Bone fracture healing is a complex process that proceeds through several stages: inflammation and hematoma formation, cellular proliferation and soft callus formation, hard callus formation and consolidation. It is influenced by local, chemical, vascular, systemic and treatment factors. Recent advances to enhance healing include bone grafts, bone marrow aspirate, growth factors, platelet rich plasma, laser therapy, and tissue engineering techniques.

1. Bone Healing
Guided by
Dr. Sandeep Kalia
Presented by
Dr. Rahul Bhardwaj
Dated 24.07.2017

2. Fracture
Fracture is defined as
● Break in continuity of bone either partial / complete.
● Result in loss of its mechanical stability
● partial destruction of blood supply
but following fracture a bone is fomed instead of
scar
bone healing is appropriately called as
BONE REGENRATION

3. Healing Of Fracture
● Fisrt described by Ham and Harris in 1956 on rabbit
model
● Healing starts as soon as fracture occurs
● Healing proceeds through several stages until the
bone is consolidated
● The pattern of healing is different for different bones
in different circumstances

4. FRACTURE HEALING
● Complex process require recruitment of cells
● Subsequent expression of genes at time and location
● A fracture initiates a sequence of inflammation,
repair, remodelling that can restore the injured bone
to original or near original state

5. Repair of Tubular Bones
Stages
● Stage of haematoma
● Stage of subperiosteal and endosteal cellular
proliferation.
● Stage of callus formation
● Stage of consolidation
● Remodelling
However stages are not sharply demarcated

7. Haematoma
Haematoma acumulates within the medullary
canal, b/w the fracture ends and beneath elevated
periosteum
Damaged blood supply will lead to death of
osteocytes upto the collaterals leaving the area
without cells
Damaged periosteum and marrow also contribute
to necrotic material.

9. Inflamation and cellular proliferation
●Inflammatory mediators are released from
platelets and dead and injured cells
●Exudation of plasma will cause local swelling
●Inflammatory cell migrate including PMN followed
by macrophages and lymphocytes and
mesenchymal stem cells
●These cells release cytokines(BMP,TGF Beta
etc.) and stimulate angiogenesis.

10. Cont..
● Delivery of progenitor cells from periosteal layers.
● Osteoclast start removing necrotic bone
● Soon the necrotic tissue and exudate is reabsorbed
● Fibrin fibres stabilise the haematoma.

12. Callus
●Derived from latin name callum meaning thick
skin
●Fibroblast and chondrocytes appear and start
producing a new matrix.
●Can be divided in two
Soft callus
Hard callus

13. Soft callus
● New blood vessels invade haematoma
● Fibroblast from periosteum colonise haematoma and
produce collagen fibres
● Collagen fibres loosly link bone fragments
● Granulation tissue gradually differentiates into
fibrous tissue and subsequently fibrocartilage.
● Progenitor cells differentiate according to
strain,Oxygen tension and local conditions

14. Hard callus
● Once # ends linked by soft callus,hard callus stage
starts
● Osteoblast lay down woven bone from
periphery( intramembranous ossification)
● Fibrocartilagenous callus bridges fracture site
chondroid matrix calcifies. New woven bone is laid
down (endochondral ossification)
● Cascade of cellular differentiation converts
haematoma to progressivly stiffer tissue

17. Healing in cancellous bone
● Different pattern
● Bone is uniformly spongy texture so easy
penetration of bone forming tissue
● Union can occur directly without the medium of
external callous
● Fracture will lead to haematoma formation
● The blood vessels and proliferating osteogenic cells
from # ends penetrate until they meet similar tissue
from opposite ends
● Osteoblast lay down matrix which calcify to form
woven bone.

18. Fracture union
● Union is complete repair and ensheathing callus is
calcified
● Clinically the fracture site is little tender but bone
moves in one piece, attempted angulation is painful
● X ray shows the fracture line clearly visible, with
fluffy callus around it
● Repair is incomplete so not safe to put to use

20. union
● Clincal union
progressive increase stiffness, strength given by
minrelaisation process makes fracture site stable,
pain free
● Radiological Union
Xray show bone trabeculae or cortical bone crossing
fracture site

22. WOLFFs LAW
● For a uniform or constant fact or principle, more
specifically, that a bone, either normal or abnormal,
will devlop the structure most suited to resist the
forces acting on it.
● Stress adaptive remodelling
● Bone grows or remodel in response to force or
demand applied to it.

24. HEUTERS VOLKMANN LAW
● Remodelling also occurs under the influence of
1. Distractive Strain (Traction)
2. Compressive strain ( compression)

25. Distraction

28. Remodelling
● Its a continous process
● Its more evident after fracture and continues even
after function restoration and radiological union
● Continues for years

29. Influencing factors
● Local factors
● Chemical factors
● Vascular factors
● Systemic factors
● Electromagnetic factors
● Treatment factors

30. Local factors
● Type of bone
● Degree of trauma
● Vascular injury
● Degree of immobilisation
● Types of fracture
● Others (bone death is caused by)
radiation
thermal, chemical burns
infections.

31. Chemical factors
● Messangers
serotonin
Prostaglandin
histamine
thromboxane
● Permeabilty factors
protease
polypeptides
Amines
● Growth factors
TGF
FGF
insulin like GF
Bone morphogenic proteins

32. Vascular factors
● Metalloproteinase
degrade catilage, bone to allow vessel invasion
● Angiogenic factors
promotes neo-angiogenesis, endothelial cell specific
mitogens
● angiopoitein(l&ll)
regulate formation of large vessel and branches

33. Systemic factors
● Age
young pt. Heal rapidly and remodel remarkably than
old
● Nutrition
sufficient protein, carbohydrates , vit, minerals
● Systemic Diseases
immunocompromised states delay healing
Marfans/ Ehlers Danlos cause abn. healing

34. Hormones
● ESTROGEN stimulate fracture healing through
receptor mechanism
● THYROID hormone & GLUCOCORTICOIDS
stimulate osteoclastic bone resorption
● PARATHYROID HORMONE accelerates callus
formation, remodelling, biomechanical properties of
healing # .
● GROWTH HORMONE increase callus formation
and fracture strength.

35. Electromagnetic factors
● Based on wolffs law,
exogenous electromagnetic field may stimulate
mechanical loading and stimulate bone growth and
repair.
● Types are
ultrasound
direct electric current
pulsed electromagnetic fields (PEMF)

36. Recent updates
● Bone Grafts
Autogenous :- iliac crest, fibula
allogenic :- from cadaver
Synthetic :- collagen, demineralised bone matrix,
collagen, ceramics, polymer- Si, PMMA
Emerging products:-
Tricalcium phosphate composite
hydroxyapatite compound – marine coral

37. Bone marrow aspirate
● Contain mesenchymal stem cells, proginators
● mesenchymal stem cell- differentiate into
osteoblasts, chondrocytes
● proginators- contribute to adult vasculogenesis

38. Serological bone markers
● To monitor callus devlopment and fracture healing
● Ex:-
bone specific ALP
Osteocalcin
Procollagen type-1N terminal propeptidase PINP
Procollagen type-1C terminal propeptidase PICP
PINP is superior marker to monitor callus formation
and fracture healing.

39. Laser photo biomodulation
● Effective
● Causes increase neo bone formation
● Effect depends on total dose, irradiation time and
mode
● Energy density and intensity accounts for success
and failure of treatmet

40. Other techniques
● Growth factor therapy
have shown promising results
● Aplication of platelet rich plasma
improve cellular proliferation,chondrogenesis(early)
increase mechanical strength of callus (later on)
● Tissue engineering, Stem Cells, Gene Therapies
these techniques have been implicated in # healing
and articular cartilage regenration.

41. THANK YOU