POSTGRADUATE ORTHOPEDIC INSTRUCTION

 

Hip Growth Disturbances in Childhood

 

María Gabriela Miranda,*,** Claudio A. Fernández**

*Orthopedics and Traumatology Service, Hospital de Niños “Sor María Ludovica”, La Plata, Buenos Aires, Argentina

**School of Medical Sciences, Universidad Nacional de La Plata, Buenos Aires, Argentina

 

ABSTRACT

Growth disturbances of the proximal femur, described in the medical literature as avascular necrosis, osteochondritis, or post-reduction epiphysitis, are associated almost exclusively with the treatment of developmental dysplasia of the hip. Some of these disturbances can lead to later joint degeneration, with clinical, functional, and social implications. Various treatment-related factors have been identified. However, preexisting idiosyncratic, morphological, and vascular factors also determine specific risk profiles. This study aims to analyze the natural history of these disturbances and identify possible strategies to prevent them or reduce their sequelae. Understanding hip growth, development, and vascular supply is essential to understanding their pathogenesis. Diagnosis and treatment of developmental dysplasia of the hip during the neonatal period remain the gold standard, given the extremely low rates of treatment failure and residual abnormalities.

Keywords: Developmental dysplasia of the hip; femoral growth disturbance; natural history; children.

Level of Evidence: V

 

Alteraciones del crecimiento de la cadera en la infancia

 

RESUMEN

Las alteraciones del crecimiento del fémur proximal, referidas en la literatura médica como necrosis avascular, osteocondritis o epifisitis posreduccional, se relacionan casi exclusivamente con la terapéutica empleada en la displasia del desarrollo de la cadera. Algunas de ellas condicionan la ulterior degeneración articular con sus implicancias clínicas, funcionales y sociales. Se han individualizado una diversidad de factores relacionados con el tratamiento. Sin embargo, otras variables preexistentes idiosincrásicas, morfológicas y vasculares conFiguren perfiles de riesgo específicos. El objetivo de esta investigación es analizar la historia natural de estas alteraciones y establecer posibles formas de prevención o reducir sus secuelas. Una síntesis del crecimiento, el desarrollo y la vascularización de la cadera es imprescindible para la compresión de la patogenia. El diagnóstico y el tratamiento de la displasia del desarrollo en el período neonatal siguen siendo el método de referencia, dado las ínfimas tasas de fracaso terapéutico y anomalías residuales.

Palabras clave: Displasia del desarrollo de la cadera; alteración del crecimiento femoral; historia natural; niños.

Nivel de Evidencia: V

 

INTRODUCTION

Proximal femoral growth disturbances (PFGDs) in childhood are morphological abnormalities involving the epiphysis, physis, femoral neck, or a combination of these structures. Although PFGDs are predominantly associated with the treatment of developmental dysplasia of the hip (DDH), they have also been observed in the contralateral, nondysplastic hip after immobilization.1 The untreated hip may also show signs of dysplasia at skeletal maturity in 13%–40% of cases, consistent with the term “developmental dysplasia.”2,3 PFGDs may be transient and reversible or permanent and irreversible, with various deformities and joint degeneration that remain clinically silent for years, reflecting a discrepancy between radiographic and clinical findings.

This study aims to analyze the natural history of PFGDs and identify ways to prevent or reduce their sequelae. In DDH, the primary driver of deformity lies in the acetabulum, whereas in PFGDs, the initial changes occur in the proximal femur and acetabular involvement is secondary. The terms avascular necrosis, post-reduction osteochondritis, and epiphysitis are used synonymously in the scientific literature. Histological uncertainty has led many investigators to favor the euphemism “proximal femoral growth disturbance.”1,4-6 Proposed etiopathogenic mechanisms include mechanical factors (excessive joint pressure) and ischemia, hypotheses supported by experimental studies in pigs.7 These mechanisms may also interact (Figure 1).8

 

 

 

 

 

The reported prevalence of PFGDs varies widely, from 0% to 73%, possibly reflecting differences in diagnostic rigor and follow-up duration. Numerous predisposing factors have been described: age >6 months at reduction, an unossified femoral head nucleus, greater cartilage volume, high dislocations, an inverted labrum, soft tissue interposition, nonconcentric reduction, preoperative traction, all surgical modalities, forceful reduction, immobilization in ≥60° of abduction combined with internal rotation, prolonged immobilization, and surgery after failed treatment.1,9-11 In a prospective multicenter study of dysplastic hip dislocations, 20% of children already had epiphyseal abnormalities and femoral neck widening before treatment. During follow-up, 42% met the criteria for PFGDs, demonstrating that these abnormalities are not iatrogenic but pre-existing.6 Similarly, a pretreatment MRI study revealed impaired perfusion and an immature microcirculatory pattern.12 Comparable findings have been reported with real-time contrast-enhanced ultrasound (CEUS; Optison®).13 The prevalence of PFGDs with devices such as the Pavlik harness, von Rosen splint, and Frejka pillow is exceptionally low, at 0%–1%. However, delaying treatment by several weeks or persisting with treatment after failed reduction raises the risk above 25%.2,11,12,14 Rates of PFGDs following closed reduction under general anesthesia and various surgical procedures range from 20% to 60%.3-6,8,11,14-16 Even without PFGDs, joint quality may deteriorate over time, as dysplasia cannot be regarded solely as a mechanical fetal disorder. Regardless of treatment, the risk of PFGDs is related to the high position of the proximal femur, underscoring the importance of classification systems with excellent intra- and interobserver reliability (Figures 2 and 3).17-20

 

 

 

 

 

 

 

 

HIP GROWTH AND DEVELOPMENT

The proximal femur and acetabulum arise from the same embryonic mesenchyme. During the eleventh week of intrauterine life, the fully formed hip begins to differentiate into cartilage, following the pattern of endochondral ossification, supplemented after birth by periosteal bone apposition. In the newborn, both joint components consist of hyaline cartilage (Figure 4).1

The femoral epiphysis and greater trochanteric apophysis are spherical chondroepiphyses. Their growth is centripetal, driven by the metabolic activity of peripheral epiphyseal chondrocytes, whereas ossification is centrifugal and radial, proceeding from the center toward the periphery. The proximal femoral growth plate is linear and resembles an inverted L with three segments: the physeal or discoid segment, perpendicular to the femoral neck axis; the cervicotrochanteric segment; and the isthmus, which connects the other two and contributes to femoral neck thickness.1 The calcification front of this configuration may occasionally be visible on radiographs as Harris lines. Interruption or distortion of these lines is considered predictive of PFGDs (O’Brien’s sign) (Figure 5).1

 

 

 

 

 

 

 

 

Physiological physeal closure begins in the lateral, superior, and slightly posterior regions of the physis and then progresses in all directions.21,22 The blood supply comes from an extracapsular vascular network at the base of the femoral neck, supplied by the circumflex arteries. The medial circumflex artery passes between the iliopsoas muscle, enters the joint through the retrotrochanteric fossa, and gives rise to the retinacular vessels, particularly the posterosuperior vessels, which provide 80% of the blood supply to the epiphysis, isthmus, and much of the femoral metaphysis. The anterior retinacular branches arising from the lateral circumflex artery provide a supplementary supply. This vascular network forms a bipartite system: the retinacular vessels perfuse the epiphyseal ossification center and physis for the synthesis of ground substance and osteoid, while the metaphyseal system contributes to substrate mineralization and bone resorption according to the Hueter–Volkmann law. This vascular network does not follow a fixed pattern; it shows substantial anatomical variation according to sex, ethnicity, the number and diameter of the arteries, and the variable presence of intra-articular vascular rings.

 

Classification and characterization of PFGDs

Several authors have proposed classifications of PFGDs. In chronological order, these include: Salter and Kostuik,7 Bucholtz and Ogden,2 Kalamchi and MacEwen,23 and Kruczynski24 (Figure 6). All have moderate interobserver reliability.6 Given their similarity and widespread use in the specialized literature, the Kalamchi–MacEwen and Bucholtz–Ogden classifications will be considered together in this analysis. Type I is characterized by delayed ossification and an appearance of epiphyseal fragmentation. Although reversible, these changes may precede lesions with a poorer prognosis (Figure 7).

 

 

 

 

 

 

 

 

   The type II pattern has a prevalence of 25% and is defined by epiphysiodesis or a lateral physeal bar, which causes valgus tilt of the epiphysis relative to the femoral neck and may lead to secondary subluxation (Figure 8A). One study evaluated 58 hips in 48 patients with type II PFGDs treated by closed reduction (n = 36) or surgery through an inguinal approach (n = 22), with a follow-up of 21 years (range, 10–55). The abnormality became radiographically apparent at 10 years of age (range, 4–14). Outcomes were classified as Severin groups I/II in 59% of hips; the remainder had unsatisfactory outcomes (Table).4,24

 

 

 

 

 

Another study included 155 dislocated hips treated by closed reduction at a mean age of 15 months. Type II PFGDs were present in 23% and were detected at a mean age of 8.9 years (range, 3–12). Sixty-six percent were classified as Severin grades I/II, while the remainder had suboptimal outcomes (Figures 8A and 9).25

 

 

 

 

 

 

 

 

This phenomenon appears to reproduce physiological proximal femoral physeal closure prematurely.22

Type III PFGDs have a prevalence of 14%–30% and are the most damaging deformities, causing progressive joint and functional deterioration. They involve severe epiphyseal and physeal damage, leading to reduced femoral neck growth and varus deformity, lower limb shortening, relative elevation of the greater trochanter with gluteus medius dysfunction, and coxa magna. Severe ischemia is the presumed cause (Figures 8B and C, 10A-C).2 In a study that followed 29 hips in 22 patients over four decades, the abnormality became radiographically visible a mean of 10 months (range, 5–19) after closed reduction or surgery through an inguinal approach. High dislocations (Tönnis grade IV) had an odds ratio of 3.43 for joint deterioration compared with grades II and III.

At skeletal maturity, 90% of hips were classified as Severin grades III/IV. By 39 years of age, 32% of patients had undergone total hip replacement (Table).5,24

In light of these findings, some surgeons opted for an anterolateral approach combined with femoral and pelvic osteotomies. The results were also disappointing, however, as 32% developed type II/III PFGDs (Figure 7B and C).15 Thus, type III PFGD represents the worst treatment outcome, regardless of the method used. Type IV is a medial epiphyseal–metaphyseal defect characteristic of longstanding dislocations or subluxations and is observed before any treatment (Figure 8D) Finally, 25% of cases show unclassifiable or mixed patterns (Figure 10D and E).

 

 

 

 

 

CONCLUSIONS

The gold standard for preventing PFGDs or mitigating their sequelae is neonatal or perinatal diagnosis and treatment of DDH. Beyond the epidemiological and treatment-related variables associated with DDH, individual anatomical characteristics (both morphological and vascular) also predispose patients to PFGDs, as demonstrated by advances in imaging technology and recent clinical research. Following children throughout growth is essential for a definitive and accurate assessment of the outcome.

 

REFERENCES

 

1.     Weinstein SL, Dolan LA. Proximal femoral growth disturbance in developmental dysplasia of the hip: what do we know? J Child Orthop 2018;12(4):331-41. https://doi.org/10.1302/1863-2548.12.180070

2.     Bucholz R, Ogden JA (eds.). Patterns of ischemic necrosis of the proximal femur in nonoperative treated congenital hip disease. St. Louis: C.V. Mosby; 1978.

3.     Kobayashi D, Satsuma S, Kuroda R, Kurosaka M. Acetabular development in the contralateral hip in patients with unilateral developmental dysplasia of the hip. J Bone Joint Surg Am 2010;92(6):1390-7. https://doi.org/10.2106/JBJS.I.00840

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M. G. Miranda ORCID ID: https://orcid.org/0000-0003-4949-9407

 

Received on June 16th, 2026. Accepted after evaluation on July 7th, 2026 • Dr. CLAUDIO A. FERNÁNDEZ • claudioalfredofernandez619@gmail.com • https://orcid.org/0000-0003-2350-3885

 

How to cite this article: Miranda MG, Fernández CA. Hip Growth Disturbances in Childhood. Rev Asoc Argent Ortop Traumatol 2026;91(5):510-518. https://doi.org/10.15417/issn.1852-7434.2026.91.5.2411

 

 

Article Info

Identification: https://doi.org/10.15417/issn.1852-7434.2026.91.5.2411

Published: October, 2026

Conflict of interests: The authors declare no conflicts of interest.

Copyright: © 2026, Revista de la Asociación Argentina de Ortopedia y Traumatología.

License: This article is under Attribution-NonCommertial-ShareAlike 4.0 International Creative Commons License (CC-BY-NC-SA 4.0).