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Bone & Joint Research
Vol. 14, Issue 3 | Pages 236 - 244
14 Mar 2025
Park BK Lee K Park K Park H Ko EA Lee JW Kim HW Park K

Aims. It remains unclear which factors influence overgrowth of the tibia, resulting from the metaphyseal hole created during anterior cruciate ligament (ACL) reconstruction in skeletally immature patients. This study aimed to investigate the effects of growth stimulation by creating a metaphyseal hole in a rabbit model, based on its distance from the physis and type of interposition material. Methods. In Experiment 1, 38 skeletally immature male New Zealand white rabbits were randomized into one of four groups: a metaphyseal hole created at 5, 10, or 15 mm distal to the physis of the left proximal tibia with the hole filled with bone wax, or a sham control group. In Experiment 2, after establishing the distance associated with the most overgrowth, a defect was created at 10 mm distal to the physis in 20 additional rabbits, which were randomly assigned to have the defect filled with Tisseel, or be left unfilled. The rabbits were euthanized six weeks postoperatively. Results. The length and rate of overgrowth were higher in the groups with holes drilled 5 and 10 mm distal to the physis compared to the sham group. A significant increase in new bone width was observed in the 10 mm distal hole group. Growth stimulation in both radiological and histological analyses was not significant in the unfilled and Tisseel groups. Valgus deformities were observed in all groups with metaphyseal holes compared to the sham group. Conclusion. Creating a metaphyseal hole 10 mm distal to the physis of the proximal tibia can significantly stimulate longitudinal growth and induce tibia valga in rabbits; however, the effect varies depending on the type of interposition material. Notably, overgrowth was significant only in the group with holes filled with bone wax. Based on this study, the location of the metaphyseal hole during ACL reconstruction or physeal bar excision could be optimized. Cite this article: Bone Joint Res 2025;14(3):236–244


Bone & Joint Research
Vol. 9, Issue 10 | Pages 709 - 718
1 Oct 2020
Raina DB Liu Y Jacobson OLP Tanner KE Tägil M Lidgren L

Bone is a dynamic tissue with a quarter of the trabecular and a fifth of the cortical bone being replaced continuously each year in a complex process that continues throughout an individual’s lifetime. Bone has an important role in homeostasis of minerals with non-stoichiometric hydroxyapatite bone mineral forming the inorganic phase of bone. Due to its crystal structure and chemistry, hydroxyapatite (HA) and related apatites have a remarkable ability to bind molecules. This review article describes the accretion of trace elements in bone mineral giving a historical perspective. Implanted HA particles of synthetic origin have proved to be an efficient recruiting moiety for systemically circulating drugs which can locally biomodulate the material and lead to a therapeutic effect. Bone mineral and apatite however also act as a waste dump for trace elements and drugs, which significantly affects the environment and human health.

Cite this article: Bone Joint Res 2020;9(10):709–718.


Bone & Joint Research
Vol. 8, Issue 8 | Pages 405 - 413
1 Aug 2019
Huang J Bao X Xia W Zhu L Zhang J Ma J Jiang N Yang J Chen Q Jing T Liu J Ma D Xu G

Objectives

X-linked hypophosphataemic rickets (XLHR) is a disease of impaired bone mineralization characterized by hypophosphataemia caused by renal phosphate wasting. The main clinical manifestations of the disorder are O-shaped legs, X-shaped legs, delayed growth, and bone pain. XLHR is the most common inheritable form of rickets, with an incidence of 1/20 000 in humans. It accounts for approximately 80% of familial cases of hypophosphataemia and serves as the prototype of defective tubular phosphate (PO43+) transport, due to extra renal defects resulting in unregulated FGF23 activity. XLHR is caused by loss-of-function mutations in the PHEX gene. The aim of this research was to identify the genetic defect responsible for familial hypophosphataemic rickets in a four-generation Chinese Han pedigree and to analyze the function of this mutation.

Methods

The genome DNA samples of all members in the pedigree were extracted from whole blood. We sequenced all exons of the PHEX and FGF23 genes, as well as the adjacent splice site sequence with Sanger sequencing. Next, we analyzed the de novo mutation c.1692 del A of the PHEX gene with an online digital service and investigated the mutant PHEX with SWISS-MODEL, immunofluorescence, and protein stability detection.