4. DEFINITION
“Direct structural and functional connection between
ordered, living bone and surface of a load carrying implant”
by Branemark et al. in 1977 .
“Functional ankylosis” by Schroeder et al. in 1981.
“A biomechanical phenomenon whereby clinically
asymptomatic rigid fixation of the implant is achieved and
maintained in bone during functional loading.” by
Albrektson and Johansson in 2001.
4
10. TISSUE RESPONSE
Biological response to the host tissue following the
placement of the implant:
1. Cellular injury
2. Inflammation and Coagulation
3. Repair and Regeneration
10
11. CELLULAR INJURY
injury: oxygen deprivation
reversible injury: cellular swelling
irreversible injury: point of no return
11
Najjar T. FONSECA: oral and maxillofacial surgery. Reconstructive and Implant
surgery
12. 12
Najjar T. FONSECA: oral and maxillofacial surgery. Reconstructive and Implant
surgery
13. Injured mesenchymal cells at the surgical site are not
conductive for osseointegration of the implant.
The aim is to reduce ischemia and anoxia to a minimal
degree and for a very short duration during the surgical
phase of implant placement.
13
Najjar T. FONSECA: oral and maxillofacial surgery. Reconstructive and Implant
surgery
16. The micro-thrombin that are formed immediately after
surgery at the implant bone interface constitute the
framework for osseointegration to take place.
16
Najjar T. FONSECA: oral and maxillofacial surgery. Reconstructive and Implant
surgery
17. REPAIR AND REGENERATION
Branemark PI. Tissue-integrated prosthesis: osseointegration in clinical
dentistry Chicago: Quintessence Publishing Co.; 1985.
17
Bone may react in three different ways as a response to the
necrosis
18. Conditions for bone repair at an implant site depend on the
presence of:
1. Adequate cells
2. Adequate nutrition to these cells
3. Adequate stimulus for bone repair
18
Branemark PI. Tissue-integrated prosthesis: osseointegration in clinical
dentistry Chicago: Quintessence Publishing Co.; 1985.
19. ADEQUATE CELLS
Osteoclasts Creeping substitution Osteoblasts
Osteoclasts propagates at a rate of 50ɥm per day
Undifferentiated mesenchymal cells
19
Branemark PI. Tissue-integrated prosthesis: osseointegration in clinical
dentistry Chicago: Quintessence Publishing Co.; 1985.
21. ADEQUATE STIMULUS FOR BONE REPAIR
21
Branemark PI. Tissue-integrated prosthesis: osseointegration in clinical
dentistry Chicago: Quintessence Publishing Co.; 1985.
22. STAGES OF OSSEOINTEGRATION
1. Incorporation by woven bone formation
2. Adaptation of bone mass to load (lamellar and parallel
fibered bone deposition)
3. Adaptation of bone mass structure to load (bone
remodeling)
22
Schenk RK. Osseointegration: a reality. Periodontology 2000. 1998; 17: p. 22-
35.
23. WOVEN BONE FORMATION
The first bone tissue formed is woven bone. It is
characterized by a random, felt-like orientation of its
collagen fibrils, numerous, irregularly shaped osteocytes
and, at the beginning, a relatively low mineral density
It grows by forming a scaffold of rods and plates and
thus is able to spread out into the surrounding tissue at a
relatively rapid rate.
Woven bone formation clearly dominates the scene within
the first 4 to 6 weeks after surgery.
23
Schenk RK. Osseointegration: a reality. Periodontology 2000. 1998; 17: p. 22-
35.
24. LAMELLAR AND PARALLEL FIBERED BONE
DEPOSITION
Lamellar bone deposition Parallel fibered bone
deposition
24
The linear apposition rate:
1-1.5 ɥm/day 3-5 times larger than lamellar
bone
Schenk RK. Osseointegration: a reality. Periodontology 2000. 1998; 17: p. 22-
35.
25. Both types of bone grow by apposition on a preformed solid
base.
Three surfaces are qualified as a solid base for deposition of
parallel- fibered and lamellar bone:
Woven bone formed in the first period of osseointegration
Pre-existing or pristine bone surface
The implant surface.
25
Schenk RK. Osseointegration: a reality. Periodontology 2000. 1998; 17: p. 22-
35.
26. BONE REMODELING
It starts around the third month and after several weeks of
increasingly high activity, slow down again, but continues for
the rest of life.
In cortical, as well as in cancellous bone, remodeling occurs
in discrete units, often called a bone multicellular unit, as
proposed by Frost.
Remodeling starts with osteoclastic resorption, followed by
lamellar bone deposition.
26
Schenk RK. Osseointegration: a reality. Periodontology 2000. 1998; 17: p. 22-
35.
27. Remodeling in the third stage of osseointegration
contributes; to an adaptation of bone structure to load in two
ways:
It improves bone quality by replacing pre-existing, necrotic bone
and/or initially formed more primitive woven bone with mature, viable
lamellar bone.
It leads to a functional adaptation of the bone structure to load by
changing the dimension and orientation of the supporting elements.
Continuous replacement of old bone by new bone prevents
accumulation of micro-damage and fatigue as one possible
cause of aseptic implant loosening.
27
Schenk RK. Osseointegration: a reality. Periodontology 2000. 1998; 17: p. 22-
35.
28. MECHANISM OF INTEGRATION
OSBORN AND NEWESLEY – 1980
Distance osteogenesis Contact osteogenesis
28
Davies J. Mechanisms of Endosseous Integration. The International Journal of
Prosthodontics. 1998; 11(5): p. 391-401.
29. MECHANISM OF INTEGRATION
DAVIES - 1998
Contact osteogenesis:
Osteoconduction
De novo bone formation
Bone remodeling at discrete sites
29
Davies J. Mechanisms of Endosseous Integration. The International Journal of
Prosthodontics. 1998; 11(5): p. 391-401.
31. Osborn (1979)categorized this bio-response into
the following three groups:
Biotolerant type: characterized by distance
osteogenesis, the implant is not rejected from the
tissue, but it is surrounded by a fibrous connective
tissue
Bioinert type: characterized by contact
osteogenesis, the osteogenic cells migrate directly to
the surface where they will establish de novo bone
formation, and
Bioreactive type: the implant allows new bone
formation around itself, thereby exchanging ions to
create a chemical bond with the bone.
31
Davies J. Mechanisms of Endosseous Integration. The International Journal of
Prosthodontics. 1998; 11(5): p. 391-401.
32. DE NOVO BONE FORMATION
32
Secretion of two collagenous
proteins: osteopontin and
bone sialoprotein
Calcium phosphate
nucleation at the calcium
binding sites of one or more
of this protein.
Crystal growth phase
Collagen production and
subsequent collagen
mineralization
Davies J. Mechanisms of Endosseous Integration. The International Journal of
Prosthodontics. 1998; 11(5): p. 391-401.
33. Initial protein layer with arginine-glycine-aspartic acid motif
adhesion. (Fibronectin, vitronectin, laminin, serum albumin
and collagen)
Osteogenic cells attached to these binding motif using
membrane receptors (Integrins)
Binding will provoke integrin-mediated cellular signaling
cascades and results in migration, proliferation and
differentiation of osteogenic cells. (Sawyer 2005)
33
Davies J. Mechanisms of Endosseous Integration. The International Journal of
Prosthodontics. 1998; 11(5): p. 391-401.
34. TIME COURSE OF INTERFACE DEVELOPMENT FOR
ENDOSSEOUS IMPLANTS IN CORTICAL BONE
Surface modeling
Stage 1: Woven callus 6 weeks
Stage 2: Lamellar compaction 18 weeks
Remodeling, maturation
Stage 3: interface remodeling 18 weeks
Stage 4: compact bone maturation 54 weeks
Misch C. Contemporary Implant Dentistry, 3e. 3rd ed.; 2008.
34
36. REFERENCES
36
Najjar T. FONSECA: oral and maxillofacial surgery. Reconstructive and
Implant surgery
Branemark PI. Tissue-integrated prosthesis: osseointegration in clinical
dentistry Chicago: Quintessence Publishing Co.; 1985.
Davies J. Mechanisms of Endosseous Integration. The International
Journal of Prosthodontics. 1998; 11(5): p. 391-401.
Ramazanoglu M. Osseointegration and Bioscience of Implant Surfaces -
Current Concepts at Bone-Implant Interface, Implant Dentistry- A
Rapidly Evolving Practice Turkyilmaz PI, editor.: Intech; 2001.
Misch C. Contemporary Implant Dentistry, 3e. 3rd ed.; 2008.
Editor's Notes
Modelling: net change in size and shape
Remodelling: turnover or internal restructing
Osteocytes: helps to control calcium and phosphate levels in the microenviroment and detect mechanical forces and translate them into biological activity- process called mechnao-transduction.
Modelling / Remodelling
Macrophage colony stimulating factor (M-CSF) precusor cell to osteoclasts
Osteoclasts arise from hematopoietic precursors of monocytes/ macrophage lineage.
Receptor activated nuclear factor KB
All three belong to TNF superfamily
The degree on injury depends on duration and degree of surgical trauma
Oxygen deprivation: caused due to ischemia and activation of partially reduced oxygen species
Increased intracellualer Ca. released for intracelluar stores, activity of protease and phospholipase, membrane damage-influx of extracelluar Ca,
Ca leads to paralysis of ATP driven sodium pump…accumulation of intracelluar Na and diffusion of Potassium. Iso-osmotic gain of water
Hypoxia continue…worsening mitochondria fun…increase permeability…..point of no return.
Activation of clotting system, complement and kinin system
Burheads
The repair of the cortical necrotic border zone around an implant will to a large extent depends on one particular type of coupled osteoclasts/osteoblasts action called creeping substitution
Cortical bone: Haversian canal (Alinged along long axis of the bone)
Volkmann’s canal: perpendicular
Burwell in 1966: dying cells differentiate mesenchymal cells or some differentiated cells remain alive
Urist 1968
Yasuda 1953: Piezoelectric forces acted over the fracture gap and stimulate the bone healing
Lamellar bone Packing of the collagen fibrils into parallel layers with alternating course gives it the highest ultimate strength
Parallel-fibered bone is an intermediate between woven and lamellar bone: the collagen fibrils run parallel to the surface but without a preferential orientation in that plane
. The term “Osteoconduction” refers to the migration of these cells to the proposed site. derived at bone remodeling sites from undifferentiated peri-vascular connective tissue cells.
Fibrin retraction
Fibrin the reaction product of thrombin and fibrinogen…adhere to implant surface and via which osteogenic cells migrate.
4 stages:
Cement lines: non collagenous protein….interface between new and old bone….0.5micro meter thick
Bonding of collagen and implant surface: interdigitation with chemically active surface….micromechanical interlocking.