Basic Sciences
I. Histologic Features of Bone
III. Conditions of Bone Mineralization, Bone Mineral Density, and Bone Viability
SECTION 3 NEUROMUSCULAR AND CONNECTIVE TISSUES
SECTION 4 CELLULAR AND MOLECULAR BIOLOGY, IMMUNOLOGY, AND GENETICS OF ORTHOPAEDICS
SECTION 5 ORTHOPAEDIC INFECTIONS AND MICROBIOLOGY
SECTION 6 PERIOPERATIVE PROBLEMS
SECTION 7 IMAGING AND SPECIAL STUDIES
section 1 Bone
A Types (Figure 1-1; Table 1-1)
Table 1-1
Modified from Brinker MR, Miller MD: Fundamentals of orthopaedics, Philadelphia, 1999, WB Saunders, p 1.
1. Normal bone: lamellar, either cortical or cancellous
2. Immature and pathologic bone: woven; more random, more osteocytes, increased turnover, weaker
Constitutes 80% of the skeleton
Consists of tightly packed osteons or haversian systems
Connected by Haversian (or Volkmann’s) canals
Contains arterioles, venules, capillaries, nerves, possibly lymphatic channels
Interstitial lamellae: between osteons
Nutrition provided by intraosseous circulation
Characterized by slow turnover rate, higher Young’s modulus of elasticity, more stiffness
B Cellular biology (Figure 1-2)
Form bone by generating organic, nonmineralized matrix
Derived from undifferentiated mesenchymal stem cells
Have more endoplasmic reticulum, Golgi apparatus, and mitochondria than do other cells (for synthesis and secretion of matrix)
Bone surfaces lined by more differentiated, metabolically active cells
“Entrapped cells”: less active cells in “resting regions”; maintain the ionic milieu of bone
Osteoblast differentiation in vivo effected by the following:
Receptor-effector interactions in osteoblasts (Table 1-2)
Osteoblasts produce the following:
Osteoblast activity stimulated by intermittent (pulsatile) exposure to parathyroid hormone (PTH)
Osteoblast activity inhibited by tumor necrosis factor-α (TNF-α)
2. Osteocytes (see Figure 1-1)
Constitute 90% of the cells in the mature skeleton
Long interconnecting cytoplasmic processes projecting through the canaliculi
Less active in matrix production than are osteoblasts
Important for control of extracellular calcium and phosphorus concentration
This activity occurs both normally and in certain conditions, including multiple myeloma and metastatic bone disease.
Multinucleated, irregular giant cells
Possess a ruffled (“brush”) border and surrounding clear zone
Bone resorption occurs in depressions: Howship’s lacunae
Osteoblasts (and tumor cells) express RANKL (Figure 1-3), which acts as follows:
Synthesize tartrate-resistant acid phosphate
Bind to bone surfaces through cell attachment (anchoring) proteins
Produce hydrogen ions through carbonic anhydrase
Have specific receptors for calcitonin
Potent stimulator of osteoclast differentiation and bone resorption
Inhibit osteoclastic bone resorption.
Categorized into two classes on the basis of presence or absence of a nitrogen side group
Nitrogen-containing bisphosphonates are up to 1000-fold more potent in their antiresorptive activity.
Nitrogen-containing bisphosphonates
Non–nitrogen-containing bisphosphonates
Decreases skeletal events in multiple myeloma
Associated with osteonecrosis of the jaw
Table 1-3
1. Organic components: 40% of the dry weight of bone
Collagen (90% of organic component)
Collagen is primarily type I (mnemonic: “bone” contains the word “one”).
Hole zones (gaps) exist within the collagen fibril between the ends of molecules.
Pores exist between the sides of parallel molecules.
Mineral deposition (calcification) occurs within the hole zones and pores (Figure 1-4).
Cross-linking decreases collagen solubility and increases its tensile strength.
Matrix proteins (noncollagenous)
2. Inorganic (mineral) components: 60% of the dry weight of bone
Cortical and cancellous bone is continuously remodeled throughout life by osteoclastic and osteoblastic activity (Figure 1-5).
Wolff’s law: Remodeling occurs in response to mechanical stress.
Piezoelectric remodeling occurs in response to electrical charge.
Bone receives 5% to 10% of the cardiac output.
Long bones receive blood from three sources (systems):
Nutrient arteries branch from systemic arteries, enter the diaphyseal cortex through the nutrient foramen, enter the medullary canal, and branch into ascending and descending arteries (Figure 1-7).
Further branching into arterioles in the endosteal cortex enables blood supply to at least the inner two thirds of the mature diaphyseal cortex via the Haversian system (Figures 1-8 and 1-9).
G Types of bone formation (Table 1-4)
1. Enchondral bone formation and mineralization
Undifferentiated cells secrete the cartilaginous matrix and differentiate into chondrocytes.
The matrix mineralizes and is invaded by vascular buds that bring osteoprogenitor cells.
Osteoclasts resorb calcified cartilage, and osteoblasts form bone.
Bone replaces the cartilage model; cartilage is not converted to bone.
Embryonic formation of long bones (Figures 1-11 and 1-12)
These bones are formed from the mesenchymal anlage, at 6 weeks of gestation.
The cartilage model increases in size through appositional (width) and interstitial (length) growth.
Arterial supply is rich during development, with an epiphyseal artery (terminates in the proliferative zone), metaphyseal arteries, nutrient arteries, and perichondrial arteries (Figure 1-13).
Two growth plates exist in immature long bones: (1) horizontal (the physis) and (2) spherical (growth of the epiphysis).
The perichondrial artery is the major source of nutrition of the growth plate.
Delineation of physeal cartilage zones is based on growth (see Figure 1-13) and function (Figures 1-14 and 1-15).
Reserve zone: Cells store lipids, glycogen, and proteoglycan aggregates; decreased oxygen tension occurs in this zone.
Normal matrix mineralization occurs in the lower hypertrophic zone: chondrocytes increase five times in size, accumulate calcium in their mitochondria, die, and release calcium from matrix vesicles.
Osteoblasts migrate from sinusoidal vessels and use cartilage as a scaffolding for bone formation.
This zone widens in rickets (see Figure 1-15), with little or no provisional calcification.
Mucopolysaccharide diseases (see Figure 1-15) affect this zone, leading to chondrocyte degeneration.
Physeal fractures probably traverse several zones, depending on the type of loading (Figure 1-16).
This is adjacent to the physis and expands with skeletal growth.
Osteoblasts from osteoprogenitor cells align on cartilage bars produced by physeal expansion.
Collagen hole zones are seeded with calcium hydroxyapatite crystals through branching and accretion (crystal growth).
Hormones and growth factors (Figure 1-17; Table 1-5)
Table 1-5
Effects of Hormones and Growth Factors on the Growth Plate
From Simon SR, editor: Orthopaedic basic science, ed 2, Rosemont, Ill, 1994, American Academy of Orthopaedic Surgeons, p 196.
1. A Continuum: inflammation to repair (soft callus followed by hard callus) ending in remodeling
2. Blood supply (bone blood flow): the most important factor
Bleeding creates a hematoma, which provides hematopoietic cells capable of secreting growth factors.
Osteoblasts from surrounding osteogenic precursor cells and fibroblasts proliferate.
Primary callus response within 2 weeks.
For bone ends not in continuity, bridging (soft) callus occurs.
Soft callus is later replaced through enchondral ossification by woven bone (hard callus).
Medullary callus supplements the bridging callus, forming more slowly and later (Figure 1-18).
Fracture healing varies with treatment method (Table 1-7).
