Thickening of the long bone: mechanisms and clinical implications

doi:10.3969/j.issn.2095-4344.2017.36.022

Abstract

Abstract:

BACKGROUND: The thickening of living bone is an important natural rule, and genetic, nutritional and endocrine factors play critical roles in the bone thickening; however, these factors are site-blind.
OBJECTIVE: To analyze the mechanism underlying the thickening of the long bone.
METHODS: Clinical cases and literature were analyzed. Medline and CNKI databases were retrieved using the keywords of “bone growth in width, skeletal thickening, bone thickening, periosteal apposition” in English and Chinese, respectively. Totally 12 eligible articles were included for result analysis.
RESULTS AND CONCLUSION: The mechanical environment of the bone plays a key role in the bone remodeling, which is a site-specific process. The thickening of the long bone is completed through the periosteal apposition, and the coupling effect of stress-angiogenesis-osteogenesis induced by overloading is the pathological basis of bone thickening. The periosteal apposition and periosteal resorption belong to a lifelong dynamic process, and the bending stress is the most important factor to maintain the periosteal osteogenesis. If the bone is shielded from bending stress to a certain extent by the metal fixators, it may lead to bone resorption and thinning, nonunion and other serious consequences. Therefore, the strength of the fixators should match the patient body mass and the thickness of the bone. The marrow cavity is a natural low stress region, so intramedullary fixation theoretically has little effect on the width growth of bone.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Skeleton, Periosteum, Biomechanics, Tissue Engineering

CLC Number:

R318

Liu Zhen-dong1, Zhou Da-peng2, Qin Si-he3. Thickening of the long bone: mechanisms and clinical implications[J]. Chinese Journal of Tissue Engineering Research, 2017, 21(36): 5868-5872.

Figures/Tables 7

References

[1] Gkiatas I, Lykissas M, Kostas-Agnantis I et al. Factors affecting bone growth. Am J Orthop (Belle Mead NJ). 2015； 44(2):61-67.

[2] Rauch F. Bone growth in length and width: the Yin and Yang of bone stability. J Musculoskelet Neuronal Interact. 2005；5(3):194-201.

[3] Buckwalter JA, Glimcher MJ, Cooper RR, et al. Bone Biology. J Bone Joint Surg.1995;77A(8):1276-1289.

[4] Wohl GR, Towler DA, Silva MJ. Stress fracture healing: fatigue loading of the rat ulna induces upregulation in expression of osteogenic and angiogenic genes that mimic the intramembranous portion of fracture repair. Bone. 2009；44(2):320-330.

[5] Schipani E, Maes C, Carmeliet G, et al. Regulation of osteogenesis-angiogenesis coupling by HIFs and VEGF.J Bone Miner Res. 2009;24(8):1347-1353.

[6] 刘振东,马梦然. 骨折愈合理论研究现状[J].中国矫形外科杂志, 2010,18(16);87-91.

[7] Nakamura K, Matsushita T, Mamada K, et al. Changes of callus diameter during axial loading and after fixator removal

in leg lengthening.Arch Orthop Trauma Surg. 1998;117(8): 464-467

[8] May C, Yen YM, Nasreddine AY, et al. Complications of plate fixation of femoral shaft fractures in children and adolescents. J Child Ortho. 2013;7(3):235-243.

[9] Seeman E. Periosteal bone formation--a neglected determinant of bone strength. N Engl J Med. 2003; 349(4): 320-323

[10] Devmurari KN, Song HR, Modi HN, et al. Callus features of regenerate fracture cases in femoral lengthening in achondroplasia. Skeletal Radiol. 2010 ;39(9):897-903.

[11] 刘振东,范清宇.应力遮挡效应—寻找丢失的钥匙[J].中华创伤骨科杂志,2002,4(1):62-64.

[12] Trias A,Feri A.Cortical circulation of long bones. J Bone Joint Surg.1979;61A:1052-1059.

[13] 刘振东,范清宇,马保安，等.成年狗股骨微波高温灭活后的再血管化研究[J].中华骨科杂志,1998,18(11):682-685.

[14] Rhinelander FW. Tibial blood supply in relation to fracture healing. Clin Orthop Relat Res.1974;(105):34-81.

[15] 刘振东,秦泗河. 骨痂的形成和分类[J]. 中国矫形外科杂志, 2016,24(4):332-337.