by Dr Praveen Kumar Reddy G; DNB TRAINEE;LISIE HOSPITAL;KOCHI

1. BONE AND FRACTURE HEALING
By Dr Praveen

2. • Bone and cartilage healing are central to the
practice of orthopedic surgery.
• Orthopaedic treatments should attempt to
optimize the cells, scaffold, molecules, and
blood supply required for healing.

3. • Bone heals with new tissue that is
indistinguishable from its preinjured state.
• Fractures heal through the parallel processes
of endochondral and intramembranous
ossification, with most fractures exhibiting
both types of healing.

4. • The fracture repair process is intimately
influenced by the mechanical and biologic
environments at the fracture site.

5. Cells
• Inflammatory cells--Debride necrotic tissues
• Progenitor cells --Signal for upregulation of
synthetic functions
• Chondrocytes --Form repair tissues
• Osteoblast and Osteoclast--Remodel healed
bone for optimal strength/weight ratio

6. scaffold
• Hematoma--Support cellular function
• Collagen--Inflammatory cell chemotaxis
• Noncollagenous proteins--Scaffold for
mineralization

7. Blood Supply
• Blood vessels--Supply inflammatory cells to
injury site and Reverse hypoxic environment
• Supporting cells (pericytes)--Deliver building
blocks of repair tissues

8. Molecules
• Matrix-embedded proteins,Locally produced
factors,Systemic hormones
• Regulate cellular function and proliferation
during fracture healing process

9. Types of Bone Healing
•Endochondral
•Intramembranous

10. Endochondral
• This healing response was associated with
motion at the fracture site
• Obtained when # are treated conservatively
(splints/casts) or by external fixation, IM
nailing or bridge plating.
• Cartilaginous anlage is replaced by bone

12. • In unstable fractures, cartilage is found
during the early phase of fracture healing
and, as stated previously, chondrocytes
hypertrophy and are replaced by osteoblasts
as vessels invade the cartilage callus.

13. • In the past, the predominance of
endochondral ossification was referred to as
secondary bone healing, which proceeded
through three sequential phases: soft callus,
hard callus, and remodeling.
• No porosis of bone occurs

14. 5 mo
Postop
Relative stability

15. Stages of Enchondral Fracture Repair
– early hematoma stage
– inflammation
– soft callus
– hard callus
– remodeling

16. • They can overlap one another in time during
the healing process.
Hematoma Formation
– debris from bone
– platelets,
– erythrocytes,
– immune cells

18. • The oxygen tension is decreased significantly
over the first 72 hours after fracture.
• The fracture hematoma is bioactive.
• Increased concentration of
• TNF α
• IL-6
• IL-8

19. Inflammation
• The presence of cellular debris initiates an
inflammatory response mediated by both local and
infiltrating inflammatory cells, including
– platelets,
– polymorphonuclear cells (PMN),
– macrophages, and
– Lymphocytes
• Phagocytose necrotic tissue and produce cytokines

20. • surgical interventions typically occur during
this early phase of fracture healing, and
therefore they can disrupt the hematoma or
inflammatory stages of fracture healing.

21. • Animal models have demonstrated that the
removal of hematoma early during fracture
repair (2 to 4 days) and repeated debridement
of the fracture site (for the first 2 days) after
fracture can result in both delayed union and
nonunion

22. Soft Callus
• Differentiation of progenitor cells into
chondrocytes and osteoblasts.
• Begins by 3 weeks in humans.
• Types I and II collagen are produced in order to
form a matrix that restores stability to the bone
ends.

23. • Radiographically, the fracture site does not
appear united at this stage, but a fluffy
appearance of the early mineralizing callus
may start to be detected

24. Hard Callus
• conversion of cartilage to a calcified cartilage
matrix with terminal differentiation of the
chondrocytes.
• Occurs several weeks after a fracture in
humans
• Concurrently, with the wave of calcification,
hypertrophic chondrocytes senesce and
blood vessels invade the callus.

25. • Dominant cell types during the hard callus
phase are the osteoblast and osteoclast.
• Seen as the calcification and consolidation
of the fracture callus on radiographs.
• .

26. • During cast or traction treatment of fractures,
the hard callus phase is also accompanied by a
clinically evident reduction in pain and
increased sense of stability at the fracture site

27. Remodeling
• Returns the previously damaged tissue
nearer to its pre-injured state.
• continues for months or years

28. • To accomplish the stress-induced remodeling
of bone, the actions of osteoclasts and
osteoblasts are coupled in the functional unit
of bone remodeling—the cutting cone.
• osteoclasts first remove the disorganized
woven bone.
• Then osteoblasts follow and lay down
lamellar bone in an organized pattern around
a central blood vessel.

30. • The activity of bone resorption by
osteoclasts and bone formation by
osteoblasts is linked through the actions of
RANK, RANKL, and osteoprotegerin
(OPG).

34. Intramembranous
• Direct bone formation without a cartilaginous
intermediate
• Results when there is rigid internal fixation.
• Seen in fractures treated by compression
technique using plates and in case of impacted
fractures

35. Rigid stabilisation

36. • In first few days there is minimal activity near
fracture.
• Hematoma reabsorbed
• Swelling subsides and surgical wound heals
• After 3 to 4 weeks the Haversian system starts
to remodel the bone internally

37. • Schenk and Willenegger described 2 types of
primary bone healing
–Gap healing
–Contact healing
gap
contact

38. Contact healing
• A cluster of osteoclasts cuts across the
fracture , osteoblasts following the
osteoclasts deposit new bone and blood
vessels follow the osteoblasts.

39. Direct bone healing
Gap healing
• Gaps between bone fragments are invaded by
blood vessels which appear within the first 8
days.
• Accompanied by osteoblasts which deposit
osteoid, giving rise to lamellae oriented 90° to
the long axis of the bone.

40. • From 4th week onwards haversian remodelling
begins with cutting cones traversing the new
bone in the fracture gap depositing lamellar
bone and forming axially oriented osteons.

41. In brief
• Mechanical instability favors
endochondral ossification
• Mechanical stability favors
intramembranous ossification

42. • The histologic examination of the fracture
calluses demonstrated an increased
predominance of cartilage 14 days after
fracture when the fracture stabilization was
delayed 24 hours or greater, suggesting that
cell fate is determined early in the fracture
healing process.

43. Biological plate fixation
Current plating methods attempt to preserve
periosteal blood supply
These methods provide relative stability and in the presence of
preserved vascularity heal by stronger callus formation
(Indirect healing).
Decreasing contact
Elevated application Bridge & Wave platingIndirect reduction &MIPO

44. Intramedullary nailing
• Reaming and intramedullary nailing destroys
the medullary and endosteal blood supply
• centrifugal reversed to centripetal
• Gradual revascularisation of endosteum
occurs over a few weeks.
• bone healing occurs with callus formation.

45. Failures of Healing—Etiologies
and Overview of Treatment Strategies
• Biologic failures---atrophic nonunion
• Mechanical failures—hypertrophic nonunion

46. Variables Influence Fracture Healing
INJURY VARIABLES
Open Fractures
Impeding or preventing formation # Hematoma
 Delaying formation repair tissue
 Risk of infection

47. 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

48. Patient Variables
AGE
NUTRTION
 HEALING PROCESS NEEDS
Energy
Proteins & carbohydrates

49. Patient Variables cont….
Systemic hormones
 Corticosteroid ( )
 Growth hormone
 Thyroid hormone
 Calcitonin
 Insulin
 Anabolic steroids
 DM
 Hypervitaminosis D
 Rickets
Inhibit fracture healing ( Vascularization?)
Nicotine
Ratefracture healing
Rate fracture healing

50. Tissue Variables
 Cancellous or cortical bones
 Bone necrosis
 Infection

51. Bone disease
 Osteoprosis
 Osteomalacia
 Primary malignant bone tumors
 Metastatic bone tumors
 Fibrous dysplacia
 Benign bone tumors
 Bone cysts
 Osteogenesis imperfecta
 Paget’s disease
 Hyperparathyroidism

52. Treatment Variables
Apposition of fracture fragments
Loading & micromotion
 Loading a fracture site stimulates bone
formation
 Micromotion promotes fracture healing

53. Treatment Variables
Fracture stabilization
 Traction
 Cast Imm
 Ext.Fixation
 Int.Fixation
Facilitate fracture healing by Preventing
repeated disruption of Repair tissue

54. COMPLICATIONS OF FRACTURE HEALING
• MALUNION
• DELAYED UNION
• NONUNION

55. 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

56. MALUNION contd…
MALUNION can IMPAIR FUCNTION by
ABNORMAL JOINT SURFACE
ROTATION or ANGULATION
OVERRIDING
MOVEMENT OF NEIGHBOURING JOINT MAY
BE BLOCKED

57. CHARACTERISTICS FOR ACCEPTABILITY
OF FRACTURE REDUCTION
ALIGNMENT (MOST IMPORTANT)
 ROTATION
 RESTORATION OF NORMAL LENGTH
ACTUAL POSITION OF FRAGMENTS
(LEAST IMPORTANT)

58. ANALYSIS OF DEFORMITY
• RIES and O’NEILL developed
TRIGNOMETRIC ANALYSIS of DEFORMITY and
designed E-GRAPH to determine the
true maximal deformity on AP and LATERAL X-
Ray views.

59. MALUNION contd….
• 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.
• Surgeon should look for before surgery--
 OSTEOPROSIS
 SOFT TISSUE
 HOW MUCH FUNCTION CAN BE GAINED

60. MALUNION contd….
ILIZAROV TECHNIQUE is BEST
Simultaneous restoration of
ALIGNMENT
 ROTATION
LENGTH

61. Delayed Union
• The exact time when a given fracture should
be united cannot be defined
• Union is delayed when healing has not
advanced at the average rate for the location
and type of fracture (Btn 3-6 mths)
• Treatment usually is by an efficient cast that
allows as much function as possible can be
continued for 4 to 12 additional weeks

62. Delayed Union cont.
• If still nonunited a decision should be made to
treat the fracture as nonunion
• External ultrasound or electrical stimulation
may be considered
• Surgical treatment should be carried out to
remove interposed soft tissues and to oppose
widely separated fragments

63. • Iliac grafts should be used if plates and
screws are placed but grafts are not usually
needed when using intramedullary nailing,
unless reduction is done open

64. Nonunion
• 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)

65. Atrophic Nonunion
• Absence of any visible bone formation on
radiographs
• The major factors that contribute include
– infection,
– compromised nutrition,
– smoking,
– medications,
– surgeon-controlled factors such as fracture
vascularity.

66. Hypertrophic Nonunion
• lack of adequate stability at the fracture site
• Macroscopic movement of fracture fragments
prevents normal vascular invasion and the
associated senescence of chondrocytes and
mineralization of the cartilage matrix seen in
optimally stable fractures.

67. • Morphologically, hypertrophic nonunions are
identified by a persistent fracture line with a
large fusiform callus that has been compared
to the shape of two elephants’ feet, sole-to-
sole

68. • With revision surgery to provide adequate
stability, a hypertrophic nonunion typically
goes on to heal uneventfully without the
need to augment local biology with bone graft
or growth factor stimulation.

69. Systemic Pharmacologic Treatments
Influencing Bone Healing
• After bone fracture, bisphosphonates do not
appear to interfere with the early phases of
repair, rather continued bisphosphonate use
in one study resulted in a larger, stronger
callus.
• Although time-to-union was not affected, a
marked delay in the completion of remodeling
was seen

70. • Although not completely elucidated, the
mechanism of improved fracture healing with
PTH treatment is felt to relate to the increase
in chondroprogenitor and osteoprogenitor
cells in the early fracture callus

71. • corticosteroids inhibit
– osteogenic differentiation of MSCs,
– osteoblast and osteocyte apoptosis,
– reduction in organic matrix synthesis

72. COX 2
INCREASE PG E2
upregulation of Cbfa1 (or Runx2)
(transcription factor necessary for osteoblastogenesis)

73. • NSAIDs have not definitively demonstrated
impaired healing with both nonspecific and
COX-2–specific NSAIDs.
• clinician weigh the current theoretical risk of
impaired fracture healing against the benefits
of improved pain relief.