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Dr. Shrikant Gore 
Prof. of Orthopaedics 
Govt. Medical College, 
Latur
Fracture Healing 
Bone is vital & pulsating tissue 
Every hour & every day bone grows 
& remodels & lives again
Stages of # Healing 
Broken Bone - Broken vessels – Hematoma 
Release of proliferating factors 
Proliferation of endothelial cells, bone cells, 
mesenchymal cells 
Differentiation of proliferating cells 
according to the need & environment 
provided
Stages of # Healing 
Blockage of capillaries to various extent-bone 
necrosis (marrow-cortex- 
Periosteum) 
Proliferation factor released by plasma 
cells as a response to trauma to vascular 
channels 
Cells with osteogenic potential derived 
from endothelial cells, deeper layer of 
periosteal cells , bone cells proliferate
External Callus 
Most active proliferating cells from deeper 
layer of Periosteum forms collar around the 
# bone ends thickening & growing towards 
each-other to bridge the # gap by merging 
with each-other forming the OUTER 
CALLUS 
The deeper layer gets vascularized – 
osteoblastic activity –laying new Trabicular 
bone
External Callus 
The intermediate layer actively 
proliferating- compact , less vascular-differentiate 
in cartilage – Gradually being 
replaced by bone through endochondral 
ossification- calcification-cell death- 
Vascularization- osteoblats - trabicular new 
bone 
The outer layer of actively proliferating cells
Internal Callus 
Within 2 days of injury marked vascular 
proliferation in the marrow cavity – neo 
Vascularization – infiltration of mesenchymal cells 
– differentiating in pre- osteoblats -Osteoblasts – 
laying new bone trabeculae- bridging the # 
fragments – INTERNAL CALLUS 
Vascular sprouts start invading the dead bone at # ends 
with osteoclastic activity & removal of dead bone – 
replaced by Osteoblastic activity & replacement by bone
Callus
Maturation of callus & Remodeling 
Initial callus is loosely woven bone like 
cancellous bone 
Trabicular pattern as per the requirement – 
mechanical stresses 
Marrow callus- hemopiotic marrow 
cortex- compact bone with thickening along 
the lines of stress resorption of extra callus
Remodelling
Remodelling
Maturation of callus
Summary 
Biochemical factors -Cellular response – vascular 
response 
Osteoblastic & osteoclastic activity 
laying down immature bone –Osteoid 
mineralization to form- The CALLUS 
Having irregular trabicular pattern unlike 
cancellous bone 
Remodeling to suit the functional 
requirements
Stages of Bone Healing
Requirements 
Reasonable opposition (Anatomical Reduction) 
Sufficient protection (rigid immobilization) 
Good blood supply (Quantity, Cellular) 
Healthy bone (cortical/ Cancellous / pathological) 
Environment (Foreign / Dead material /intra-articular#) 
Nutrition (Deficiencies, Metabolic ) 
Immunological status (HIV, Corticosteroids)
General factors 
Age- 
Young – 
Bones are soft vascular and have very good capacity to form 
new bone and remold 
Growing ends –likely to get damaged resulting in growth 
disturbance 
Adult- 
Strong muscle force difficulty in getting &maintaining 
reduction 
Old – 
Poor bone quality &blood supply- associated diseases-osteoporosis
General factors 
Sex- 
Postmenopausal osteoporosis 
Nutrition- 
Hemoglobin 
Calcium, Vit. D, Vit. C, & other vitamins - minerals 
Immunity – 
Immuno – suppressive drugs, Chronic debilitating diseases – DM, 
HT, TB, Malignancy, Chr. Lung diseases, Vascular diseases 
Habits- 
Tobacco, alcohol 
Neurological diseases
Local Factors at fracture site 
Reduction – Gap 
Soft tissue interposition , excessive traction, bone loss, 
severe communition, loss of soft tissue attachment, 
improper fixation maintaining gap, 
Movement – Poor immobilization 
shearing, torsional, bending, stresses 
repeated trauma –hyperemia – resorption of bone ends 
fibrous & cartilaginous differentiation of osteogenic 
cell
Vascularity 
Anatomical susceptibility 
Soft tissue damage 
Crushed bone 
Excessive intra- medullary reaming 
Edema & inflammation 
Vascular injuries 
Vascular diseases- DM, Atherosclerosis, TAO, 
Varicose veins, Smoking
Anatomical susceptibility
Poor blood supply at one end
Environment 
Intra-articular # 
Presence of synovial fluid having anti-thrombotic 
activity 
Tamponade 
Infection 
Hyperemia at # site 
Bacterial toxins 
Bone destruction, 
Vascular damage, 
Damage to immature bone
Bone Quality 
Type of bones – Cancellous bone, 
Cortical bone, Flat bones, 
Intra-articular fractures 
Pathology – 
Developmental, 
Metabolic, Radiational, 
Neoplastic, infection 
Osteoporosis
Hypertrophic Nonunion
Delayed union
Surgical Interference 
Periosteal damage, 
Damage to blood supply , 
soft tissue damage 
Metal reaction, 
skeletal traction 
Infection
Local Factors

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3 fracture healing

  • 1. Dr. Shrikant Gore Prof. of Orthopaedics Govt. Medical College, Latur
  • 2. Fracture Healing Bone is vital & pulsating tissue Every hour & every day bone grows & remodels & lives again
  • 3. Stages of # Healing Broken Bone - Broken vessels – Hematoma Release of proliferating factors Proliferation of endothelial cells, bone cells, mesenchymal cells Differentiation of proliferating cells according to the need & environment provided
  • 4. Stages of # Healing Blockage of capillaries to various extent-bone necrosis (marrow-cortex- Periosteum) Proliferation factor released by plasma cells as a response to trauma to vascular channels Cells with osteogenic potential derived from endothelial cells, deeper layer of periosteal cells , bone cells proliferate
  • 5.
  • 6. External Callus Most active proliferating cells from deeper layer of Periosteum forms collar around the # bone ends thickening & growing towards each-other to bridge the # gap by merging with each-other forming the OUTER CALLUS The deeper layer gets vascularized – osteoblastic activity –laying new Trabicular bone
  • 7. External Callus The intermediate layer actively proliferating- compact , less vascular-differentiate in cartilage – Gradually being replaced by bone through endochondral ossification- calcification-cell death- Vascularization- osteoblats - trabicular new bone The outer layer of actively proliferating cells
  • 8. Internal Callus Within 2 days of injury marked vascular proliferation in the marrow cavity – neo Vascularization – infiltration of mesenchymal cells – differentiating in pre- osteoblats -Osteoblasts – laying new bone trabeculae- bridging the # fragments – INTERNAL CALLUS Vascular sprouts start invading the dead bone at # ends with osteoclastic activity & removal of dead bone – replaced by Osteoblastic activity & replacement by bone
  • 10. Maturation of callus & Remodeling Initial callus is loosely woven bone like cancellous bone Trabicular pattern as per the requirement – mechanical stresses Marrow callus- hemopiotic marrow cortex- compact bone with thickening along the lines of stress resorption of extra callus
  • 13.
  • 15. Summary Biochemical factors -Cellular response – vascular response Osteoblastic & osteoclastic activity laying down immature bone –Osteoid mineralization to form- The CALLUS Having irregular trabicular pattern unlike cancellous bone Remodeling to suit the functional requirements
  • 16. Stages of Bone Healing
  • 17. Requirements Reasonable opposition (Anatomical Reduction) Sufficient protection (rigid immobilization) Good blood supply (Quantity, Cellular) Healthy bone (cortical/ Cancellous / pathological) Environment (Foreign / Dead material /intra-articular#) Nutrition (Deficiencies, Metabolic ) Immunological status (HIV, Corticosteroids)
  • 18. General factors Age- Young – Bones are soft vascular and have very good capacity to form new bone and remold Growing ends –likely to get damaged resulting in growth disturbance Adult- Strong muscle force difficulty in getting &maintaining reduction Old – Poor bone quality &blood supply- associated diseases-osteoporosis
  • 19. General factors Sex- Postmenopausal osteoporosis Nutrition- Hemoglobin Calcium, Vit. D, Vit. C, & other vitamins - minerals Immunity – Immuno – suppressive drugs, Chronic debilitating diseases – DM, HT, TB, Malignancy, Chr. Lung diseases, Vascular diseases Habits- Tobacco, alcohol Neurological diseases
  • 20. Local Factors at fracture site Reduction – Gap Soft tissue interposition , excessive traction, bone loss, severe communition, loss of soft tissue attachment, improper fixation maintaining gap, Movement – Poor immobilization shearing, torsional, bending, stresses repeated trauma –hyperemia – resorption of bone ends fibrous & cartilaginous differentiation of osteogenic cell
  • 21. Vascularity Anatomical susceptibility Soft tissue damage Crushed bone Excessive intra- medullary reaming Edema & inflammation Vascular injuries Vascular diseases- DM, Atherosclerosis, TAO, Varicose veins, Smoking
  • 23. Poor blood supply at one end
  • 24. Environment Intra-articular # Presence of synovial fluid having anti-thrombotic activity Tamponade Infection Hyperemia at # site Bacterial toxins Bone destruction, Vascular damage, Damage to immature bone
  • 25. Bone Quality Type of bones – Cancellous bone, Cortical bone, Flat bones, Intra-articular fractures Pathology – Developmental, Metabolic, Radiational, Neoplastic, infection Osteoporosis
  • 28. Surgical Interference Periosteal damage, Damage to blood supply , soft tissue damage Metal reaction, skeletal traction Infection