27:e1043-e1051.
21. Miller ST, Sleeper LA, Pegelow CH, et al.: Prediction of adverse outcomes in children with sickle cell disease. New Engl J Med 2000;342:83-89.
22. Zempsky WT, Loiselle KA, McKay K, Lee BH, Hagstrom JN, Schechter NL: Do children with sickle cell disease receive disparate care for pain in the emergency department?. J Emerg Med 2010;39:691-695.
23. Haywood C Jr, Tanabe P, Naik R, Beach MC, Lanzkron S: The impact of race and disease on sickle cell patient wait times in the emergency department. Am J Emerg Med 2013;31:651-656.
24. Al Farii H, Zhou S, Albers A: Management of osteomyelitis in sickle cell disease: Review article. J Am Acad Orthop Surg Glob Res Rev 2020;4:e20.00002-e20.00010.
25. Kosaraju V, Harwani A, Partovi S, et al.: Imaging of musculoskeletal manifestations in sickle cell disease patients. Br J Radiol 2017;90:20160130.
26. Milner PF, Kraus AP, Sebes JI, et al.: Sickle cell disease as a cause of osteonecrosis of the femoral head. N Engl J Med 1991;325:1476-1481.
27. Fassihi SC, Lee R, Quan T, Tran AA, Stake SN, Unger AS: Total hip arthroplasty in patients with sickle cell disease: A comprehensive systematic review. J Arthroplasty 2020;35:2286-2295.
28. Ryan LM, Brandoli C, Freishtat RJ, Wright JL, Tosi L, Chamberlain JM: Prevalence of vitamin D insufficiency in african American children with forearm fractures: A preliminary study. J Pediatr Orthop 2010;30:106-109.
29. James JR, Massey PA, Hollister AM, Greber EM: Prevalence of hypovitaminosis D among children with upper extremity fractures. J Pediatr Orthop 2013;33:159-162.
30. Zavatsky JM, Peters AJ, Nahvi FA, et al.: Disease severity and treatment in adolescent idiopathic scoliosis: The impact of race and economic status. Spine J 2015;15:939-943.
31. Elsamadicy AA, Koo AB, David WB, et al.: Impact of race on outcomes and healthcare utilization following spinal fusion for adolescent idiopathic scoliosis. Clin Neurol Neurosurg 2021;206:106634.
32. Alomari S, Planchard R, Azad TD, Larry Lo SF, Bydon A: Association of race with early outcomes of elective posterior spinal fusion for adolescent idiopathic scoliosis: Propensity-matched and subgroup Analysis. World Neurosurg 2021;150:e176-e181.
33. da Silva PHA, Aiquoc KM, da Silva Nunes AD, et al.: Prevalence of access to prenatal care in the first trimester of pregnancy among black women compared to other races/ethnicities: A systematic review and meta-analysis. Public Health Rev 2022;43:1604400.
34. Chen D, Huang M, Yin Y, et al.: Risk factors of cerebral palsy in children: A systematic review and meta-analysis. Transl Pediatr 2022;11:556-564.
35. Durkin MS, Maenner MJ, Benedict RE, et al.: The role of socio-economic status and perinatal factors in racial disparities in the risk of cerebral palsy. Dev Med Child Neurol 2015;57:835-843.
36. Zhao C, Starke M, Tompson JD, Sabharwal S: Predictors for nonaccidental trauma in a child with a fracture: A national inpatient database study. J Am Acad Orthop Surgeons 2020;28:e164-e171.
37. Ards S, Chung C, Myers SL: The effects of sample selection bias on racial differences in child abuse reporting. Child Abuse Neglect 1998;22:103-115.
38. Blatz AM, Gillespie CW, Katcher A, Matthews A, Oetgen ME: Factors associated with nonaccidental trauma evaluation among patients below 36 months old presenting with femur fractures at a level-1 pediatric trauma center. J Pediatr Orthopaedics 2019;39:175-180.
39. McCormack SE, Chesi A, Mitchell JA, et al.: Relative skeletal maturation and population ancestry in nonobese children and adolescents. J Bone Miner Res 2017;32:115-124.
40. Somerson JS, Bhandari M, Vaughan CT, Smith CS, Zelle BA: Lack of diversity in orthopaedic trials conducted in the United States. J Bone Joint Surg 2014;96:e56.
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