Comparative Skeletal Structure


The sophisticated organization of the skeleton achieves a structure that can withstand the extremes of functional load‐bearing. The growth, development and repair of the skeletal structure is realized through the tightly regulated remodelling of bone tissue, orchestrated by cells that specifically form or resorb the matrix.

Keywords: bone; ligament; tendon; cartilage; skeleton; connective tissue

Figure 1.

Bone can be categorized into two morphological components: cortical and cancellous bone. The dense cortical bone envelopes the entire structure, while cancellous – or trabecular – bone is typically found towards the ends of the bone. The internal spaces of bone are filled with marrow. Reprinted, with permission, from Lynch SE, Genco RJ and Marx RE (1999) Tissue Engineering: Applications in Maxillofacial Surgery and Periodontics. Quintessence.

Figure 2.

Diagram depicting a section of the cortical shaft of a long bone, showing the arrangement of the lamellae in the osteons, the interstitial lamellae, and the outer and inner circumferential lamellae. The outer surface is protected by the periosteum, while the inner surface is covered by the endosteum. Within the cortical shell, the branching out of the buttressing trabeculae can be seen. Reprinted, with permission, from Bloom W and Fawcett DW (1986) A Textbook of Histology, 11th edn. Saunders.

Figure 3.

Bone may be categorized into three microstructural components: (1) bone cells, which include osteoblasts, osteocytes and osteoclasts (stained with a modified Goldner trichrome stain); (2) an organic matrix consisting of collagenous and noncollagenous factors, such as the bone morphogenetic proteins (the mineralized matrix has been removed and cells have been coloured green to distinguish them from the organic framework); (3) an inorganic component consisting primarily of calcium and phosphate; this component has been stylized as an array of hexagonal crystals. Reprinted, with permission, from Lynch SE, Genco RJ and Marx RE (1999) Tissue Engineering: Applications in Maxillofacial Surgery and Periodontics. Quintessence.

Figure 4.

Osteoclasts (red) and osteoblasts (dark green) interact through cytokines released into the bone micromilieu. Macrophages secrete macrophage colony‐stimulating factor (MCSF), various interleukins and tumour necrosis factor, all of which promote osteoclast differentiation from haematopoietic stem cells, from the colony forming unit for granulocyte‐macrophages (CFU‐GM) and the CFU‐M (CFU for macrophage) to terminal osteoclast phenotype. Osteoblasts interact by expressing factors which affect osteoclasts, mainly RANKL and MCSF, as well as factors affecting bone mineralization and progression of their own phenotype, such as insulin‐like growth factors and basic fibroblast growth factors. Importantly, disuse will also upregulate osteoclast activity, while increases in mechanical factors will elevate bone formation.

Figure 5.

Development of a long bone as shown in longitudinal sections (A–J), and in cross‐sections A′, B′, C′ and D′. Pale blue is cartilage; purple, calcified cartilage; black, bone; red, arteries. A, The original cartilage model of the bone; B, a periosteal collar of bone appears before any calcification of cartilage occurs; C, cartilage begins to calcify; D, vascular mesenchyme enters the calcified cartilage and divides it into two zones of ossification (E and F); G, blood vessels and mesenchyme penetrate the epiphyseal cartilage and the epiphyseal ossification centre develops within it; H, a similar ossification centre develops in the lower epiphyseal cartilage; as the bone ceases to grow in length, the lower epiphyseal plate disappears first (I) and then the upper epiphyseal plate (J). The marrow cavity then becomes continuous throughout the length of the bone, and the blood vessels of the diaphysis, metaphyses and epiphyses intercommunicate. Reprinted, with permission, from Bloom W and Fawcett DW (1986) A Textbook of Histology, 11th edn. Saunders.

Figure 6.

The cutting–filling cone has a head of osteoclasts that cut through the bone, and a tail of osteoblasts that form a new secondary osteon. The velocity through bone is determined by measuring between two tetracycline labels (1 and 2) administered 1 week apart. Reprinted, with permission, from Graber T and Vanarsdall RL (2000) Orthodontics:Current Principles and Techniques, 3rd edn. Mosby.


Further Reading

Alsina M, Guise T and Roodman GD (1996) Cytokine regulation of bone cell differentiation. Vitamins and Hormones 52: 63–98.

Baron R, Ravesloot JH, Neef L et al. (1993) Cellular and molecular biology of the osteoclast. In: Noda M (ed.) Cellular and Molecular Biology of Bone, pp. 445–495. San Diego: Academic Press.

Bilezikian JP, Raisz LG and Rodan GA (eds) (1996) Principles of Bone Biology. San Diego: Academic Press.

Buckwalter JA, Einhorn TA and Sheldon RS (eds) (2000) Orthopaedic Basic Science. Rosemont, Illinois: American Academy of Orthopaedic Surgeons.

Cowin SC (1989) Bone Mechanics. Boca Raton, FL: CRC Press.

Ducy P and Karsenty G (1998) Genetic control of cell differentiation in the skeleton. Current Opinion in Cell Biology 10: 614–619.

Ferguson CM, Miclau T, Hu D, Alpern E and Helms JA (1998) Common molecular pathways in skeletal morphogenesis and repair. Annals of the New York Academy of Sciences 857: 33–42.

Hall BK and Miyake T (1992) The membranous skeleton: the role of cell condensations in vertebrate skeletogenesis. Anatomy and Embryology 186: 107–124.

Lian B and Stein GS (1992) Concepts of osteoblast growth and differentiation: basis for modulation of bone cell development and tissue formation. Critical Reviews in Oral Biology and Medicine 3(3): 269–305.

Martin RB, Burr DB and Sharkey NA (1998) Skeletal Tissue Mechanics. New York: Springer.

Niiweide PJ, Ajubi NE and Aarden EM (1998) Biology of osteocytes. Advances in Organ Biology 5B: 529–542.

Owen TA, Aronow M, Shalhoub V, Lian JB and Stein GS (1990) Progressive development of the rat osteoblast phenotype in vitro – reciprocal relationships in expression of genes associated with osteoblast proliferation and differentiation during formation of the bone extracellular matrix. Journal of Cellular Physiology 143: 420–430.

Reddi AH (1994) Bone and cartilage differentiation. Current Opinion in Genetics and Development 4(5): 737–744.

Rubin CT (1984) Skeletal strain and the functional strain significance of bone architecture. Calcified Tissue International 36: S11–S18.

Rubin CT and Lanyon LE (1984) Dynamic strain similarity in vertebrates: an alternative to limb bone scaling. Journal of Theoretical Biology 107: 321–327.

Rubin CT and Rubin J (2000) Biology, physiology and morphology of bone. In: Harris E, Ruddy S and Sledge C (eds) Kelly's Textbook of Rheumatology, 6th edn, pp. 1611–1634. Philadelphia, PA: WB Saunders.

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Rubin, Clinton, Alikhani, Mani, and Rubin, Janet(Apr 2001) Comparative Skeletal Structure. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1038/npg.els.0001860]