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histology of bone

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Histology of Bone

Source: Junqueira's Basic Histology, 17e & Histology: A Text and Atlas (Ross & Pawlina)

1. Overview

Bone is a specialized connective tissue composed of cells embedded in a hard, mineralized extracellular matrix (ECM). It differs from other connective tissues because its matrix is calcified - approximately 70% inorganic (mainly hydroxyapatite crystals: Ca₁₀(PO₄)₆(OH)₂) and 30% organic (mainly type I collagen + proteoglycans + glycoproteins).

2. Types of Bone

Macroscopic Types

Cross section showing compact bone (dense outer layer) and cancellous bone (porous inner lattice of trabeculae)

Type	Also Called	% of Total	Location	Structure
Compact bone	Cortical bone	~80%	Outer region (diaphysis of long bones)	Dense, parallel lamellae / osteons
Cancellous bone	Spongy / trabecular bone	~20%	Inner region (epiphyses), around marrow cavities	Interconnected trabeculae / spicules covered by endosteum

Microscopic Types

Type	Features	Found In
Woven (primary) bone	Irregular, random collagen arrangement; lightly calcified; rapidly formed	Fetal bone, fracture callus
Lamellar (secondary) bone	Ordered parallel collagen in lamellae 3-7 μm thick; heavily calcified	All adult normal bone

Key exam point: Woven bone is replaced by lamellar bone during remodeling. Under polarized light, lamellar bone shows alternating bright and dark bands due to the orthogonal shift in collagen fiber orientation between successive lamellae - this is birefringence.

3. Bone Cells

Trichrome-stained bone showing osteocytes (Oc) embedded in blue matrix, osteoblasts (Ob) lining the surface, and a large multinuclear osteoclast (Ocl) with surrounding mesenchyme (M)

A. Osteoprogenitor Cells

Origin: mesenchymal stem cells (periosteum and endosteum)
Flat, spindle-shaped cells with pale-staining nuclei
Can proliferate and differentiate into osteoblasts
Found in inner cellular layer of periosteum and in endosteum

B. Osteoblasts (Ob)

Bone-forming cells
Single layer of cuboidal cells on bone surfaces
Basophilic cytoplasm (rich in RER) - actively synthesize osteoid
Secrete: type I collagen, proteoglycans, osteonectin, osteocalcin
Alkaline phosphatase activity - essential for mineralization
Joined by gap junctions and adherent junctions
Fate: become osteocytes (trapped in matrix), bone lining cells, or undergo apoptosis

C. Osteocytes (Oc)

Most numerous bone cell
Former osteoblasts trapped in lacunae within calcified matrix
Flattened cell body with long dendritic processes in canaliculi
Processes connect to adjacent osteocytes and to central canal via gap junctions
Maintain bone matrix; act as mechanosensors
Cannot divide; metabolites exchanged via canalicular network

D. Osteoclasts (Ocl)

Bone-resorbing cells
Very large, multinucleated (up to 50 nuclei) - formed by fusion of blood monocytes
Located in shallow resorption pits = Howship's lacunae
Ruffled border (brush border) - greatly increases surface area for resorption
Secrete: HCl (dissolves mineral) + cathepsin K (degrades collagen)
Sealing zone - ring of tight contact between osteoclast and bone
Acidophilic (eosinophilic) cytoplasm

Cell	Origin	Function	Key Feature
Osteoprogenitor	Mesenchyme	Stem cell	Flat, pale
Osteoblast	Mesenchyme	Forms bone (osteoid)	Cuboidal, basophilic, on surface
Osteocyte	Osteoblast	Maintains matrix, mechanosensor	In lacunae + canaliculi
Osteoclast	Blood monocyte	Resorbs bone	Multinuclear, ruffled border, Howship's lacuna

4. Bone Matrix

Organic Component (30%)

Type I collagen (90% of organic matrix) - provides tensile strength
Non-collagenous proteins: osteonectin (binds collagen to mineral), osteocalcin, osteopontin, proteoglycans, bone morphogenetic proteins (BMPs)
The unmineralized organic matrix is called osteoid

Inorganic Component (70%)

Mainly hydroxyapatite [Ca₁₀(PO₄)₆(OH)₂]
Also carbonate, citrate, fluoride, magnesium
Provides compressive strength and hardness

5. The Osteon (Haversian System) - Structural Unit of Compact Bone

Osteon cross-section showing central canal (CC), concentric lamellae (L), osteocytes in lacunae (O), canaliculi (C), and interstitial lamellae (I)

The osteon is 100-250 μm in diameter and consists of:

Component	Description
Haversian canal (central canal)	Contains blood vessels, nerves, loose connective tissue, endosteum
Concentric lamellae	4-20 rings of calcified matrix surrounding the canal
Lacunae	Small spaces between lamellae, each housing one osteocyte
Canaliculi	Tiny channels radiating from lacunae, containing cell processes
Cement line	Outer boundary of osteon; rich in non-collagen proteins, poor in collagen
Interstitial lamellae	Remnants of old, remodeled osteons between current osteons

Canal System

Haversian canals - run longitudinally (parallel to long axis of bone)
Volkmann's (perforating) canals - run perpendicular/oblique, connect Haversian canals to each other and to the periosteum and marrow

6. Periosteum and Endosteum

Periosteum (outer covering)

Outer fibrous layer: dense connective tissue, fibroblasts, blood vessels
Inner cellular (cambium) layer: osteoprogenitor cells, osteoblasts, bone lining cells
Sharpey's (perforating) fibers - collagen bundles anchoring periosteum into bone matrix

Endosteum (inner covering)

Lines marrow cavities and covers trabeculae of cancellous bone
Thin layer of osteoprogenitor cells and bone lining cells
Covers surfaces of all haversian and Volkmann canals

7. Bone Formation (Ossification)

A. Intramembranous Ossification

Direct from mesenchyme - no cartilage template
Forms: flat bones of skull, clavicle, mandible
Mesenchymal cells → osteoprogenitor cells → osteoblasts → deposit osteoid → calcification
Forms woven bone first, then remodeled to lamellar bone

B. Endochondral Ossification

Uses hyaline cartilage model as template
Forms: long bones, short bones, base of skull, vertebrae, ribs
Zones of epiphyseal growth plate (from epiphysis toward diaphysis):
1. Zone of reserve (resting) cartilage - no proliferation
2. Zone of proliferating cartilage - chondrocytes dividing (coin-stack columns)
3. Zone of hypertrophic cartilage - cells enlarge, matrix calcifies
4. Zone of calcified cartilage - chondrocytes die (apoptosis), cartilage calcifies
5. Zone of ossification (bone deposition) - osteoblasts deposit bone on calcified cartilage spicules

8. Histological Preparation Note

Bone cannot be sectioned routinely because of its hardness. Two methods are used:

Decalcification - immerse in acid or EDTA to remove mineral, then paraffin-embed and section
Ground sections - bone is ground down to thin slices without decalcification (used to study Haversian systems)

Quick Summary for Exams

Feature	Compact Bone	Cancellous Bone
% of bone mass	80%	20%
Structure	Osteons (Haversian systems)	Trabeculae / spicules
Surface covering	Periosteum outside	Endosteum on all surfaces
Location	Diaphysis of long bones	Epiphyses, around marrow

Key associations to remember:

Osteoblast = Basophilic cytoplasm (lots of RER)
Osteoclast = Multinucleated, ruffled border, Howship's lacuna
Osteocyte = Lacuna + canaliculi
Haversian canal = longitudinal; Volkmann canal = transverse/oblique
Bone mineral = hydroxyapatite

- Junqueira's Basic Histology, 17e, pp. 353-370 - Histology: A Text and Atlas with Correlated Cell and Molecular Biology (Ross & Pawlina)

action potentials in nerve fibres

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Action Potentials in Nerve Fibres

Source: Guyton and Hall Textbook of Medical Physiology & Neuroscience: Exploring the Brain, 5e

1. Resting Membrane Potential

Before discussing action potentials, the resting state must be understood:

Resting membrane potential (RMP) = -70 mV (inside negative relative to outside)
Maintained by: Na⁺-K⁺ ATPase pump (pumps 3 Na⁺ out, 2 K⁺ in), K⁺ leak channels, and ionic concentration gradients
K⁺ is more concentrated inside the cell; Na⁺ is more concentrated outside
The membrane is said to be "polarized" at rest

2. What is an Action Potential?

An action potential (AP) is a rapid, self-propagating, all-or-none change in membrane potential that travels along the nerve fibre. It is the electrical signal by which nerve impulses are transmitted.

Key property: All-or-None Law - once threshold is reached, the AP fires at full amplitude regardless of stimulus strength. Stimulus strength is encoded by frequency of APs, not their size.

3. Phases of the Action Potential

Action potential waveform from Guyton showing resting (-70mV), threshold, depolarization (rising phase), overshoot (+35mV), repolarization (falling phase), and hyperpolarization

Detailed action potential diagram (Neuroscience: Exploring the Brain) showing resting potential, graded depolarization, threshold, rising phase, overshoot, falling phase, and undershoot with equilibrium potentials E_Na and E_K marked

Phase-by-Phase Breakdown

Phase	mV Range	Ion Movement	Channel Event
Resting	-70 mV	None	Na⁺ channels closed; K⁺ leak channels open
Graded depolarization	-70 → -55 mV	Small Na⁺ inflow	Stimulus brings membrane toward threshold
Threshold	~-55 mV	-	Critical point - AP becomes inevitable
Rising phase (depolarization)	-55 → +35 mV	Rapid Na⁺ influx	Voltage-gated Na⁺ channels open (activation gate opens)
Overshoot	~+35 mV peak	Na⁺ influx at peak	Vm approaches E_Na (+60 mV) but doesn't reach it
Falling phase (repolarization)	+35 → -70 mV	K⁺ efflux	Na⁺ channels inactivate (inactivation gate closes); K⁺ channels open
Undershoot (after-hyperpolarization)	Below -70 mV	Excess K⁺ efflux	K⁺ channels remain open too long
Restoration	back to -70 mV	Na⁺-K⁺ pump restores gradients	K⁺ channels close; Na⁺-K⁺ ATPase active

Total duration: ~2 milliseconds

4. Voltage-Gated Ion Channels (The Molecular Basis)

Voltage-gated sodium channel in three states (Resting, Activated, Inactivated) and voltage-gated potassium channel in two states (Resting, Slow activation) from Guyton Figure 5.7

Voltage-Gated Na⁺ Channel - THREE STATES

The Na⁺ channel has two gates:

Activation gate (outer) - opens rapidly with depolarization
Inactivation gate (inner) - closes slowly after activation

State	Membrane Potential	Activation Gate	Inactivation Gate	Na⁺ Flow
Resting (closed)	-70 mV	Closed	Open	None
Activated (open)	-55 to +35 mV	Open	Open	Inward (rapid)
Inactivated	Returning to -70 mV	Open	Closed	None

Key point: The channel cannot re-open from the inactivated state until the membrane repolarizes back to near resting potential. This is the basis of the absolute refractory period.

When depolarization occurs, permeability to Na⁺ increases 500-5000 fold.

Voltage-Gated K⁺ Channel - TWO STATES

Has only one gate (activation gate)
Opens more slowly than Na⁺ channels (delayed rectifier)
Opens during repolarization phase (after Na⁺ channels inactivate)
Stays open a little too long → causes after-hyperpolarization (undershoot)
No inactivation gate - simply closes slowly as membrane repolarizes

Positive Feedback (Hodgkin Cycle)

Depolarization → Na⁺ channels open → Na⁺ rushes in → more depolarization → more Na⁺ channels open...

This explosive positive feedback explains the all-or-none, spike-like nature of the AP.

5. Refractory Periods

Period	Duration	Mechanism	Can AP be fired?
Absolute Refractory Period (ARP)	~1 ms (during AP + early repolarization)	Na⁺ channels are inactivated - cannot open regardless of stimulus strength	No
Relative Refractory Period (RRP)	~1-2 ms after ARP	Na⁺ channels recovering; K⁺ channels still partially open (membrane hyperpolarized)	Yes, but needs supramaximal stimulus

Significance: Refractory periods ensure:

APs travel in one direction only (forward, never backward)
APs are discrete, separated signals
Limits maximum firing frequency (~500-1000 Hz)

6. Propagation of the Action Potential

Unmyelinated fibres (continuous conduction)

Na⁺ influx at active site creates local currents that depolarize adjacent membrane
This brings adjacent membrane to threshold → AP propagates forward
Cannot go backward because that region is in the refractory period
Like a burning fuse - the flame moves forward, can't go back because the material behind it is spent

Myelinated fibres (saltatory conduction)

Myelin sheath insulates the axon between nodes of Ranvier
AP can only be generated at nodes (where ion channels are concentrated)
Electrical current "jumps" from one node to the next - saltatory conduction (Latin: saltare = to jump)
Much faster and more energy-efficient than continuous conduction

Feature	Unmyelinated	Myelinated
Conduction velocity	0.5-2 m/s	Up to 120 m/s
Type of conduction	Continuous	Saltatory
Energy cost	Higher	Lower
Example	C fibres (pain, temperature)	Aα fibres (motor, proprioception)

7. Nerve Fibre Classification

Fibre Type	Myelin	Diameter	Velocity	Function
Aα	Thick	12-20 μm	70-120 m/s	Skeletal muscle motor, proprioception
Aβ	Medium	5-12 μm	30-70 m/s	Touch, pressure
Aγ	Thin	3-6 μm	15-30 m/s	Muscle spindle (intrafusal)
Aδ	Thin	2-5 μm	5-30 m/s	Fast pain, cold temperature
B	Thin	<3 μm	3-15 m/s	Preganglionic autonomic
C	None	0.2-1.5 μm	0.5-2 m/s	Slow pain, warmth, postganglionic autonomic

8. Factors Affecting Conduction Velocity

Myelin - increases velocity dramatically (saltatory conduction)
Axon diameter - larger diameter = faster conduction (less resistance)
Temperature - higher temperature = faster conduction (cold slows or blocks conduction - used in cryoanesthesia)

9. Role of the Na⁺-K⁺ ATPase Pump

Works continuously in the background to restore ionic gradients
Pumps 3 Na⁺ out and 2 K⁺ in per cycle (electrogenic - contributes ~-4 mV)
A single AP barely changes ionic gradients - 100,000 to 50 million APs can fire before gradients run down significantly
Activity increases ~8-fold when intracellular Na⁺ doubles (concentration-sensitive)
Requires ATP - explains why neurons are highly sensitive to ischemia/hypoxia

10. Clinical Relevance

Clinical Condition	Mechanism
Local anesthetics (lidocaine)	Block voltage-gated Na⁺ channels → prevent AP generation
Tetrodotoxin (TTX)	Blocks Na⁺ channel activation gate from outside
Multiple sclerosis	Demyelination slows/blocks saltatory conduction
Hypocalcemia	Ca²⁺ normally stabilizes Na⁺ channel gating; low Ca²⁺ → hyperexcitability, tetany
Hyperkalemia	Reduces RMP (less negative) → partial inactivation of Na⁺ channels → weakness/paralysis

Quick Exam Summary

RMP: -70 mV (Guyton) / -65 mV (Neuroscience texts)
Threshold: ~-55 mV (about 15 mV above RMP)
Peak overshoot: ~+35 mV
Duration: ~2 ms
Depolarization: Na⁺ in (via voltage-gated Na⁺ channels)
Repolarization: K⁺ out (via voltage-gated K⁺ channels)
Na⁺ channel has 3 states: Resting → Activated → Inactivated
ARP: Na⁺ channels inactivated → no AP possible
RRP: Partial recovery → suprathreshold stimulus needed
Saltatory conduction: Jumps between nodes of Ranvier → fast + efficient

- Guyton and Hall Textbook of Medical Physiology, 14e, pp. 79-90 - Neuroscience: Exploring the Brain, 5e, Chapter 4

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