Bone Remodeling: Involves comparison of the locations and remodeling functions of osteoblasts, osteocytes, and osteoclasts.
Hormonal Regulation: Explanation of how hormones and physical stress regulate bone remodeling.
6.6 Bone Remodeling
Overview:
Bone remodeling is a continuous process that replaces approximately 5–10% of bone every year.
Duration of Replacement:
Spongy Bone: Replaced every 3–4 years.
Compact Bone: Replaced every 10 years.
Components of Remodeling:
Consists of both bone deposition and bone resorption.
Occurs at surfaces of both the periosteum and endosteum.
Remodeling Units: The process is coordinated by packets of adjacent osteoblasts and osteoclasts.
Bone Deposition
Mechanism:
New bone matrix is deposited by osteoblasts.
Osteoid Seam: A band of unmineralized bone matrix that indicates the area of new matrix deposition.
Calcification Front: The sudden transition zone between the osteoid seam and older mineralized bone.
Triggers for Bone Deposit (not fully confirmed but may include):
Mechanical signals.
Increased concentrations of calcium and phosphate ions, essential for hydroxyapatite formation.
Matrix proteins that bind and concentrate calcium ions.
Adequate enzyme alkaline phosphatase for proper mineralization.
Bone Resorption
Function: Primarily performed by osteoclasts.
Process:
Osteoclasts dig depressions or grooves in the bone surface.
They secrete lysosomal enzymes and protons (H+) to digest the bone matrix.
The acidic environment converts calcium salts into soluble forms for absorption.
Phagocytosis:
Osteoclasts also phagocytize the demineralized matrix and dead osteocytes.
Waste products are transcytosed and released into interstitial fluid, eventually entering the bloodstream.
Following completion of resorption, osteoclasts undergo apoptosis (programmed cell death).
Activation: Osteoclast activation is influenced by parathyroid hormone (PTH) and proteins from immune T cells.
Control of Remodeling
Regulation: Remodeling occurs continuously and is controlled by two primary loops:
Maintaining homeostasis through hormonal negative feedback, notably involving PTH.
Ensuring bone strength through mechanical and gravitational forces acting on bones.
Hormonal Controls
Importance of Calcium Levels:
Maintaining extracellular fluid calcium levels is crucial for the membrane potential of all cells, essential for:
Nerve firing.
Muscle contraction.
Of the total 1200–1400 g of calcium in the body, 99% is found in bone minerals.
Blood Calcium Levels:
Hormones maintain blood calcium levels at 9–11 mg/dL.
Parathyroid Hormone (PTH):
Produced by parathyroid glands in response to low blood calcium levels.
Stimulates osteoclasts to resorb bone, releasing calcium into the blood and raising its levels (stops when homeostasis is restored).
Calcitonin:
Produced by parafollicular cells of the thyroid gland in response to high blood calcium levels.
Effects are negligible at normal levels but can lower blood calcium levels temporarily when present at abnormally high doses.
Clinical—Homeostatic Imbalance 6.1
Neuromuscular Problems:
Even slight fluctuations in blood calcium levels can lead to severe neuromuscular issues:
Hypocalcemia: Low calcium levels result in hyperexcitability of the nervous system.
Hypercalcemia: High calcium levels lead to nonresponsiveness.
Sustained elevated blood calcium can result in deposits of calcium salts in blood vessels or kidneys, leading to kidney stones.
Response to Mechanical Stress
Stress on Bones:
Bones adapt to the stresses they experience (e.g., weight bearing, muscle pulls).
Wolf’s Law:
States that bones will grow or remodel in response to demands placed upon them:
Stress is typically off-center, causing bones to bend, compressing one side and stretching the other.
Diaphysis is thickest where bending stresses are greatest.
Bone can be hollow as compression and tension forces offset each other in the center of the bone.
Applications of Wolf’s Law
Handedness:
Right- or left-handed individuals have thicker and stronger bones in the corresponding upper limb.
Curved Bones:
Curved bones are thickest at points likely to buckle.
Trabeculae Formation:
Trabeculae are formed along lines of stress, reinforcing bone structure.
Muscle Attachment:
Large bony projections occur where strong, active muscles attach (e.g., weightlifters exhibit notable thickenings at muscle attachment sites).
Activity Level:
Bones of fetuses and bedridden individuals often lack features due to insufficient stress.
Physiological Mechanisms
Mechanical Stress: Produces electrical signals when bone is deformed:
Regions under compression and tension develop opposite charges.
Changes in fluid flow within the canaliculi can stimulate remodeling processes.
Interaction of Hormones and Mechanical Stress:
Hormonal controls dictate whether and when remodeling occurs in response to changes in blood calcium levels, whereas mechanical signals determine the location of remodeling.
6.7 Bone Repair
Fractures: Defined as breaks in bone, with varying causes based on age:
Youth: Most fractures result from trauma.
Old Age: Most fractures result from bone weakness due to thinning.
Fracture Classification
Three Classifications Based on Criteria:
Position of Bone Ends:
Nondisplaced: Bone ends retain normal position.
Displaced: Bone ends are out of normal alignment.
Completeness of Break:
Complete: Bone is broken all the way through.
Incomplete: Bone is not completely broken.
Skin Penetration:
Open (compound): Skin is penetrated by the broken bone.
Closed (simple): Skin is not penetrated.
Additional Descriptions: Can describe fractures by location, external appearance, and nature.
Table 6.3 Common Types of Fractures
Comminuted Fracture:
Bone fragments into three or more pieces, common in older adults due to brittleness.
Compression Fracture:
Bone is crushed, often in porous bones like in osteoporotic individuals subjected to trauma (e.g., fall).
Spiral Fracture:
Ragged break due to excessive twisting forces, commonly seen in sports injuries.
Epiphyseal Fracture:
The epiphysis separates from the diaphysis at the epiphyseal plate during calcification of cartilage cells.
Depressed Fracture:
Broken bone portion is pushed inward, typical in skull fractures.
Greenstick Fracture:
Incomplete break on one side while the other side bends, typically occurring in children due to more pliable bone compositions.
Fracture Treatment and Repair
Realignment: Treatment involves the realignment of broken bones, a process known as reduction:
Closed Reduction: The physician manipulates the bone back into position without surgery.
Open Reduction: Surgical intervention using pins or wires to secure ends.
Immobilization: Necessary via casting or traction for healing.
Healing Time: Dependent on the severity of the break, type of bone affected, and age of the patient.
Major Stages of Bone Repair
Hematoma Formation: Torn blood vessels create a mass of clotted blood (hematoma), resulting in swelling, pain, and inflammation.
Fibrocartilaginous Callus Formation:
Capillaries grow into the hematoma.
Phagocytes clear debris.
Fibroblasts secrete collagen fibers to connect the broken ends, forming a mass of repair tissue called the fibrocartilaginous callus.
Bony Callus Formation:
Within a week, new trabeculae appear, converting the fibrocartilaginous callus into a hard bony callus over approximately two months.
Bone Remodeling:
Begins during bony callus formation and may continue for several months, involving the removal of excess materials and the renewal of the compact bone to restore the original bone structure, responsive to the same mechanical stressors.
Figure 6.15: Stages in the Healing of a Bone Fracture
Illustrative representation capturing the sequential stages of bone fracture healing and repair processes.