Presentan:

I Dewa Ayu Raina Kenovita Ardani

Mentor:
dr. Muhamad Naseh Sajadi Budi Irawan,
Sp.OT(K)

THE BIOLOGIC RESPONSE TO

ORTHOPAEDIC IMPLANTS
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BIOMATERIALS
Biomaterials
 natural or synthetic materials that treat, augment, or replace tissues and
organs
 have the ability to remain in contact with tissues from the human body
without creating too much adverse or a hostile response,
 able to resist mechanical forces and chemical effects
 exhibit osseointegration properties
The biomaterials most commonly used in orthopedic surgery
 metallic implants steel, cobalt-chrome, or titanium alloys provide
satisfactory mechanical performance.
The success of these implants is highly dependent on
 the properties of the biomaterial (mechan- ical, chemical, and tribological)
 the biocompatibility of the implant
 the condition of the recipient tissue/the competency of the surgeon.

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 The Biologic Response

Host response

Inflammatory process

Mediators of the response

IMPLANT FIXATION &
OSTEOINTEGRATION
The major modes of
implant fixation

Cemented fixation
Cementless fixation
Polymethyl-
 Biologic attachment
methacrylate (PMMA)
 as an adhesive
 Host bone quality
Surgical technique
Factors involved in Implant alignment
the integrity
& longevity Implant characteristic
fixation
Implant wear issues

Local biology
3 PHASES OF HEALING

Initial repair stabilization

Dynamic
Injury or tissue Load transfer
osteointegration
destruction Local biologic
consequences
INITIAL PHASE
mechanical

vascular
Local tissue
necrosis at cement-
bone interface
thermal

chemical
REPAIR PHASE
Fibrous membran is formed Tissue regeneration

Repair phase

Vascularization is establish osteointegration

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 Component design
patient

Quality &
integrity the Implant wear debris
interface

Host bone characteristic Cement technique

THE BIOLOGIC RESPONSE OF SURROUNDING BONE
TO THE PROSTHESIS IS CALLED ADDAPTIVE
REMODELLING

Direct apposition of
host bone
Characterized by DenseText
shell of bone

Rare intervening Text

fibrous tissue
CEMENTLESS IMPLANT
Surgical technique Bone quality

Quality of
biologic fixation
Patient
with cementless related
implant factors

Implant design

Initial implant stability

HEALING PHASE OF CEMENTLESS
IMPLANT
Early phase

Intramembranous bone
formation

HEALING
osteointegration
stabilization
CEMENTLESS IMPLANT

Cobalt-chromium
Titanium sintered beads
Titanium fiber metal
Titanium plasma spray
Diffusion-bonded plasma

Provide osseous ingrowth or ongrowth

Provide biologic fixation
Good clinical function
FACTORS ENHANCING IMPLANT OSTEOINTEGRATION

Factors Aposition
Pore size of enhancing of the
Bone ingrowth implant
surface To host
bone

New design
biomaterial
ADAPTIVE BONE LOSS & POTENTIAL
THERAPIES
 refers to changes in bone mass & geometry in respons to alteration inmechanical
forces & environment
The mechanism for adaptation involve a multistep of cellular mechanotransduction
THE MECHANISM FOR ADAPTATION

Mechanocoupling
• conversion of mechanical forces into local mechanical signal such as a
fluid shear stress that initiate a response by bone cells
Biochemical coupling
• transduction of mechanical signal to a biochemical response within the
cell membrane & cytoskeleton
Cell-to-cell signaling from the sensor cells
• to effector cells (osteoblast or osteoclast)
The effector response
• bone formation/resorption to cause appropiate architectural changes
STRUCTURAL CHANGES

1. Bone adaptation is driven by dynamic rather than static loading

2. Extending the loading duration has a diminishing effect on further bone
adaptation
3. Bone cells accommodate to a mechanical environment
Stress shielding  contribute net bone loss
Factors that determined :
1. geometry & material properties
2. host bone
INHIBITION BONE LOSS
Inhibition osteoclast activity
Bisphosphonat
A new generation of osteoclast inhibitors (osteoprotegerin/OPG)
Receptor activator of nuclear factor-kappaB (RANK)-fc
Etanercept
Selective inhibitors of tyrosine kinases
RESPONSE TO IMPLANT DEBRIS &
INFLAMATORY BONE LOSS
Implant  foreign body
Wear debris occurs immediately
The causes :
1. micromotion
2. corrotion
3. oxidative reaction
Intial response  localized anti inflamatory response
Formation of fibrous tissue
Synovial fluid & thick synovial lining membrane
Granulomatous tissue
Abundance of macrophage, fibroblast & lymphocyte
ASEPTIC LOOSENING

Characterized by :
Poorly vascularized connective tissue
Dominated by fibroblast & macrophages
Secretion of proinflamatory factors, gelatinase, & protease
The cellular & inflamatory response  occur during progression & late stage
of osteolysis
Excessive motion & physical strain  loosening of implant
The ammount of particulate debris  aseptic loosening
BIOLOGY OF OSTEOLYTIC CASCADE

Cellular response
 fagocyte, macrophage, osteoclast, fibroblast, osteoblast/stromal cells
Recognition  interaction  endotoxin/bacterial protein  induced
inflamatory response
POTENTIAL THERAPIES FOR
INFLAMATORY BONE LOSS
Molecular approach to arrest osteoclast activity
Several approach regarding osteoclast-based Therapy :
1. targeting osteoclast precusors cells
2. targeting precusor which are stimulated by particle-mediated celluler
response
3. targeting activation mechanism of mature osteoclast
INHIBITION OSTEOCLAST
DIFFERENTIATION
RANKL decoy molecules
OPG
RANK-fc
C-fms
C-fos
NF-kB
C-src
Protein adenosin triphosphate
INHIBIT OSTEOCLAST FUNCTION
Bisphosphonate
 also induced its apoptosis
 preventing particle-induced osteolysis
ANTI-INFLAMATORY STRATEGIES
Pharmacologic intervention  macrophage
Local cytokine inhibition
IL-1 receptor antagonist protein (IL-1Ra)
Anti-inflamatory cytokine
IL-10
T-lymphocyte secreted IL-10, IL-4 interferon (IFN)-γ
Antagonist proinflamatory cytokines
Inhibit osteoclast formation
Inhibit bone resorption
Titanium, alumunium, vanadium, cobalt, chromium & nickel  toxic

Toxicity range : normal celluler response  immunologic  carcinogenesis

 Adverse reaction depend on :
1. Metal quantities
2. Tissue distribution
3. Metal properties

Most reactive metal :

Nickel
Cobalt
chromium
RESPONSE TO AUTOGRAFT &
ALLOGRAFT
Bone graft provide mechanical support
 act as weight bearing space fillers
Bone graft act as osteoconductive/ osteoinductive agents
 enhance osseous healing
 5 STAGE OF INCORPORATION OF BONE
GRAFT

Acute vascularizat osteoinduc osteointegrati remodelling

inflamatory ion tion on
Cellular
response
AUTOGRAFT
Cancelous autograft
 highly osteogenic
 revascularized
 integrates rapidly in host tissue
 large content of osteoblast & osteogenic precursor cells.
Cortical autograft
 nonvascularized & vascularized
 nonvascularized  awaits osteoclastic resorption for vascular invation
 vascularized  implanted with functional blood supply
ALLOGRAFT
Healing  solely mediated by invasion of graft by host tissue
Union process depend on remodelling, new bone formation & mineralization
Types :
- allogenic demineralized bone matrix
- morcelized
- cancelous bone
- corticocancelous bone
- cortical bone
THANK YOU