Connective Tissue - Bone Study Guide

General Structure of Bone

• Cortical Bone (Compact Bone): Tough outer layer; constitutes the majority of bone mass; covered by periosteum rich in blood vessels.
• Cancellous Bone (Trabecular or Spongy Bone): Features spongy, mesh-like plates; in direct contact with bone marrow.

Cellular and Non-cellular Components of Bone

• Cellular Component:

  • Osteoblasts: Immature bone cells responsible for secreting the extracellular matrix; can differentiate into osteocytes, bone lining cells, or undergo apoptosis.
  • Osteocytes: Mature bone cells that maintain the extracellular matrix and respond to mechanical loading and hormonal changes.
  • Osteoclasts: Responsible for breaking down the extracellular matrix, releasing minerals into the bloodstream, and creating space for osteoblast activity.
  • Bone Lining Cells: Play a role in maintaining the bone surface.

• Non-cellular Component:

  • Non-mineralized Matrix: Known as osteoid; primarily consists of collagen.
  • Mineralized Matrix: Composed chiefly of hydroxyapatite, providing rigidity.

Classifications of Bone Maturity

• Immature Bone (Woven Bone):

  • Also referred to as primary bone; typically found during fracture repair and fetal development; characterized by irregular collagen structure and lower mineral content, making it weaker.

• Mature Bone (Lamellar Bone):

  • Known as secondary bone; results from the remodeling of woven bone under stress; exhibits an organized osteon structure with concentric rings, providing greater strength and higher mineral content.

• Bone Types: Both cortical and cancellous bones can present in immature forms.

Process of Fracture Repair

• Regeneration and Remodeling: Repair process aims to restore optimal bone function without forming scars.

• Healing Duration: Influenced by factors such as fracture site, type, treatment, soft tissue involvement, and individual traits (age, immune health, nutritional status).

• Phases of Healing:

  • Initial Response: Internal bleeding leads to cell influx at injury site, secreting growth factors and facilitating clot formation (involves fibroblasts, platelets, osteoprogenitor cells, and inflammatory cells).
  • Hematoma Formation: Develops and persists for about a week post-injury.
  • Inflammatory Phase: Formation of granulation tissue, including fibrosis and neovascularization (new blood vessel formation).

Tissue Types

• Tissue organization hierarchy: chemical level → cellular level → tissue level → system level.
• Extracellular matrix (ECM) consists of fluids and molecules secreted by cells, influencing tissue structure and function.
• Common ECM molecules:
  • Collagen: Provides structure and strength; has a triple helix structure.
  • Elastin: Allows elasticity in tissues.
  • Proteoglycans: Fill space and attract water, crucial for tissue softness (e.g., cartilage).
  • Integrins: Connect cells to other cells and ECM components.

Categories of Tissue

• Epithelial Tissue: Protects, lines organs, and produces secretions (e.g., skin, mucous).
• Connective Tissue: Fills spaces, provides support (e.g., bone, cartilage), and stores energy (e.g., adipose).
  • Fibroblasts are key cells producing ECM components and aiding tissue repair.
• Muscle Tissue: Contracts for movement; includes skeletal (voluntary), smooth (involuntary), and cardiac muscles.
• Nervous Tissue: Transmits electrical impulses for communication throughout the body.

Cellular Injury / Adaptation

• Factors influencing injury reversal: mechanism, duration, and severity of injury.
• Free Radical Theory: Reactive oxygen species (ROS) can damage cells; excess ROS leads to oxidative stress, implicated in many diseases.
• Antioxidants neutralize ROS, preventing DNA and cell damage.
  • Endogenous antioxidants: e.g., glutathione, peroxidase, catalase.
  • Exogenous antioxidants: e.g., vitamins C, E, beta-carotene.
• Exercise generates ROS but also encourages the development of endogenous antioxidants; excessive exercise can induce oxidative stress.

Genetic Alterations

• Genetic changes causing injury:
  • Chromosomal abnormalities (e.g., Down's syndrome).
  • Single gene mutations affecting protein function (e.g., sickle cell anemia).
  • Multi-gene interactions with environmental factors (e.g., Type II diabetes, obesity).

Cellular Responses to Physical Stress

• Possible responses include:
  • Atrophy: Decreased stress tolerance; examples include muscle and bone loss.
  • Maintenance of current state.
  • Hypertrophy: Increased cell size due to demands or hormonal input; occurs in cardiac and skeletal muscles, e.g., left ventricular hypertrophy.
  • Hyperplasia: Increased cell number often from hormonal or physical stimulation; examples include callus formation and smooth muscle proliferation.
  • Injury and Death occur under severe stress.

Reversible Cellular Injury

• Process involves:
  • Increased sodium and calcium in cells leading to swelling.
  • Impaired organelle function, particularly mitochondria affecting ATP production.
  • Successful reversal depends on the nucleus remaining intact, restoring energy sources, and neutralizing toxins.

Chronic Cellular Stress Responses

• Responses to chronic stress include:
  • Atrophy: Reduction in organ or cell size, e.g., muscle wasting.
  • Hypertrophy: Growth in cell size due to demand.
  • Hyperplasia: Increase in cell numbers in response to stimulation.
  • Metaplasia: Transformation of one cell type to another, e.g., airway epithelium changes in smokers.
  • Dysplasia: Increased cell numbers with loss of morphology and organization, often in chronic injury contexts.

Irreversible Cell Injury

• Consequences and processes of irreversible injury lead to cell death, characterized by severe damage that cannot be repaired.