Identical Twins with Legg-Calve-Perthes Disease: A Report of Two Cases.
- 1Department of Orthopaedic Surgery, Saint Louis University, Saint Louis, Missouri, United States.
- 2Saint Louis University School of Medicine, Saint Louis, Missouri, United States.
Abstract
Legg-Calvé-Perthes disease (LCPD) is an idiopathic avascular necrosis of the femoral head in children, with proposed etiologies, including genetic mutations and coagulation abnormalities. While familial clustering has been reported, the role of genetic predisposition remains incompletely understood, particularly in monozygotic twins. We report monozygotic male twins born at 35 weeks' gestation who developed LCPD sequentially. Twin A presented at 3 years and 4 months with a 2-week history of antalgic gait. Initial imaging was unremarkable, but follow-up radiographs demonstrated progressive changes consistent with LCPD, ultimately classified as lateral pillar Class A. He was managed conservatively with observation and showed clinical and radiographic improvement at 1 year. During Twin A's 1-year follow-up, Twin B presented with similar symptoms of antalgic gait and mild right hip pain. Imaging revealed early fragmentation and mild lateral pillar height loss, consistent with early-stage LCPD. Given the favorable course in Twin A, Twin B was also managed non-operatively. This case highlights the occurrence of LCPD in monozygotic twins raised in a shared environment, supporting a potential genetic contribution to disease pathogenesis. Prior studies have implicated hereditary thrombophilia and mutations in type II collagen in LCPD development. Although larger twin studies suggest low concordance rates, limited sample sizes restrict definitive conclusions. This case adds to existing reports suggesting a possible genetic predisposition, while also acknowledging the influence of shared environmental factors. The sequential development of LCPD in identical twins underscores the importance of considering genetic susceptibility in disease etiology. Increased clinical vigilance and early evaluation in siblings may facilitate timely diagnosis. Further research is needed to better define the genetic mechanisms contributing to LCPD.
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BibTeX
@article{lane2026identical,
title = {{Identical Twins with Legg-Calve-Perthes Disease: A Report of Two Cases.}},
author = {Gabriel Lane and Gavin Christy and Dustin Baker and Sivashanmugam Raju and Mehmet Erkilinc},
journal = {Journal of orthopaedic case reports},
year = {2026},
month = nov,
doi = {10.13107/jocr.2026.v16.i11.8438},
url = {https://europepmc.org/article/MED/42997007},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Identical Twins with Legg-Calve-Perthes Disease: A Report of Two Cases.
AU - Gabriel Lane
AU - Gavin Christy
AU - Dustin Baker
AU - Sivashanmugam Raju
AU - Mehmet Erkilinc
PY - 2026
DA - 2026/11/01
JO - Journal of orthopaedic case reports
DO - 10.13107/jocr.2026.v16.i11.8438
UR - https://europepmc.org/article/MED/42997007
AB - Legg-Calvé-Perthes disease (LCPD) is an idiopathic avascular necrosis of the femoral head in children, with proposed etiologies, including genetic mutations and coagulation abnormalities. While familial clustering has been reported, the role of genetic predisposition remains incompletely understood, particularly in monozygotic twins. We report monozygotic male twins born at 35 weeks' gestation who developed LCPD sequentially. Twin A presented at 3 years and 4 months with a 2-week history of antalgic gait. Initial imaging was unremarkable, but follow-up radiographs demonstrated progressive changes consistent with LCPD, ultimately classified as lateral pillar Class A. He was managed conservatively with observation and showed clinical and radiographic improvement at 1 year. During Twin A's 1-year follow-up, Twin B presented with similar symptoms of antalgic gait and mild right hip pain. Imaging revealed early fragmentation and mild lateral pillar height loss, consistent with early-stage LCPD. Given the favorable course in Twin A, Twin B was also managed non-operatively. This case highlights the occurrence of LCPD in monozygotic twins raised in a shared environment, supporting a potential genetic contribution to disease pathogenesis. Prior studies have implicated hereditary thrombophilia and mutations in type II collagen in LCPD development. Although larger twin studies suggest low concordance rates, limited sample sizes restrict definitive conclusions. This case adds to existing reports suggesting a possible genetic predisposition, while also acknowledging the influence of shared environmental factors. The sequential development of LCPD in identical twins underscores the importance of considering genetic susceptibility in disease etiology. Increased clinical vigilance and early evaluation in siblings may facilitate timely diagnosis. Further research is needed to better define the genetic mechanisms contributing to LCPD.
SN - 2250-0685
SN - 2321-3817
ER -