osseointegration

- DEFINITION
- MICRO & MACRO EXPLANATION
- MICROSEAL
OSSEOINTEGRATION
Sunil Gurram

INTRODUCTION
The successful replacement of lost natural
teeth by tissue-integrated tooth root
analogues is a major advancement over
last 25 years. Today the continued high
rate of success achieved with these
osseointegrated dental implants allow a
greater number of patients to enjoy the
benefits of fixed rather than removable
restorations.

Throughout history, many researchers
have attempted to use dental implants as
a solution to edentulism and partial
edentulism. Unfortunately much of this
work has resulted in failure. However,
without the work of the early investigators
to build upon, we would not enjoy the
success that we now have. It is critically
important to understand how oral
implantology has evolved in order to
understand where we have been, and
where we are going.

Evolution of Osseo integration
concept:
In the past, direct contact (without
interposed soft tissue layers) between
bone and metallic implants was regarded
as impossible to achieve (Fibro-osseous
integration). The supporters of this theory
were Linkow (1970) James (1975) and
Weiss (1986).

 The term “Osseointegration” was coined
by Dr Per-Ingvar Branemark (Fig-1),
Professor at the Institute for Applied
Biotechnology, University of Goteborg,
Sweden in the year 1985 to describe the
direct connection between a living bone
and load-carrying endosseous implant at
the light microscopic level.

In January 1986, the Branemark clinic for
osseointegration implant treatment was
established within the School of dentistry
at Goteborg University. Since then the
science of osseointegration evolved in
both laboratory and clinical environments
and also as a result of extensive
multidisciplinary co-operation. Branemark
has also been credited for finding out the
most biocompatible implant material as
titanium

DEFINITIONS
According to Branemark, Zarb, and
Albrektsson (1985)
Osseointegration is the direct structural
and functional connection between
ordered, living bone and the surface of a
load–carrying implant.

According to Branemark’s histologic
point of view: (1985)
Osseointegration is a direct connection
between a living bone and load-carrying
endosseous implant at the light
microscopic level

 According to Glossary of Prosthodontic
terms (J Prosthet Dent 2005; 94: p58)
 Osseointegration is defined as 1: the apparent
direct attachment or connection of osseous
tissue to an inert, alloplastic material without
intervening connective tissue 2: the process and
resultant apparent direct connection of an
exogenous material’s surface and the host bone
tissues, without intervening fibrous connective
tissue present 3: the interface between
alloplastic materials and bone.

According to the American Academy of
Implants Dentistry (1986)
Osseointegration is the contact
established without interposition of non-
bone tissue between normal remodeled
bone and an implant entailing a sustained
transfer and distribution of load from the
implant to and within the bone tissue.

According to Zarb and Albrektsson
(1991)
Osseointegration is a time-dependent
healing process whereby clinically
asymptomatic rigid fixation of alloplastic
materials is achieved, and maintained, in
bone during functional loading.

BONE HEALING:
An injured bone heals either by primary or
secondary process. Primary bone healing
occurs at the fracture site with a clean
break. The sites are positioned by pressed
fixation or closely approximated. In this
type of healing there is a well-organized
bone formation with minimal granulation
tissue formation. When implants are
considered this type of healing is ideal.

Hence to duplicate this healing process,
the surgery should be performed on
healthy bone, free from infection or
necrotic tissue.
 Secondary healing occurs when a
large defect or large fracture site
precludes close approximation of the two
sites. This type of healing is prolonged
due to infection and granulation tissue
formation. This type of healing may result
in fibrous tissue formation, which is
undesirable in case of implants.

Bone healing around an inserted implant
Three phases
1st
phase – injury phase – starts
immediately after insertion of implant
2nd
phase – granulation phase – 3-2 weeks
after implantation. Formation of new local
connective tissue, new capillaries and new
supporting cells.
3rd
phase – callus phase – 4-6 weeks after
injury – evidence of new bone formation

BONE REMODELING:
Osseointegration requires new bone
formation around the fixture, a process
resulting from remodeling within bone
tissue. Remodeling, bone resorption, and
apposition helps to maintain blood calcium
levels and does not change the mass
quantity of bone. In spongy bone, with an
abundance of osteoblasts and osteoclasts
available remodeling occurs on the
surface of bone trabeculae.

Occlusal forces applied to spongy bone
act as a stimulus to the recipient area.
This stimulation causes bone cells to
differentiate into osteoclasts involved in
bone resorption, while the same stimulus
causes osteoprogenitor cells to
differentiate into osteoblasts involved in
bone formation. The same phenomenon
occurs in compact bone at the remodeling
sites.

FOREIGN BODY REACTION:
 Organization or an antigen-antibody
reaction occurs when a foreign body is
present in the body. Organization is the
process by which the body attempts to
isolate the foreign body by surrounding it
with granulation tissue then connective
tissue.

 An antigen-antibody reaction is the process of
formation of an antibody in response to the
foreign body. An antigen is formed after a latent
period as a protective mechanism. This reaction
occurs in the presence of protein, but with
implant materials devoid of protein, there is no
antigen-antibody reaction.

CONDITIONS AFFECTING BONE
REPAIR AT AN IMPLANT SITE:
(CELLULAR BACKGROUND)
In principle, bone may react in three
different ways as a response to the
necrosis
1. Fibrous tissue formation may occur.
2. Dead bone may remain as sequester
without repair.
3. New bone healing or Osseointegration
(bone formation = bone resorption)

Bone repair of the necrotic implant cortex
will depend on the presence of
1. Adequate cells
2. Adequate nutrition to these cells
3. Adequate stimulus for bone repair.

In case of bone healing, the adequate
stimulus has been regarded by various
authors as based on a cell-to-cell contact,
soluble matrix molecules or stress-
generated electric potentials.

Tissue-implant biological seal
The concept of the role of the gingival
epithelium in forming a biologic seal is one
of the great importance in implant dentistry

All dental implants, whether endosteal,
transosteal or subperiosteal, must have a
super structure or coronal portion
supported by a post that must pass
through the submucosa (lamina propria)
and the covering stratified squamous
epithelium into the oral cavity.

This permucosal passage creates a “weak
link” between the prosthetic attachment
and the predicted bony support of the
implant .
This is the area where intial tissue break
down begins that can result in eventual
tissue necrosis and destruction around the
implant

The biologic seal thus becomes an
important and pivot factor in dental implant
longevity. The seal as a physiological
barrier must be effective enough to
prevent the ingress of bacterial plaque,
toxins, oral debris, and other deleterious
substances taken into the oral cavity.

if seal is violated
Adjacent tissue will become inflamed
Osteoclastic activity is stimulated
Chronic resorption of supporting bone

Discrepency will fill with granulation tissue
and implant becomes mobile
Percolation of bacteria and toxins
Acute suppurative inflammation

Excessive mobile.
Support of dental prosthesis impractical
Removal of implant
Decrease support of other new implants to
place or any restorative procedure.

So how is this seal formed
Implant surgery
attached gingiva
regenerates around
the implant
epithelial cuff /free gingival
margin(more appropriate term)
regenerating epithelium forms the free
gingival margin & a gingival sulcus

epithelium regenerate
into the sulcus
Non keratinized sulcular (crevicular)
epithelium & a zone of epithelial cells at
the base of the sulcus that interface the
implant surface.
Series of biologic attachment structures

Formation of a basal lamina collagenous
structure (type IV)
attachment

In addition, the epithelial cells produce an
enzyme called laminin, which serves as an
additional molecular bonding agent
between the epithelial cells and the
various component layers of the basal
lamina.

 Biologic structures creating biologic seal
following surgical placement of an implant
Epithelial cell with cell membrane
Basal lamina outside cell membrane
lamina lucida
lamina densa
sublamina lucida
Hemidesmosomes on cell membrane
peripheral densities
pyramidal particles
fine filaments
Linear body on the implant face

THEORIES ON BONE TO IMPLANT
INTERFACE
There are two basic theories regarding the
bone-implant interface.
a) Fibro-osseous integration (Linkow
1970, James 1975, and Weiss 1986)
b) Osseointegration (supported by
Branemark, Zarb, and Albrektsson 1985)

A. FIBRO-OSSEOUS INTEGRATION:
Fibro-osseous integration refers to a
presence of connective tissue between the
implant and bone. In this theory, collagen
fibers functions similarly to Sharpey’s
fibers found in natural dentition. The fibers
affect bone remodeling where tension is
created under optimal loading conditions.

In 1986, the American Academy of
Implants Dentistry (AAID) defined fibrous
integration as “tissue-to-implant contact
with healthy dense collagenous tissue
between the implant and bone”

Weiss stated that the presence of collagen
fibers at the interface between the implant
and bone is a peri-implant membrane with
an osteogenic effect. He believed that the
collagen fibers invest the implant,
originating at the trabeculae of cancellous
bone on one side, weaving around the
implant, and reinserting into a trabeculae
on the other side.

Failure of fibro-osseous theory
Conventional implant systems have
always had a fibrous capsule or fibrous
tissue interface along the surface of the
implant, which has been referred to as a
pseudo-peri-implant membrane. It was felt
that, this membrane gave a cushion effect
and acted as similar as periodontal
membrane in natural dentition.

However, there was no real evidence to
suggest that these fibers functioned in the
mode of periodontal ligament. Hence
when in function the forces are not
transmitted through the fibers as seen in
natural dentition. Therefore, remodeling
was not expected to occur in fibrous
integration. Moreover the forces applied
resulted in widening fibrous encapsulation,
inflammatory reactions, and gradual bone
resorption there by leading to failure.

B. THEORY OF OSSEOINTEGRATION
Meffert et al, (1987) redefined and
subdivided the term osseointegration into
“adaptive osseointegration” and
“biointegration”. “Adaptive
osseointegration” has osseous tissue
approximating the surface of implant
without apparent soft tissue interface at
the light microscopic level. “Biointegration”
is a direct biochemical bone surface
attachment confirmed at the electron
microscopic level.

 Unlike fibro-osseous integration,
osseointegration was able to distribute
vertical and slightly inclined loads more
equally in to surrounding bone. To obtain
a successful osseointegration Branemark
and coworkers proposed numerous
factors. According to the proponents the
oxide layer should not be contaminated or
else inflammatory reaction follows
resulting in granulation tissue formation.

The temperature during drilling should be
controlled by copious irrigation, if not can
inhibit alkaline calcium synthesis there by
preventing osseointegration.
 The first month after fixture insertion is
the critical time period for initial healing
period. When loads are applied to the
fixture during this period primary fixation is
destroyed.

Osseointegration Vs Biointegration:
. In 1985, DePutter et al. observed that
there are two ways of implant anchorage
or retention; mechanical and bioactive.

Mechanical retention basically refers to
the metallic substrate systems such as
titanium or titanium alloy. The retention is
based on undercut forms such as vents,
slots, dimples, screws, and so forth and
involves direct contact between the
dioxide layer on the base metal and bone
with no chemical bonding.

Bioactive retention is achieved with
bioactive materials such as hydroxyapatite
(HA), which bond directly to bone, similar
to ankylosis of natural teeth. Bone matrix
is deposited on the HA layer as a result of
some type of physiochemical interaction
between the collagen of bone and the HA
crystals of the implant.

MECHANISM OF OSSEOINTEGRATION
(BONE TISSUE RESPONSE)
MECHANISM OF INTEGRATION: (Davies
- 1998)
MECHANISM OF INTEGRATION:
(Osborn and Newesley – 1980)

MECHANISM OF INTEGRATION:
(Osborn and Newesley – 1980)
The terms “Distance and Contact
osteogenesis” were first described by
Osborn and Newesley in 1980 and it
refers to the relationship between forming
bone and the surface of an implanted
material. Their terms described essentially
two distinctly different phenomena by
which bone can become juxtaposed to an
implant surface.

a. Distance osteogenesis:
In distance osteogenesis, new bone is
formed on the surface of bone in the peri-
implant site. Similar to normal appositional
bone growth, the existent bone surfaces
provide a population of osteogenic cells
that lay down new matrix, which as
osteogenesis continues, encroaches on
the implant itself

Thus, an essential observation here is that
new bone is not forming on the implant
itself, but rather that the implant becomes
surrounded by bone. In these
circumstances, the implant surface will
always be partially obscured from bone by
intervening cells and general connective
tissue extra-cellular matrix which makes
bone bonding impossible to achieve.

b. Contact osteogenesis:
 In contact osteogenesis, new bone forms
first on the implant surface. Since no bone
was present on the surface of the implant
upon implantation, the implant surface
must become colonized by a population of
osteogenic cells before initiation of bone
matrix formation. This occurs at
remodeling sites were an old bone surface
is populated with osteogenic cells before
new bone can be laid down. These
osteogenic cells migrate to the implant
surface.

 While both distance and contact
osteogenesis will result in the juxtaposition
of bone to the implant surface, the biologic
significance of these different healing
reactions is of considerable importance in
both attempting to unravel the role of
implant design in endosseous integration,
and in elucidating the differences in
structure and composition of the bone-
implant interface.

MECHANISM OF INTEGRATION:
(Davies - 1998)
Davies divided the contact osteogenesis
into two distinct early phases of
osteogenic cell migration
(Osteoconduction) and de novo bone
formation and a third tissue response that
consist of bone remodeling at discrete
sites.

a. Osteoconduction:
The term “Osteoconduction” refers to the
migration of differentiating osteogenic cells
to the proposed site. These cells are
derived at bone remodeling sites from
undifferentiated peri-vascular connective
tissue cells. A more complex environment
characterizes the peri-implant healing site
since this will be occupied transiently by
blood.

In this case, as in fracture healing,
migration of the connective tissue cells will
occur through the fibrin that forms during
clot resolution. Fibrin, the reaction product
of thrombin and fibrinogen released into
the healing site can be expected to adhere
to almost all surfaces. It is via this that the
osteogenic cells get migrated.

 The migration of cells through a
temporary matrix such as fibrin will cause
retraction of the fibrin scaffold. Thus, the
ability of an implant surface to retain fibrin
attachment during this wound contraction
phase of healing is critical in determining if
the migrating cells will reach the former.

The phenomenon of osteoconduction
relies on the migration of differentiating
osteogenic cells to the implant surface.
Implant design can have a profound
influence on osteoconduction by
maintaining the anchorage of the
temporary scaffold through which these
cells reach the implant surface

It can be predicted that roughened
surfaces would promote osteoconduction
by both increasing available surface area
for fibrin attachment, and by providing
surface features with which fibrin could
become entangled. In addition, the
chemistry of some implant surfaces may
increase both the adsorption and retention
of macromolecular species from the
biologic milieu, and thus potentiate
osteoconduction.

b. De novo bone formation:
An essential prerequisite of de novo bone
formation is the recruitment of potentially
osteogenic cells to the site of future matrix
formation. Differentiating osteogenic cells,
which reach the implant surface initially,
secrete a collagen-free organic matrix that
provides nucleation sites for calcium
phosphate mineralization

Two noncollagenous bone proteins
Osteopontin and bone Sialoprotein has
been identified in this initial organic phase,
but no collagen. Calcium phosphate
crystal growth follows nucleation, and
concomitant with crystal growth at the
developing interface, there will be initiation
of collagen fiber assembly.

Finally, calcification of the collagen
compartment will occur both in association
with individual collagen fibers or in the
interfiber compartment. Thus, in this
process of de novo bone formation, the
collagen compartment of bone will be
separated from the underlying substratum
by a collagen-free calcified tissue layer
containing non-collagenous bone proteins.

Bone bonding in de novo bone
formation:
 Bonding of de novo bone will occur by the
fusion, or micromechanical interlocking of
the biologic cement line matrix with the
surface reactive layer of the substratum. In
other areas where connective tissue
collagen is in contact with the implant, it
will become encrusted in the surface
reaction layer of so-called “bioactive”
materials to produce the ultrastrustural
appearance of collagen interdigitation.

Bone remodeling:
During the long-term phase of peri-implant
healing, it is only through those
remodeling osteons that actually impinge
on the implant surface that de novo bone
formation will occur at these specific sites
on the transcortical implant

The remainder of the transcortical portion of the
implant will be occupied by old, dead bone or
connective tissue space created by peri-implant
necrosis and lysis of bone tissue. Although
trabecular remodeling occurs this is not vital to
implant stability.
 Calcium phosphates accelerate early peri-
implant bone healing by potentiating
osteoconduction through structural protein
adsorption and retention during early healing.

In this view it is possible to envision that
biologic design strategies for dental
implants have surfaces that are replaced
by bone during normal tissue remodeling.
Moreover, it is also seen that calcium
phosphate coating (Fig-22) can be site-
specifically resorbed by osteoclasts.

STAGES OF OSSEOINTEGRATION
 According to Misch there are two stages (Fig-23)
in osseointegration, each stage been again
divided into two substages. They are:
 Surface modeling
 Stage 1: Woven callus (0-6 weeks)
 Stage 2: Lamellar compaction (6-18 weeks)
 Remodeling, Maturation
 Stage 3: Interface remodeling (6-18 weeks)
 Stage 4: Compacta maturation (18-54 weeks)

STAGE 1: (Woven callus)
This stage undergoes from 0-6 weeks of
implantation. During this stage woven
bone is formed at implant site. It is often
considered as a primitive type of bone
tissue and characterized by a random, felt-
like orientation of collagen fibrils,
numerous irregularly shaped osteosites
and at the beginnings relatively low
mineral density

. It grows by forming a scaffold of rod and
plates and thus is able to spread out in to
the surrounding tissue at a relatively rapid
rate. It starts growing from the surrounding
bone towards the implant except in narrow
gaps, where it is simultaneously deposited
upon the implant surface. Woven bone
formation clearly dominates the seen
within the first four to six weeks after
surgery.

STAGE 2: (Lamellar compaction)
 This stage starts from 6th week of
implantation and continues till 18th week.
During this stage the woven callus
matures as it is replaced by lamellar bone.
This stage helps in achieving sufficient
strength for loading.

STAGE 3: (Interface remodeling)
This stage begins at the same time when
woven callus is completing lamellar
compaction. During this stage callus starts
to resorb, and remodeling of devitalized
interface begins. The interface remodeling
helps in establishing a viable interface
between the implant and original bone.

Remodeling of non-vital interface is
achieved by cutting/filling cones
emanating from the endosteal surface.
The mechanism is similar to typical
cortical remodeling except that many of
the cutting/filling cones are oriented
perpendicular to the usual pathway.

STAGE 4: (Compacta maturation)
 This occurs form 18th week of
implantation and continues till the 54th
week. During this stage compacta matures
by series of modeling and remodeling
processes. The callus volume is
decreased and interface remodeling
continues.

It was previously believed that maturation
involved two physiologic transients.
a. Regional acceleratory phenomenon
(RAP)
b. Secondary mineralization of newly
formed bone

 According to this a new bone get
strengthened only after 12 months through
secondary mineralization process. But
now it is thought that because of rapid
remodeling at the impact site, bone
mineralization could occur faster.

 Osseointegration, once looked upon with skepticism, is
now even regarded by some investigators as a frequently
occurring, primitive foreign body reaction to an implanted
material. A biomechanical factor alone is thought to
determine whether a fibrous encapsulation or a bone
covering will develop around an implanted device
Conclusion

New developments of oral implants have,
generally, been focused on changes in the
hardware of the implant, i.e. new
materials, designs or surfaces have been
introduced with simultaneous claims of
these been superior to those used in the
past.

The future of oral implants will mean a
greater understanding of the important
contributions by the responsible surgeon
and prosthodontist.

osseointegration

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