• Clinical science

Bone tissue (Osseous tissue)

Summary

The musculoskeletal system is comprised of bones and connective tissue structures, such as cartilage, ligaments, and tendons. These structures are brought into motion by skeletal muscles. To withstand resultant forces, bone tissue resists pressure and tension and is minimally elastic. Bone tissue mainly consists of bone cells (osteoblasts, osteocytes, and osteoclasts) and a mineralized extracellular matrix that is primarily made up of collagen fibrils and hydroxyapatite crystals. Ossification, or bone formation, begins with a framework that consists of either mesenchymal connective tissue (intramembranous ossification) or cartilage (endochondral ossification). Woven bone is formed, which is replaced by the more solid and layered lamellar bone. The outer cortical layers can be macroscopically differentiated from the branched center of the trabeculae.

Overview

Function of bone

  • Supportive function
  • Protective function
  • Storage (calcium and phosphorus reservoir)
  • Hematopoiesis

Types of bone

References:[1][2]

Bone composition

Overview

The exact composition or organization of individual bone components differs in the various bones types and maturation stages. All human bones are composed of the same basic elements:

Bone cells

Characteristics of bone cells
Definition Function [3] Location
Osteoprogenitor cells
  • Barely differentiated precursor bone cells that originate from the mesenchyme
Osteoblasts [4]
Osteocytes
Osteoclasts
  • Bone-dissolving multinucleated phagocytes that degrade mineralized bone
  • Derive from the fusion of monocyte and macrophage precursor cells
  • Have calcitonin receptors

Bone matrix

Composed of organic and inorganic material:

Bone membranes

The periosteum and the endosteum consist of the same type of bone cells.

Bone marrow

Development and maturation

Development of bone

Ossification

Overview of the ossification process
Endochondral ossification Intramembranous ossification
Definition
Process
  1. Mesenchymal cells differentiate into osteoblasts at the ossification center.
  2. Osteoblasts deposit osteoids → osteocytes form after osteoid mineralization → formation of a bone segment
  3. The osteoblasts on the outer surface of the bone segment deposit osteoid layers → appositional growth
  4. Several bone segments fuse to primary trabecular bone.
  5. Blood vessels and undifferentiated mesenchymal cells invade the trabecular bone → formation of bone marrow
  6. Simultaneous construction and remodeling of bone (woven bone → lamellar bone)
  7. Mesenchymal layers that do not become ossified → formation of endosteum and periosteum
Examples

The skull undergoes both processes: some bones (e.g., frontal, parietal bones) are derived from the neural crest and undergo membranous ossification, whereas other bones (e.g., sphenoid, occipital bones) are derived from the paraxial mesoderm and undergo endochondral ossification.

Stages of bone maturity

Bones are arranged into woven bone (primary bone) during embryonic development or bone healing. The structure of woven bone is disorganized and transformed into organized tissue of lamellar bone (secondary bone) through continuous remodeling.

Stages of bone maturity
Woven bone Lamellar bone
Definition
Histology
  • Disorganized collagen fibers
  • Less mineralized bone substance with a high water content
  • Rich in cells

Characteristics

  • Mechanically strong
Remodeling
  • Usually successively remodeled to more stable lamellar bones
  • Load-dependent, continuous remodeling of bone according to acting forces

The direction of collagen fibers of the bone extracellular matrix is an important distinguishing characteristic between immature woven bone and mature lamellar bone.

Trabecular bone (spongy or cancellous bone)

Cortical bone (compact bone)

Lamellar bones vascularization and canals

The course of lamellar bone vessels is strictly defined by the Haversian and Volkmann canal structures. In contrast, woven bone vessels are disorganized.

Development of long bones

Epiphyseal plate

The part of the bone where longitudinal growth takes place. Layers include (from epiphysis to diaphysis):

  1. Zone of resting cartilage: deposits undifferentiated precursor chondrocytes that provide the proliferation zone with new chondrocytes
  2. Proliferation zone: mitosis of chondrocytes
  3. Zone of hypertrophy: enlarges cartilage through chondrocyte hypertrophy, which leads to collagen (type X) production by hypertrophic chondrocytes and mineralization of the longitudinal septa
  4. Zone of calcification
  5. Zone of ossification: colonization of the mineralized longitudinal septae by osteoblasts osteoid formation → mineralization

References:[5]

Bone remodeling and healing

The human skeleton is in a continuous dynamic state of remodeling. Not only does this apply to the replacement of immature woven bone by lamellar bone, but also for adaptation of adult bones to their individual load.

Bone remodeling [6]

Blasts build, clasts crumble.

Bone remodeling in cortical bone

Bone remodeling in trabecular bone

Regulation of bone remodeling [7]

Estrogen has a positive effect on bone balance because it inhibits osteoclast formation and activation and increases OPG formation.

Bone healing [8]

Fractures occur when bones are strained beyond their maximum load. Fractures can heal in two different ways.

During childhood or adolescence, a fracture near a joint may damage the unclosed epiphyseal plate, which can result in growth disorders (e.g., asymmetry, inhibition, acceleration) during healing.

References:[9][10]

Clinical significance

  • 1. Sadler TW, Langman J. Langman's Medical Embryology. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.
  • 2. Hill MA. Musculoskeletal System - Skull Development. https://embryology.med.unsw.edu.au/embryology/index.php/Musculoskeletal_System_-_Skull_Development. Updated May 9, 2018. Accessed June 28, 2018.
  • 3. Blair HC, Larrouture QC, Li Y, et al. Osteoblast differentiation and bone matrix formation in vivo and in vitro. Tissue Engineering Part B: Reviews. 2017; 23(3): pp. 268–280. doi: 10.1089/ten.teb.2016.0454.
  • 4. Kwan Tat S, Padrines M, Théoleyre S, Heymann D, Fortun Y. IL-6, RANKL, TNF-alpha/IL-1: interrelations in bone resorption pathophysiology. Cytokine Growth Factor Rev. 2004; 15(1): pp. 49–60. pmid: 14746813.
  • 5. Patton KT, Thibodeau GA. Anthony's Textbook of Anatomy & Physiology. Maryland Heights, MO: Mosby; 2014.
  • 6. Rucci N. Molecular biology of bone remodelling. Clin Cases Miner Bone Metab. 2008; 5(1): pp. 49–56. pmid: 22460846.
  • 7. Ross MH, Pawlina W. Histology. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
  • 8. Sela JJ, Bab IA. Principles of Bone Regeneration. Berlin, Germany: Springer Science & Business Media; 2012.
  • 9. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. New York, NY: McGraw-Hill Education; 2015.
  • 10. Hall JE. Guyton and Hall Textbook of Medical Physiology. Philadelphia, PA: Elsevier; 2016.
last updated 11/27/2020
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