3. FRACTU
RE
• Fracture is a break in the structural
continuity of bone or periosteum.
• Fracture results in loss of its
mechanical stability and also partial
destruction of blood supply .
• Fracture healing starts as soon as bone
breaks and continues modelling for many
years.
7. HEALING
AFTER
FRACTURE
DIRECT / PRIMARY: MECHANISM OF BONE HEALING
SEEN WHEN THERE IS NO MOTION AT THE FRACTURE
SITE (I.E. RIGID INTERNAL FIXATION).
1. CONTACT HEALING-WHEN THERE IS DIRECT
CONTACT BETWEEN THE CORTICAL BONE ENDS,
LAMELLAR BONE FORMS DIRECTLY ACROSS THE
FRACTURE LINE, BY DIRECT EXTENSION OF OSTEONS.
2. GAP HEALING- OSTEOBLASTS DIFFERNTIATE AMD
START DEPOSITING OSTEOIDS ON THE EXPOSED
SURFACES OF FRAGMNET ENDS, MOSTLY WITHOUT
A PRECEEDING OSTEOCLASTIC RESORPTION WHICH
IS LATER CONVERTED INTO LAMELLAR BONE.
8. SECONDARY HEALING:
• Callus formation occurs either fibrous or cartilagenous
• This callus is later replaced by lamellar bone.
• Mechanism for healing in fractures that are not rigidly fixed.
• Bridging periosteal (soft) callus and medullary (hard) callus re-establish structural
continuity.
• It is comparable to healing of soft tissue by filling of gaps with vascular granulation
tissue
9. Mechanism Of Bone Formation
● ENDOCHONDRAL BONE FORMATION
● INTRA MEMBERANOUS OSSIFICATION
● APPOSITIONAL NEW BONE FORMATION
10. 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).
11. INTRAMEMBRANOUS BONE FORMATION
(PERIOSTEAL)
● Mechanism by which a long bone
grows in width.
● Osteoblasts differentiate directly from
pre osteoblasts and lay down seams
of osteoid.
● Does NOT involve cartilage anlage.
12. APPOSITIONAL BONE FORMATION
● While bones are increasing in length,
they are also increasing in diameter;
growth in diameter can continue
even after longitudinal growth
ceases.
● This growth by adding to the free
surface of bone is called appositional
growth.
● Appositional growth can occur at the
endosteum or periosteum where
osteoclasts resorb old bone while
osteoblasts produce new bone
tissue.
● This remodeling of bone primarily
takes place during a bone’s growth.
13. •NEW BLOOD VESSELS
CAN INVADE THE
TRABECULAE OF
CANCELLOUS BONE AND
BONE OPPOSITION MAY
TAKE PLACE DIRECTLY
ON TO THE SURFACE OF
TRABECULUM.
HEALING IN
CANCELLOUS
BONE
“CREEPING
SUBSTITUTION”
15. 1. TISSUE DESTRUCTION AND HEMATOMA
FORMATION
Torn blood vessels hemorrhage
A mass of clotted blood (hematoma) forms at the
fracture site
Site becomes swollen, painful, and inflamed
16. 2. LOCAL INFLAMMATORY RESPONSE:
• Within 8 hrs inflammatory reaction starts, marked by
the exudation of fibrin, polymorphs, and macrophages.
• Proliferation and Differentiation of mesenchymal stem
cells.
• Secretion of TGF-B , PDGF and various BMP factors.
17. 3. INGROWTH OF GRANULATION TISSUE:
● Begins by neovascularization and proliferation of
mesenchymal cells from periosteum and
endosteum.
● Soft tissue callus is formed which joins the
fractured ends.
18. 3. Procallus Formation: Callus is composed of woven bone
and cartilage.
• Cells of inner layer has osteogenic potential and lay down
collagen and osteoid matrix in granulation tissue.
This osteoid undergoes calcification and forms woven bone
callus which unite to bridge gap between ends of fracture site
giving spindle shaped or fusiform appearance to the union.
• procallus is divided into: 1- EXTERNAL
2- INTERMEDIATE
3- INTERNAL
20. 4. OSSEOUS CALLUS FORMATION
● Procallus acts as scaffolding on which osseous
callus composed of lamellar bone is formed.
● Lamellar bone is formed by developing haversian
system concentrically around the blood vessels.
21. 5. STAGE OF
REMODELLING :
DURING THIS
OSTEOBLASTIC LAYING
AND OSTEOCLASTIC
REMOVAL IS TAKING
PLACE TO FORM THE
BONE, EXTERNAL CALLUS
IS CLEARED AWAY,
CORTEX IS FORMED IN
PLACE OF INTERMEDIATE
23. INJURY VARIABLES
Open Fractures Impeding or preventing
formation of Hematoma
Delaying formation repair tissue
Risk of infection
24. Intra articular fractures- If the alignment & congruity joint surface is not
restored it may lead to delayed healing or non union, Joint stiffness
Segmental fractures
Soft tissue interposition
Damage to the blood supply
25. PATIENT
VARIABL
ES
• AGE
• NUTRITION- HEALING PROCESS NEEDS
ENERGY PROTEINS & CARBOHYDRATES
• SYSTEMIC HORMONES - GROWTH
HORMONE, THYROID HORMONE,
CALCITONIN, INSULIN, ANABOLIC
STEROIDS, DM, HYPERVITAMINOSIS D,
CORTICOSTEROID, RICKETS
26. TISSUE
VARIABLE
S
• CANCELLOUS OR CORTICAL BONES
• BONE NECROSIS
• INFECTION
• BONE DISEASE -OSTEOPOROSIS,
OSTEOMALACIA, PRIMARY
MALIGNANT BONE TUMORS,
METASTATIC BONE TUMORS ,
FIBROUS DYSPLASIA, BENIGN BONE
TUMORS, BONE CYSTS,
OSTEOGENESIS IMPERFECTA,
PAGET’S DISEASE ,
HYPERPARATHYROIDISM
27. TREATMEN
T
VARIABLES Fracture stabilization -Traction, Cast,
Immobilisation, Ext.Fixation,
Int.Fixation Facilitate fracture healing
by Preventing repeated disruption of
tissue repair
Apposition of fracture fragments
Loading & micromotion- Loading a
fracture site stimulates bone formation
and micromotion promotes fracture
healing
30. SYSTEMIC EARLY COMPLICATIONS
Fat embolism and deep vein thrombosis
● Shock
● ARDS
● Thromboembolism
● Septicaemia
● Crush syndrome
●
31. LATE COMPLICATIONS
● THOSE WHICH OCCUR AFTER SUBSTANTIAL TIME HAS
PASSED AND ARE RESULT OF DEFECTIVE HEALING
PROCESS OR DUE TO TREATMENT ITSELF
● SUBCLASSIFIED IN 2 GROUPS-
● 1. IMPERFECT UNION OF THE FRACTURE
● 2.OTHERS
32. OTHER LATE COMPLICATIONS
● AVASCULAR NECROSIS
● SHORTENING
● JOINT STIFFNESS
● SUDECK’S DYSTROPHY
● OSTEOMYELITIS
● OSTEOARTHRITIS
33. IMPERFECT UNION OF THE FRACTURE
● 4 GROUPS-
● 1.DELAYED UNION
● 2.NON UNION
● 3.MAL UNION
● 4.CROSS UNION
34. • MAL UNION- A MALUNITED
FRACTURE IS ONE THAT HAS HEALED WITH
THE FRAGMENTS IN A NON ANATOMICAL
POSITION.
• CAUSES
• 1 INACCURATE REDUCTION
• 2 INEFFECTIVE IMMOBILIZATION
•3 IMPAIR FUCNTION BY ABNORMAL JOINT
SURFACE ROTATION OR ANGULATION
OVERRIDING MOVEMENT OF NEIGHBOURING
JOINT MAY BE BLOCKED SHORTENING OF LIMB
35. • • OPERATIVE
TREATMENT FOR
MOST MALUNITED
FRACTURE
SHOULD NOT BE
CONSIDERED
UNTIL 6 TO 12
MONTHS BUT IN
INTRA ARTICULAR
FRACTURE EARLY
OPERATIVE
TREATMENT IS
NEEDED
• ILIZAROV
TECHNIQUE IS
BEST
SIMULTANEOUS
36. NON UNION
FDA defined nonunion as
“established when a minimum of 9
months has elapsed since fracture
with no visible progressive signs of
healing for 3 months”
• Every fracture has its own timetable
(ie long bone shaft fracture 6 months,
femoral neck fracture 3 months)
37. NONUNITED FRACTURES FORM TWO TYPES OF
PSEUDOARTHROSIS:
• HYPERVASCULAR OR HYPERTROPHIC
• AVASCULAR OR ATROPHIC
Hypervascular or Hypertrophic:
1. Elephant foot (hypertophic,
rich in callus) 2. Horse foot
(mildly hypertophic, poor in
callus) Oligotrophic (not
hypertrophic, no callus)
Hypervascular nonunions.
. Avascular or Atrophic
• Torsion wedge (intermediate
fragment)
• Comminuted (necrotic
intermediate fragment)
• Defect (loss of fragment of
the diathesis) • Atrophic (scar
tissue with no estrogenic
potential is replacing the
missing fragment)
38. AVASCULAR NECROSIS
● BLOOD SUPPLY OF SOME BONES IS SUCH THAT THE VASCULARITY OF A
PART OF IT IS SERIOUSLY JEOPARDIZED FOLLOWING
FRACTURE,RESULTING IN NECROSIS OF THE PART
● IT CAUSES DEFORMATION OF BONE AND AFTER SOME TIME SECONDARY
OSTEOARTHRITIS DEVELOPS AND LIMITATION OF JOINT MOVEMENT
● COMMONEST BONES INVOLVED: SCAPHOID
● FEMORAL HEAD
39. OSTEOARTHRITIS
● FRACTURE JOINT MAY DAMAGE ARTICULAR CARTILAGE AND
GIVE RISE TO POST TRAUMATIC OSTEOARTHRITIS WITHIN
MONTHS
● LATER ALSO CAUSE JOINT STIFFNESS
44. ACUTE COMPARTMENT SYNDROME
● SIGNS N SYMPTOMS- COMPLICATIONS-
● PAIN -PERMANENT LOSS OF
FUNCTION
● PARESTHESIA -LIMB CONTRACTURE
NECROSIS
● PALLOR
● POIKILOTHERMIA
45.
46. Fracture healing involves a dynamic interplay of biological processes to
restore the original anatomic structure and mechanical function of bone.
Therefore, both structural and biomechanical evaluations are used to assess
fracture repair. The extent and quality of structural repair can be evaluated
using radiographic and histologic methods.
CONCLUSIO
N
