Basic Orthopedic Trauma for M.B.B.S. Students

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

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

9. Callus

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

11. Remodelling

12. Remodelling

14. Maturation of callus

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

22. Anatomical susceptibility

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

26. Hypertrophic Nonunion

27. Delayed union

28. Surgical Interference
Periosteal damage,
Damage to blood supply ,
soft tissue damage
Metal reaction,
skeletal traction
Infection

29. Local Factors