Fracture healing is a complex process involving inflammation, cellular proliferation, callus formation, consolidation, and remodeling. It begins immediately after injury with hematoma formation and an inflammatory response. Mesenchymal stem cells proliferate and differentiate to form fibrocartilaginous callus. New bone formation then occurs as the callus converts to bony callus over 3-4 weeks. During remodeling, excess callus is resorbed and the bone is reconstructed. Multiple factors influence healing, including fracture type, stability, soft tissue injury, patient age and nutrition, and local growth factors and cytokines.

1. PATHOPHYSIOLOGY OF FRACTURE HEALING AND REPAIR

2. INTRODUCTION
• Fracture is a break in the structural continuity of bone or
periosteum.
• The healing of fracture is in many ways similiar to the healing in
soft tissue wounds except that the end result is mineralised
mesenchymal tissue i.e. BONE.
• Fracture healing starts as soon as bone breaks and continues
modelling for many years.

3. • The essential event in fracture healing is the creation of a
bony bridge between the two fragments which can be
readily built upon and modified to suit the particular
functional demands .

4. COMPONENTS OF BONE FORMATION
• Cortex
• Periosteum
• Bone marrow
• Soft tissue

5. TYPE OF BONE FORMED
• OSTEOCHONDRAL
• INTRAMEMBERANOUS OSSIFICATION
• OPPOSITIONAL NEW BONE FORMATION
• OSTEONAL MIGRATION (Creeping Substitution)

6. FACTORS EFFECTING
• The TYPE , AMOUNT and LOCATION of bone formed depends upon--
---
• FRACTURE TYPE
• GAP CONDITION
• FIXATION RIGIDITY
• LOADING
• BIOLOGICAL ENVIRONMENT

7. FRACTURE HEALING TYPES
• Fracture healing is divided according to bone--
1. Cortical bone of the shaft.
2. Cancellous bone of the metaphyseal region of the long bones and
the small bones.

8. STAGES OF FRACTURE HEALING
• TISSUE DESTRUCTION AND HAEMATOMA FORMATION
• INFLAMATION AND CELLULAR PROLIFERATION
• STAGE OF CALLUS FORMATION
• STAGE OF COSOLIDATION
• STAGE OF REMODELLING

9. TISSUE DESTRUCTION AND HEMATOMA FORMATION

10. INFLAMATION AND CELLULAR PROLIFERATION
• Within 8 hours inflammatory
reaction starts.
• Proliferation and Differentiation
of mesenchymal stem cells.
• Secretion of TGF-B
, PDGF and various BMP factors.

11. CALLUS FORMATION
• Fibrocartilaginouscallus forms
• Granulationtissue(soft callus)
forms a few days after the
fracture
• Capillaries grow into the tissue
and phagocytic cells begin
cleaning debris

12. CALLUS FORMATION THEORY
• OSTEOPROGENITOR CELL
present in all ENDOSTEAL and
SUBPERIOSTEAL surface give
rise to CALLUS.
• CALLUS arises from NON-
SPECIALISED CONNECTIVE
TISSUE CELLS in the region of
fracture which are induced into
conversion to OSTEOBLASTS.

13. STAGE OF CONSOLIDATION
• New bone trabeculae appear in
the fibrocartilaginous callus
• – Fibrocartilaginous callus
converts into a bony (hard) callus
• – Bone callus begins 3-4 weeks
after injury, and continues until
firm union is formed 2-3 months
later

14. STAGE OF REMODELLING
• Excess material on the bone
shaft exterior and in the
medullary canal is removed
• Compact bone is laid down
to reconstruct shaft walls

18. VARIABLES INFLUENCE FRACTURE HEALING
INJURY VARIABLES
• Open Fractures
Impeding or preventing formation # Hematoma
Delaying formation repair tissue
Risk of infection

19. INJURY VARIABLES
• Intra articular fractures
• If the alignment & congruity joint surface is not restored
Delayed healing or non union
Joint stiffness
• Segmental fractures
• Soft tissue interposition
• Damage to the blood supply

20. PATIENT VARIABLES
• AGE
• NUTRTION
• HEALING PROCESS NEEDS
Energy
Proteins & carbohydrates

21. • Systemic hormones
• Corticosteroid ( )
• Growth hormone
• Thyroid hormone
• Calcitonin Rate fracture healing
• Insulin
Anabolic steroids
• DM
• Hypervitaminosis D Rate fracture healing
• Rickets
Nicotine
Inhibit fracture healing ( Vascularization?)

22. TISSUE VARIABLES
Cancellous or cortical bones
Bone necrosis
Infection

23. LOCAL REGULATION OF BONE HEALING
• Growth factors
Transforming growth factor
Bone morphogenetic proteins
Fibroblast growth factors
Platelet-derived growth factors
Insulin-like growth factors
• Cytokines
Interleukin-1,-4,-6,-11,
macrophage and granulocyte/macrophage (GM)
colony-stimulating factors (CSFs) and
Tumor Necrosis Factor
• Prostaglandins/Leukotrienes
• Hormones
• Growth factor antagonists

26. REFRENCES
• Reading : Robbins Basic Pathology, 10th Edition (2017), By: Kumar,
Abbas, Aster
• WWW.Webpathology.com
• WWW.fleshandbone.com
• WWW.studentconsult.com