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BONE HEALING

Types of Bone
Microscopically
• Lamellar Bone (cortical and spongy)
• Collagen fibers arranged in parallel layers
• Normal adult bone
• Woven Bone (non-lamellar)
• Randomly oriented collagen fibers
• In adults, seen at sites of fracture healing, tendon or ligament
attachment and in pathological conditions

Lamellar Bone
 1) Cortical bone
 Composed of osteons

(Haversian systems)

 Osteons communicate with

medullary cavity by
Volkmann’s canals

Haversian System
• Osteon with

osteocyte

central
haversian canal
containing

osteon

– Cells
– Vessels
– Nerves

• Volkmann’s

canal

– Connects

osteons

Haversian
canal

Volkmann’s
canal

Lamellar Bone • 2) Cancellous bone (trabecular or spongy bone) • Bony trabeculae that are oriented in direction of the greatest stress .

Woven Bone • Coarse with random orientation • Weaker than lamellar bone • Normally remodeled to lamellar bone .

osteonectin. glycosaminoglycans.Bone Composition • Cells – Osteocytes – Osteoblasts – Osteoclasts • Extracellular Matrix – Organic (35%) • Collagen (type I) 90% • Osteocalcin. lipids (ground substance) – Inorganic (65%) . proteoglycans.

Osteoblasts • Derived from mesenchymal stem cells • Line the surface of the bone and produce osteoid • Immediate precursor is fibroblast-like preosteoblasts .

Osteocytes • Osteoblasts surrounded by bone matrix • trapped in lacunae • Function poorly understood • regulating bone metabolism in response to stress and strain .

Osteoclasts • Derived from hematopoietic stem cells (monocyte precursor cells) • Multinucleated cells whose function is bone resorption • Reside in bone resorption pits (Howship’s lacunae) .

Components of Bone Formation • Soft tissue • Periosteum • Cortex • Bone marrow .

For Bone Healing we need • Adequate blood supply • Adequate mechanical stability .

Blood Supply • Long bones have three blood supplies • Nutrient artery (intramedullary) • Periosteal vessels • Metaphyseal vessels .

Nutrient Artery • Normally the major blood supply for the diaphyseal cortex (80 to 85%) • Enters the long bone via a nutrient foramen • Forms medullary arteries up and down the bone .

Periosteal Vessels • Arise from the capillary-rich periosteum • Supply outer 15 to 20% of cortex normally • Capable of supplying a much greater proportion of the cortex in the event of injury to the medullary blood supply .

Metaphyseal Vessels • Arise from periarticular vessels • Penetrate the thin cortex in the metaphyseal region and anastomose with the medullary blood supply .

Vascular Response in Fracture Repair • Fracture stimulates the release of growth factors that promote angiogenesis and vasodilation • Blood flow is increased substantially to the fracture site – Peaks at two weeks after fracture .

loading and interfragmentary motion promotes greater callus formation .Mechanical Stability • Early stability promotes revascularization • After first month.

Mechanisms of Bone Formation • Cutting Cones • Intramembranous Bone Formation • Endochondral Bone Formation .

Cutting Cones • Primarily a mechanism to remodel bone • Osteoclasts at the front of the cutting cone remove bone • Trailing osteoblasts lay down new bone .

.Intramembranous (Periosteal) Bone Formation • Mechanism by which a long bone grows in width • Osteoblasts differentiate directly from preosteoblasts and lay down seams of osteoid .

Endochondral Bone Formation • Mechanism by which a long bone grows in length • Osteoblasts line a cartilage precursor • The chondrocytes hypertrophy. degenerate and calcify (area of low oxygen tension) • Vascular invasion of the cartilage occurs followed by ossification (increasing oxygen tension) .

Bone healing • Heals by original tissue leaving no scar .

Contact Healing  Gap Healing -Gaps less than 200-500 microns are primarily filled with woven bone that is subsequently remodeled into lamellar bone  Contact Healing: -Direct contact between the fracture ends allows healing to be with lamellar bone immediately .

Cartilage Callus formation • iv.Stages of healing • 1. Hematoma and Granulation tissue formation • 2. Remodeling Phase • v. Woven then lamellar bone deposition • 3. Reactive Phase • i. Fracture and inflammatory phase • ii. Reparative Phase • iii. Remodeling to original bone contour .

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the first change is the presence of blood cells within the tissues adjacent to the injury site. . • Blood vessels constrict.Reactive Phase • After fracture. • Fibroblasts survive and replicate forming granulation tissue . • Within a few hours a hematoma is formed.

the cells of the periosteum replicate and transform.Reparative • Days after fracture. • The periosteal cells proximal to the fracture gap develop into chondroblasts which form hyaline cartilage. • The periosteal cells distal to the fracture gap develop into osteoblasts which form woven bone. .

.Remodeling Phase • The remodeling process substitutes the trabecular bone with compact bone. creating a shallow resorption pit known as a "Howship's lacuna". • Then osteoblasts deposit compact bone within the resorption pit. • The trabecular bone is first resorbed by osteoclasts.

the fracture callus is remodeled into a new shape which closely duplicates the bone's original shape and strength.• Eventually. The remodeling phase takes 3 to 5 years depending on factors such as age or general condition. .

Regulation of Bone Healing • Growth factors • Cytokines • Prostaglandins/Leukotrienes • Hormones • Growth factor antagonists .

Hormones • Estrogen • Stimulates fracture healing through receptor mediated mechanism • Decrease the release of a specific inhibitor of IL-1 which stimulates bone resorption • Thyroid hormones • Thyroxine and triiodothyronine stimulate osteoclastic bone resorption • Glucocorticoids • Inhibit calcium absorption from the gut causing increased PTH and therefore increased osteoclastic bone resorption .

Hormones • Parathyroid Hormone • Intermittent exposure stimulates • Osteoblasts • Increased bone formation • Growth Hormone • Increases callus formation and fracture strength .

thermal or chemical burns or infection .Local Anatomic Factors That Influence Fracture Healing  Soft tissue injury  Interruption of local blood supply  Interposition of soft tissue at fracture site  Bone death caused by radiation.

defective cross-linking and alterations in collagen sub-type ratios .Systemic Factors That Decrease Fracture Healing • Malnutrition – Causes reduced activity and proliferation of osteochondral cells • Smoking – Cigarette smoke inhibits osteoblasts – Nicotine causes vasoconstriction diminishing blood flow at fracture site • Diabetes Mellitus – Associated with collagen defects including decreased collagen content.

. 3.osteoarthorosis.growth disturbance. 6. 5.malunion.non-union.Problems In Healing 1. 7.joint instability. 2.avascular necrosis.dealyed union. 4.

CAUSES: .Delayed Union when the time healing is prolonged. • sever soft tissue damage • periosteal stripping (avoidable) • imperfect splintage • infection .biological or biochemical: • poor blood supply .

-acute pain if subjected to stress.Delayed union Clinical features: -fracture tenderness persists . On x-ray: -Fracture line remains visible -bone ends are not sclerosed or atrophied .

-causes: * separation of fragments * soft tissue b/t bony fragments * excessive movement at fracture site * poor local blood supply * sever soft tissue damage * infection * abnormal bone .Non -Union Nonunion is permanent failure of healing following a broken bone.

MALUNION -unsatisfactory position (angulation. shortening). . rotation.

head of femur 2.body of talus -it is an early complication Because of ischemia but radiological findings seen later . -certain regions more than others include: 1.AVASCULAR NECROSIS -bone death .proximal part of scaphoid 3.

-no symptoms -pain if fracture fail to unite or bony collapse -on x-ray:  increase bone density .AVASCULAR NECROSIS -Clinical features.

Thank You .