Copy of osseointegration/certified fixed orthodontic courses by Indian dental academy

INTRODUCTION :
Since tooth loss from disease and trauma has always been a feature of
mankind’s existence, it is not surprising that the history of tooth
replacement is a long one. Evidence from ancient civilizations shows that
attempts were made to replace missing teeth by banding artificial tooth
replacements to remaining teeth with metal many centuries ago. For the
mechanism of attachment, clinicians have long sought an analog for
periodontal ligament. Experiments were made to develop a fibrous
attachment that could serve the same purpose as the periodontal ligament
but all in vain. The periodontal ligament in a specialized structure which
serves not only as an efficient attachment mechanism but also as a shock
absorber and sensory organ, so it was impossible to reproduce.
HISTORY OF OSSEOINTEGRATION :
Implants may indeed be anchored in bone by means of surrounding
sheath of connective tissue, but in general this has not shown the degree of
organization and specialization that would allow it to pass as a substitute for
the periodontal ligament. In most cases, loading leads to gradual widening
of fibrous tissue layer and loosening of implant, with consequent implant
failure. In contrast to periodontal ligament, a fibrous tissue sheath is a
poorly differentiated layer of scar tissue.
Dr. Per Ingvar Branemark, an anatomist is credited as the person who
has coined the term “osseointegration”. Branemark along with his team was
working in the laboratory of the vital microscopy (1952), laboratory of
experimental Biology, University of Goteberg Sweden, (1960), Institute of
Applied biotechnology, Goteberg (1978). The main study of his group was
to understand the mechanism of bone healing and bone response to the
thermal, mechanical, chemical injuries by using vital microscopy.
Vital microscopy, is a type of the miniature microscope, which is
introduced in to the living organisms. E.g. Rabbit in their study the titanium

(Ti) chambers were used for placing the vital microscope into the rabbit’s
fibula. After the studying of the bone biomechanics in one animal, the team
used to recover the vital microscope and place it into the other animal
model. While recovering Branemark observed that the Ti chambers were
firmly adherent to the bone. By this observation they concluded that the
titanium was firmly integrated to the bone and later they used Ti screws and
Ti bars for reconstruction of the long bones and mandibles of the dogs.
After ensuring the favourable bone response to the Ti, the team tried
to replace the teeth for the dogs. The Ti implants also showed good response
for the mucosa and skin penetrating implants. The implants, which used for
replacement of the teeth in the dogs showed good integration upto 10 years
and the implants could bear the load of upto 100 Kgs without failure at the
bone-implant interface. By observing this property the integration between
the bone and Ti screws was termed as “osseointegration”.
The Ti vital microscopic chambers were used to analyze
microcirculation in the healthy and diabetic human volunteers without any
signs of inflammation around the Ti chamber. In 1965, first human
edentulous patient was treated by using the Ti screws (implants) by
reconstruction of resorbed edentulous arches using autologus tibial bone
grafts.
The salient features of Branemark and his team’s work
 About more than 50 designs of Ti screws (Implants) were tested
and used.
 The surgical protocol followed was : two stage surgery, which was
proved beneficial.
 Minimal trauma during the surgery results in bone regeneration
rather than bone repair at the implant site.
 Non-contaminated implants (sterile and clean implants) proved
good integration.

 Prosthesis and abutments were screw attached for more technical
flexibility.
 There were more mechanical failures at the interface rather than
biological failures.
Mr. Victor Kuikka helped in designing the hardware parts in this
study. In the longitudinal study of the Ti implants from 1965 to 1974
showed a success rate of 99% in mandibles and 89% in maxilla.
In the mean time Schroeder et al. (1970), the members of the
international team for development of oral implants (I.T.I) studied the Ti
plasma sprayed Cp Ti cylindrical implants in Monkey models and achieved
the firm integration between the implant and the tissues. In their study the
bone was joined to implant by fine bridges of fibrous tissue. They termed
this union as functional ankylosis.
DEFINITION AND OTHER TERMINOLOGIES :
Osseointegration :
Branemark defined it “as a direct contact between the bone and
metallic implants, without interposed soft tissues layers” (1969).
Later it is modified “as a direct structural and functional connection
between ordered, living bone and the surface of a load carrying implant”
(1977). [Structurally oriented definition]
American Academy of Implant Dentistry (1986) :
Contact established without interposition of non-bone tissue between
normal remodeled bone and an implant entailing a sustained transfer and
distribution of load from implant to and within the bone tissue.
Meffert et al. (1987) Subdivided into
Adaptive Osseointegration : Osseous tissue approximating the surface of
the implant without apparent soft tissue interface at light microscopic level.
Biointegration : Is a direct biochemical bone surface attachment confirmed
at electron microscopic level.

Zarb and T. Albrektsson (1991) : It is a process whereby clinically
asymptomatic rigid fixation of alloplastic materials is achieved and
maintained, in bone during functional loading.
Schroeder et al (1970’s) : Coined the term “Functional Ankylosis”.
[The Swiss Academy]
Other Terminologies :
Osteopreservation (Stallard R.E.) :
It is a made of tissue integration around healed functioning endosteal
dental implant in which the prime load bearing tissue at the interface is a
peri-implant ligament composed of osteostimulatory collage. It limits the
further bone resorption.
Used in case of plate/blade form endosseous implants and endodontic
stabilizers.
Periosteal integration :
It is a made of tissue integration around a healed, functioning,
subperiosteal implant in which the load bearing tissue is the sheath of dense
collagenous tissue constituting the outer layer of periosteum.
MECHANISM OF OSSEOINTEGRATION :
After the surgical placement of implants into endosteal location, the
traumatized bone around these implants begins the process of wound
healing. As mentioned previously, it can be separated into the inflammatory
phase, the proliferative phase, and the maturation phase. This is summarized
in Table along with some of the specific aspects of bone healing during
these stages.
Phase one inflammatory phase :
The placement of implants into bone involves the creation of an
osseous defects with the subsequent filling of this defect with an implant
device. Even with the most careful surgical manipulation of osseous tissues,

the generation of a thin layer of necrotic bone in the peri-implant region is
inevitable.
In addition, exact microscopic fit between the implant and the
surgical defect is not possible, leaving local areas of dead space where the
implant does not directly contact osseous tissue. When the implant is
exposed to the surgical site, it comes to contact with extracellular fluid and
cells. This initial exposure of the implant to the local tissue environment
results in rapid adsorption of local plasma proteins to the implant surface.
Shortly thereafter, these proteins are enzymatically degraded and undergo
conformational changes, degradation, and replacement by other proteins.
Platelet contact with synthetic surfaces causes their activation and liberation
of their intracellular granules resulting in release of serotonin and histamine,
leading to further platelet aggregation and local thrombosis. Blood contact
with proteins and foreign materials leads to the initiation of the clotting
cascade via the intrinsic and extrinsic pathways, causing blood coagulation
in the aforementioned peri-implant dead spaces and within the damaged
local microvascular circulation. Activation of the clotting cascade also leads
to the formation of bradykinin, which is a strong mediator of vasodilation
and endothelial permeability.
During this initial implant host interaction, numerous cytokines
(growth factors) are release from the local cellular elements. These
cytokines have numerous functions, including regulating adhesion molecule
production, altering cellular proliferation, increasing vascularization rate,
enhancing collagen synthesis, regulating bone metabolism and altering
migration of cells into a given area. Table 4.2 lists some of the cystokines
believed to be important in tissue implant integration. These initial events in
healing of implants are largely chemical in nature and correspond to the
beginning of a generalized inflammatory response that occurs with any
surgical insult.

The next events noted to occur during this phase of wound healing
consist of a cellular inflammatory response. Initially, it is nonspecific in
nature and consists mainly of neutrophil emigration into the area of
damaged tissue. Its duration is variable but generally peaks during the first 3
to 4 days following surgery. The role of this cell is primarily phagocytosis
and digestion of debris and damaged tissue. Neutrophils are accompanied by
smaller numbers of eosinophils. Eosinophils have a similar phagocytic
function and they can also digest antigen antibody complexes. These cells
are attracted to the local area by chemotactic stimuli and then migrate from
the intravascular space to the interstitial space by diapedesis. End products
of this phagocytic process are carried away from the local area by the
lymphatic circulation. Neutrophils and eosinophils are end state cells and
thus further division is not possible. They act as a type of first stage cellular
defence and their duties are later augmented by the lymphocyte and the
monocyte.
Toward the end of the first week, the generalized inflammatory
response becomes more specific in nature. Increasing numbers of thymus
dependent lymphocytes (T cells) bursa equivalent lymphocytes (B cells),
killer (K) cells, natural killer (NK) cells and macrophages are found in the
wound at this time. These cells respond to foreign antigens such as bacteria
and plaque debris that have been introduced into the area during the surgical
procedure. These antigens are processed and presented to the B and T cell
populations by macrophages. Four functionally distinct T cell populations
respond and perform regulatory, inflammatory, cytotoxic and augumentary
functions resulting in a variety of effector modalities. Cellular
intercommunication is essential for effective immunoregulatory function
and this is accomplished with the release of soluble signal molecules called
lymphokines. Lymphokines are specific cytokines released from local
cellular elements that effect immunologic function.

Macrophages are the predominant phagocytic cell found in the wound
by the fifth to sixth postoperative day. These cells are derived from
circulating monocytes, which originate from the bone marrow via
monoblast differentiation. Macrophages have the ability to ingest
immunologic and non-immunologic particles by phagocytosis and attempt
to digest these particles with lysosomal enzymes. They have cell surface
receptors that are instrumental in the killing of bacteria, fungi, and tumor
cells. As mentioned previously, macrophages also process and present
foreign antigens to lymphocytes as part of the cellular immune response. In
contrast to the neutrophil, this cell is not an end state cell and thus has the
ability to undergo mitosis. Macrophages cal also fuse to form multinuclear
foreign body giant cells to ingest larger particles. The mechanism by which
they recognize and ingest non-immunologic materials, however, is not well
understood, but it has been shown that hydrophobic materials, such as
polytetrafluoroethylene and roughened plastics, are more easily taken up by
macrophages than are hydrophilic materials. In addition, it seems that
adsorbed proteins on the surface of the foreign bodies, particle size, particle
shape, surface texture and related free surface energy play some role in the
ingestion of these particles by macrophages.
The reaction of macrophages on exposure to foreign materials
depends on the physical and chemical nature of the material. In an in vitro
experiment examining the effects of particles of commonly implantable
metals on mouse peritoneal macrophage rate demonstrated that particles of
titanium, chromium and molybdenum were phagocytized and produced no
abnormal morphologic abnormalities or release of lactate dehydrogenase
(LDH). In contrast, particles of cobalt, nickel and cobalt-chromium alloy
cause marked changes in cellular morphology and release of LDH. Some
materials act directly on the macrophage, whereas other materials act
through the immunologic involvement of lymphocytes. The mechanism by

which they induce an inflammatory response is thought to be through the
release and activation of certain mediators of inflammation, including
lysosomal

enzymes, prostaglandins, complement

and

lymphokines.

Ultimately the reaction of macrophages to an implant governs the global
tissue reaction to the material. A few macrophages not associated with an
overt inflammatory response are normally located on intact implant cells
long after implantation, however, is generally problematic in nature and
suggests the presence of a chronic inflammatory reaction and probable
implant failure.
Phase Two Proliferative Phase :
Shortly after the implant is inserted into bone, the proliferative phase of
implant healing is initiated. During this phase, vascular ingrowth occurs
from the surrounding vital tissues, a process called neovascularization. In
addition, cellular differentiation, proliferation and activation occur during
this phase, resulting in the production of an immature connective tissue
matrix that is eventually remodeled. As noted previously, this phase of bone
repair begins while the inflammatory phase is still active.
During the placement of implants into their endosseous locations,
interruption of the local microcirculation occurs in the surgical areas.
Regeneration of this circulation must eventually occur if wound healing is to
begin as early as the third postoperative day. Metabolism of the local
inflammatory cells, fibroblasts, progenitor cells and other local cells creates
an area of relative hypoxia in the wound area. This results in the
development of an oxygen gradient with the lowest oxygen tension near the
wound edges. This hypoxic state combined with certain cytokines, such as
basic fibroblast growth factor (bFGF) and platelet derived growth factor
(PDGF) is responsible for simulating this angiogenesis. bFGF seems to
activate hydrolytic enzymes, such as collagenase and plasminogen, which
help to dissolve the basement membranes of local blood vessels. This

initiates the process of endothelial budding, which progresses along the
established chemotactic gradient. Once the anastomoses of the capillary
buds are developed and a local microcirculation is reestablished, the
improved tissue oxygen tension results in a curtailment of the secretion of
these angiogenic growth factors. In addition, the new circulation provides
the delivery of nutrients and oxygen necessary for connective tissue
regeneration.
Local mesenchymal cells begin to differentiate into fibroblasts,
osteoblasts and chondroblasts in response to local hypoxia and cytokines
released from platelets, macrophages, and other cellular elements. These
cells begin to lay down an extracellular matrix composed of collagen,
glycosaminoglycans, glycoproteins and glycolipids. The initial fibrous
tissue and ground substance that are laid down eventually form into a
fibrocartilaginous callus and this callus is eventually transformed into a
bone callus with a process similar to endochondral ossification. Ossification
centers begin within secretory vesicles that are liberated from the local
osteoblasts. These vesicles called matrix vesicles, are rich in phosphate and
calcium ions and also contain the enzymes alkaline phosphatase and
phospholipase A2. This callus transformation is aided by improved oxygen
tension and enhanced nutrient delivery that occurs with improvement of
local circulation. The initial bone laid down is randomly arranged (Woven
type) bone that is eventually remodeled.
In vivo studies using an optical chamber (vital chamber) implanted in
along bones of animal models have been instrumental to the understanding
of the healing process that occurs in the peri-implant space. They have
revealed that vascular ingrowth precedes ossification. Capillary ingrowth
appears initially and it matures to be a more developed vascular network
during the first three weeks after implant insertion. Ossification is initially
visualized during the first week, peaks during the third to fourth week and

arrives at a relatively steady state by the sixth to eight week. Long term
follow up (> 1 year) of these unloaded implants reveals little change from
the picture seen at the 6 to 8 week period with only some condensation of
bone and some reorientation of the vascular pattern.
Phase Three Maturation Phase :
The necrotic bone in the peri-implant space that resulted from
operative trauma must eventually be replaced with intact living bone for
complete healing to occur. Appositional woven bone is laid down on the
scaffold of dead bone trabeculae by differentiated mesenchymal cells in the
advancing granulation tissue mass. This process occurs concurrently with
the ossification of the fibrocartilaginous callus noted previously.
Simultaneous resorption of these “composite” trabeculae and the newly
formed bone, coupled with the deposition of mature concentric lamellae
eventually results in complete bone remodeling, leaving a zone of living a
zone of living lamellar bone that is continuous with the surrounding basal
bone.
Traditional placement of endosseous implants involves a two stage
surgical procedure in which the implant is placed during the first stage and
then allowed a healing period of several months before the transmucosal
portion is placed. When the superstructure is fabricated, loading of the
implants can be initiated. Bone remodeling occurs around an implant in
response to a load transmitted through the implant to the surrounding bone.
In a histopathologic comparison of loaded and unloaded implants, Donath et
al. showed that unloaded implants contacted small bone lamellae that were
interrupted by many areas of bone marrow and parts of the haversian canal
system. Loaded implants were surrounded by a more compact type of bone
with only small bone free areas near the haversian canals. The lamellae
around the implant area remodeled according to the exposed load, which
with passage of time, shows a characteristic pattern of well organized

concentric lamellae with formation of osteons in the traditional manner. The
load dependent remodeling of bone follows the same principles that govern
fracture healing.
Under normal circumstances, healing of implants is usually associated
with a reduction in the height of alveolar marginal bone. Approximately 0.5
to 1.5 mm of vertical bone loss occurs during the first year after implant
insertion. After this point, a steady state is reached and normal bone loss
occurs at a rate of approximately 0.1 mm per year. The rapid initial bone
loss can be attributed to the generalized healing response resulting from the
inevitable surgical trauma, such as periosteal elevation, removal of marginal
bone and bone damage caused by drilling. The later steady state bone loss
probably reflects normal physiologic bone resorption. Factors such as
excessive surgical trauma, excessive loading or the presence of peri-implant
inflammation may accelerate this normal resorptive process. In a
prospective review of hydroxylapatite (HA) coated implants Block and Kent
found that the presence of keratinized gingiva in the peri-implant region
strongly correlated to bone maintenance in the posterior mandibular region.
Thus, if excessive losses of marginal bone are noted, one must consider the
possibility of inappropriate loading of the implant or the presence of periimplant inflammation and step should be taken to rectify the problem before
excessive implant support is lost.
MUCOPERIOSTEAL HEALING :
Implants are placed into their endosteal position through incisions in
the mucoperiosteum. They can be placed using a one stage technique, in
which the endosteal and transmucosal portions of he implant are allowed to
heal as a single unit, or a two staged technique, in which the endosteal
component is placed initially followed some time later by the placement of
the transmucosal portion after a period of healing. Healing of the
mucoperiosteal complex around implants is of paramount importance for the

longevity of prosthetic reconstructions. An understanding of the biologic
processes involved in generalized wound repair and how soft tissue wounds
heal around implant fixtures is vital information for appropriate
management of implant patients. As in the previous section on bone healing,
there are also three phases of wound healing in soft tissue wounds :
inflammatory, proliferative and maturation phases. In addition, there is also
significant overlap between these phases as they pertain to mucoperiosteal
wound healing.
Phase one inflammatory phase :
The inflammatory phase of wound healing for the mucoperiosteal
complex is essentially the same as that mentioned in the previous section on
bone healing. It involves an initial vascular response followed by platelet
aggregation and activation, the clotting cascade and then an initial nonspecific cellular inflammatory response consisting of infiltrates of
predominantly neutrophils. This is followed shortly thereafter by a more
specific cellular inflammatory response consisting of infiltrates of
predominantly neutrophils. This is followed shortly thereafter by a more
specific cellular inflammatory response marked by increased number of
lymphocytes and macrophages. Cytokines also play an important role in the
healing of soft tissue wounds.
Phase two proliferative phase :
The proliferative phase of wound healing begins within hours of the
injury and is characterized by the establishment of an active population of
epithelial and connective tissue cells and the beginning of he
reestablishment of wound integrity. Migration and proliferation of epithelial
cells is seen within the first 24 to 48 hours of wound healing. The stimulus
for growth and migration of thee cell results from loss of contact inhibition
and from a temporary decrease in the local level of tissue specific growth
inhibitors called chalones. A watertight seal is usually established within the

first 24 hours after primary wound closure, but little structural strength is
provided by the seal.
The main connective tissue cell involved in the proliferative phase of
soft tissue wound healing is the fibroblast. Differentiation of mesenchymal
cells and proliferation and migration of the preexisting population of local
fibroblasts occur as a result of hypoxia and the release of cytokines from
local

cellular

elements,

including

platelets

and

macrophages.

Neovascularization provides the foundation for fibroblastic proliferation by
supplying the local area with the nutritional support required to maintain
this enhanced metabolic state. Fibroblasts produce ground substance,
collagen and elastic fibers. The major components of ground substance are
proteoglycans

and

glycoproteins.

Glycoproteins

are

adhesive

macromolecules. They interact with cells and constituents of the
extracellular matrix that interact with cells to promote adhesion, migration
and proliferation and alter gene expression. Proteoglycans are large
molecules composed of protein cores to which are attached side chains of
glycosaminoglycans, which are polysaccharide chains formed from
repeating disaccharide units. Proteoglycans are classified according to their
dominant disaccharide unit and include hyaluronate, chondroitin, dermatan,
keratin and heparin. These molecules retain water and form bulky gels that
fill most of the extracellular space. The major proteoglycan in connective
tissues early in inflammation is hyaluronic acid. Its concentrations decrease
after the fifth day simultaneously with an increase in concentrations of other
proteoglycans, dermatan sulfate and chondroitin-4 sulfate, the collective
function of all of the elements of the ground substance, among other things
includes the binding of connective tissue elements, stabilization and
facilitation of collagen maturation and facilitation of cellular function.
Collagen and elastic fibers, the major protein structures in connective
tissues are also produced by the fibroblast. Collagen formation is

microscopically detected between the fourth and sixth days, but biochemical
evidence of collagen formation is noted between the second and fourth days.
During the formation of collagen, three polypeptide chains are produced and
hydroxylated which occurs under the influence of propyl hydroxylase,
which is an enzyme that requires vitamin C, molecular oxygen, ferrous iron
and  - ketoglutarate as cofactors for proper function. These molecules and
the combined to form a triple helix called procollagen. After glycosylation,
procollagen is secreted from a triple helix called procollagen. After
glycosylation, procollagen is secreted from the cell and the terminal
telopeptides are then cleaved by an enzyme, procollagen peptidase, which is
also secreted by the fibroblast. The resultant molecule, tropocollagen
combines with other tropocollagen molecules to form collagen fibrils and
the collagen fibrils are then combined to form collagen fibers. These
structures are stabilized by intermolecular and intramolecular cross linkages.
Elastic fibers are also produced in a similar fashion. Tropoelastin molecules
and secreted from the fibroblast and the resultant elastin molecules are
combined with microfibrillar proteins to form elastic fibers. Elastin is a
hydrophobic protein that provide resiliency to tissues that allows them to
stretch and return to their original form.
The proliferative phase of wound healing is marked by cellular
proliferation and synthetic activity. Collagen degradation by collagenases
secreted from fibroblasts, epithelial cells, neutrophils and macrophages,
occurs simultaneously with collagen synthesis, but the net effect during the
proliferative phase of wound healing is in favour of collagen deposition.
Termination of this phase of wound healing marked by an increase in local
collagen content and a decrease in the number of local fibroblasts. Collagen
content of the wound rises rapidly between the 6 th and the 17th day but
increases only slightly between the 17th day and the 42nd day. At the
beginning of this phase, the tensile strength of the wound is provided by

epithelialization, blood vessel growth and aggregation of proteins. Collagen
deposition increases the tensile strength significantly during this phase and
the magnitude is proportional to the collagen content of the tissues.
Phase three maturation phase :
During the final phase of wound healing, maturation of the deposited
collagen occurs. There is no sharp demarcation between the end of the
proliferative phase and the beginning of the maturation phase because
collagen maturation occurs continuously shortly after initial deposition.
Collagen deposited during earlier phases of wound healing shows a non
purposeful arrangement. Even though the collagen content of wound may be
near maximal levels after 3 weeks of wound healing, the bursting strength of
the wound in on about 15% of the normal skin level at this time. As time
proceeds however, the unorganized fibrils are replaced larger, thicker and
better organized fibers, with the final result being one of ‘lacing” the wound
edges together with a three dimensional weave. This is made possible by the
continuous turnover of collagen by fibroblasts with balanced synthesis and
degradation. Improvement in strength of the wound is thus possible without
an increase in total collagen content. The bursting strength of the wound is
noted to improve dramatically from 3 to 9 weeks, reaching a level of 70% of
normal skin by the end of this period. By 6 months, the bursting strength of
the wound is approximately 90% of the level of normal skin. It must be
noted, however, that the bursting strength of a wound plateaus after this
period and does not usually reach that of the original tissue.
IMPLANT TISSUE INTERFACE :
 It consists of implant and bone interface.
 Implant and connective tissue interface.

 Implant and epithelium interface.
Implant and bone interface :
On observing the implant and bone interface at the light microscopic
level (100X) it shows that close adaptation of the regularly organized bone
next to the Ti implants.
Scanning electron microscopic study of the interface shows that
parallel alignment of the lamellae of haversian system of the bone next to
the Ti implants. No connective tissue or dead space was observed at the
interface. Ultra microscopic study of the interface (500 to 1000X) shows
that presence of amorphous coat of glycoproteins on the implants to which
the collagen fibers are arranged at right angles and are partly embedded into
the glycoprotein layer.
Mechanism of attachment :
As a general rule cells do not bind directly to the foreign materials.
The cells binds to each other or any other foreign materials by a layer of
extracellular macro molecules (glycoproteins).
The glycoprotein layer in between the cells or in between the tissues
will be at a thickness of 10 to 20 nm (100 to 200 A0).
At the interface the glycoprotein layer of normal thickness (10-20
nm) is adsorbed on the implant surface within the help of adhesive
macromolecules like Fibronectin, Laminin, Epibiolin, Epinectin, Vitronectin
(serum spreading factor), Osteopontin, thrombospodin and others. At the
molecular level the macromolecules contains Tri-peptides made up of
Arginin-glycin-Aspertic acid (RGD). The cells like fibroblasts and other
connective tissue cells contain binding elements called as “integrins”. The
integrins recognizes the RGDs and bind to them.
The macromolecules are adherent more firmly to the metallic oxide
layer on the Ti implants. The mode of attachment between the oxide layer

and the macromolecules may be of covalent bonds, ionic bonds or van-derwalls bonding.
Implant connective tissue interface :
The connective tissue above the bone attaches to the implant surface
in the similar manner as that of the implant bone interface. The supra crestal
connective tissue fibers will be arranged parallel to the surface of the
implant. Because of this type of the attachment the interface between the
connective tissue and implant is not as strong as that of the connective tissue
and tooth interface. But the implant connective tissue interface is strong
enough to withstand the occlusal forces and microbial invasions.
Implant epithelial interface :
The implant epithelial interface is considered as Biologic seal by
many authors. At this interface the glycoprotein layer is adherent to the
implant

surface

to

which

hemidesomosomes

are

attached.

The

hemidesmosomes connect the interface to the plasma membrane of the
epithelial cells. Because of this attachment the implant epithelial interface is
almost similar to the junctional epithelium. For the endosseous implants the
sulcus depth varies from 3 to 4mm.
Factors of importance to ensure a reliable bone anchorage of an
implanted device :
In most cases whenever an implant is inserted in bone, healing will
dependent on the conditions like adequate cells, nutrition to these cells and
adequate stimuli for repair. However, bone tissue is different from soft
tissue in some aspects. In the first place bone will at least under ideal
conditions, heal without any scar formation due to ongoing creeping
substitution that will gradually replace the bone with newly formed hard
tissue. Secondly, even if the repair process is disturbed so that no (or very
little) healing ensures, the dead bone may (like a dead branch of a tree) still
be capable of carrying some loads and thereby contribute to function. This

may in clinical practice be the case in many hip and knee arthroplasties.
Such replacements may tolerate the load put upon them by an elderly
patient, but not the more heavy stress likely in young individuals where the
results are much less good than with senior citizens. The delicate balance
between bone formation and bone resorption may be exemplified through
the known coupled function between bone cellular elements of opposing
function such as osteoblasts and osteoclasts. Many authors claim that the
one cell will need the other to be in an active state. This is further
exemplified in the creeping substitution process.
Even if osseointegrated implants have been documented to result in
excellent long-term results, this does not necessarily imply that every
implant system claimed to be dependent on osseointegration will result in an
acceptable clinical outcome. On the contrary, there are several reasons for
primary as well as secondary failure of osseointegration. These failures may
be attributed to an inadequate control of the six different factors known to
be important for the establishment of a reliable, long-term osseous
anchorage of an implanted device. These factors are :
1. Implant biocompatibility
2. Design characteristics
3. Surface characteristics
4. The state of the host bed
5. The surgical technique and
6. The loading conditions
There is a need to control these factors more or less simultaneously
to achieve the desirable goal of a direct bone anchorage.
IMPLANT BIOCOMPATIBILITY :
With respect to metals, commercially pure (c.p) titanium, niobium
and possibly tantalum are known to be most well accepted in bone tissue. In
the case of c.p. titanium, there is likewise a documented positive long term

function. The reason for the good acceptance of these metals does probably
relate to the fact that they are covered with a very adherent, self-repairing
oxide layer which has an excellent resistance to corrosion. Whereas the load
bearing capacity of c.p. titanium is sufficiently documented in the case of
oral implants, there is less known about niobium in this aspect. Other metals
such as different cobalt-chromoe-molybdenum alloys and stainless steels
have demonstrated less good take in the bone bed, but it is uncertain if this
is valid for every possible such alloy and if it is biocompatibility effect
alone that is responsible for their less satisfactory incorporation into bone,
compared with c.p. titanium. A significantly impaired interfacial bone
formation compared to c.p. titanium has been found with titanium-6
aluminium-4 vanadium alloy, probably dependent on a less good
biocompatibility of the alloy. One concern with metal alloys is that one
alloy component may leak out in concentrations high enough to cause local
or systemic side effects. Ceramics such as the calcium phosphate
hydroxyapatite (HA) and various types of aluminium oxides are proved to
be biocompatible and due to insufficient documentation and very less
clinical trials, they are less commonly used. With respect to HA, the
available literature points to at least a short term (<10 weeks) enhanced
interfacial bone formation in comparison to various reference metals. This
represents a potential clinical benefit of HA, whereas the risk or coat
loosening with subsequent problems represents a potential risk.
IMPLANT DESIGN (MACRO STRUCTURE) :
There is at present, sufficient long-term documentation only on
threaded types of oral implants that have been demonstrated to function for
decades without clinical problems. However, unthreaded implants may
function too, even if there is a total lack of positive documentation with
respect to bone saucerisation, a problem that caused failure of many early
types of oral implants. With currently used cylindrical implants, many

authors reported more severe bone resorption than would have been
expected with certain screw designs. It must be observed that there are other
unthreaded implant designs that may give an excellent long term clinical
result.
The threaded implants provide more functional area for stress
distribution than the cylindrical implants. The design of the threads may
also influence the long term osseointegration. For e.g. V-shaped thread
transfer the vertical forces in a angulated path, may not be efficient in stress
distribution as that of the square shaped threads.
IMPLANT SURFACE (MICRO STRUCTURE, SURFACE
TOPOGRAPHY) :
With respect to the surface topography there is clear documentation
that most smooth surfaces do not result in an acceptable bone cell adhesion.
Such implants do therefore end up as being anchored in soft tissue despite
the material used. Clinical failure would be prone to occur. Some
microirregularities seem to be necessary for a proper cellular adhesion even
if the optimal surface topography remains to be described. With a gradual
increase of the surface topographical irregularities, problems due to an
increased ionic leakage are prone to occur. With plasma sprayed titanium
surfaces for instance, more than 1600 ppm titanium has been reported in
implant adjacent haversian systems, probable resulting in an impairment of
osteogenesis.
Another surface parameter is the energy state where a high surface
energy has been regarded as positive for implant take due to an alleged,
improved cellular attachment. One practical way of increasing the surface
energy is the use of glow discharge (plasma cleaning). However, published
reports have not been able to confirm the superiority of so artificially
enhanced implant energy levels. One reason for this lack of confirmation of
the surface energy hypothesis could be that the increased surface energy

would disappear immediately when the implant makes in contact with the
host tissues.
Many researchers recommended various procedures for improving the
surface energy or surface characteristics of the implants to improve the
osseointegration. Stefini C.M. et al. (2000) recommended to apply platelet
derived growth factor and insulin like growth factors on the implant surface
before placing into the cervical bed. According to their results this method
showed better wound healing and rapid integration.
Musthafa K. et al (2000) reported to sand blast the titanium implants
with titanium oxide particles (45-90) to achieve higher rate of cell
attachment.
Other authors like Lima Y.J. et al. (2001) and Orsini Z. et al. (2000)
reported to perform acid etching of the titanium implants by hydrofluoric
acid, aqueous nitric acid and sodium hydroxide to reduce the contact angle
less than 100 for better cell attachment and utilization of 1% hydrofluoric
acid + 30% nitric acid to clean the implant surface and to remove the
alumina particles after sand blasting which improves the osseointegration.
Nishiguchi S. et al (2001) reported to provide alkali + heat treatment
to improve the amount of bone bonding, i.e. 5 mol/lt NaOH at 60 0C for 24
hours and 6000C for 1 hour (Dog study).
Rich and Harris presented some of the salient features of fibroblasts
during healing i.e. Rugophalia: attracted towards rough surfaces,
Haptotaxis: the directional cell movement that depends upon adhesive
gradients on the substratum, Contact guidance : the tendency of the cells to
be guided in their direction of locomotion by the shape of substratum. These
properties denotes that the implant fixture with rough surface topography
and more surface energy promotes faster and complete osseointegration.

STATE OF THE HOST BED :
If available, the ideal host bed is healthy and with an adequate bone
stock. However, in the clinical reality, the host bed may suffer from
previous irradiation, ridge height resorption and osteoporosis, to mention
some undesirable states for implantation. Previous irradiation need not be an
absolute contraindication for the insertion of oral implants. However, it is
preferable that some delay is allowed before an implant is inserted into a
previously irradiated bed. Furthermore, some 10-15% poorer clinical results
must be anticipated after a therapeutical dose of irradiation. The explanation
for less satisfactory clinical outcome found in irradiated beds could be
vascular damage, at least in part. One attempt to increase the healing
conditions in a previously irradiated bed is by using hyperbaric oxygen, as a
low oxygen tension definitely has negative effects on tissue repair. This is
further verified by the finding that heavy smoking, causing among other
things a local oral vasoconstriction, is one factor that will lower the
expected outcome of an implantation procedure.
Other common clinical host bed problems involve osteoporosis and
resorbed alveolar ridge. Such clinical states may constitute an indication for
ridge augmentation with bone grafts. However, present clinical technique
for bone grafting are under debate and it appears that 6-year success of oral
implants in the 75% range is a realistic outcome after most such procedures.
This figure is slightly alarming seen against the fact that, at least in the
maxilla, 10-20% of an average edentulous population may be in need of a
bone graft to improve the host bed and allow for the insertion of implants.
On the contrary, if the bone quality and quantity in the maxilla is controlled,
the expected outcome of an oral implantation procedure is similar to that of
the mandible.
As stated by Branemark et al. and Misch, the bones with D1 and D2
bone densities shows good initial stability and better osseointegration. The

bone densities D3 and D4 shows poor prognosis. Many authors have
recommended to select suitable implants depending upon the quality and
quantity of the available bone, i.e., HA coated or Ti plasma coated implants
are better for D3 and D4 and conventional threaded implants for D1 and D2
bone qualities.
SURGICAL CONSIDERATIONS :
The main aim of the careful surgical preparation of the implant bed is
to promote regenerative type of the bone healing rather than reparative type
of the bone healing. If too violent a surgical technique is used, frictional
heat will cause a temperature rise in the bone and the cells that should be
responsible for bone repair will be destroyed. Bone tissue is more sensitive
to heat than previously believed. In the past the critical temperature was
regarded to be in the 560C range, as this temperature will cause denaturation
of one of the bone enzymes, alkaline phosphatase. However, the critical
time / temperature relationship for bone tissue necrosis is around 47 0C
applied for one minute. At a temperature of 500C applied for more than one
minute we are coming close to a critical level where bone repair becomes
severely and permanently disturbed. This critical temperature should be
seen against observed frictional heat at surgical interventions. In the
orthopaedic field, despite adequate cooling, temperatures of 900C have been
measured. High drilling temperatures in the dental field are to be expected
when drilling, particularly in the dense mandible.
Erickson R.A. recommended the importance of using well sharpened
drills, slow drill speeds, a graded series of drills (avoid making, for instance,
a 4mm hole in one step) and adequate cooling by profuse irrigation. By
using such a controlled technique it has been demonstrated in clinical
studies that overheating may be totally avoided. The mechanical injury will
of course remain and is quite sufficient to trigger a proper healing response.

Erickson also recommended bone cutting speed of less than 2000 rpm and
tapping at a speed of 15 rpm with irrigation.
Hence, the surgical preparation sequences as well as the instruments
depend upon the quality of the bone as shown in the diagram.
Another surgical parameter of relevance is the power used at implant
insertion. Too strong a hand will use in bone tension and a resorption
response will be stimulated. This means that the holding power of the
implant will fall to dangerous levels after a strong insertion torque. A
moderate power at the screwing home of an implant is therefore
recommended. With other implant designs there may be a need for
implantation of the implant at insertion and other rules may apply.
Surgical fit of the fixture : The accurate fit consists of more surface
contact, less dead space and thus better healing.
LOADING CONDITIONS :
From histological investigations of animal as well as human implants
we know that, irrespective of control of surgical trauma and other relevant
parameters, the implant will, in the early remodeling phase, be surrounded
by soft tissue. This means that some weeks after implant insertion it will be
particularly sensitive to loading that results in movements, as movement
will stimulate more soft tissue formation, leading eventually to a permanent
soft tissue anchorage. In essence, the situation is similar to that of a fracture.
Loading of an unstabilized fracture will result in soft tissue healing and poor
function, whereas stabilization with plates or plaster of Paris will ensure a
satisfying rigidity leading to bone healing of the fracture. The case of an
implant is, in principle, very similar. Premature loading will lead to soft
tissue anchorage and poor long-term function, whereas postponing the
loading by using a two stage surgery will result in bone healing and positive
long term function. The length of time loading should be avoided is
dependent on the implantation site as well as on the bone bed quality.

Furthermore, there may be cases where an almost immediate loading would
not disturb the bone healing response, but in general loading must be
controlled if osseointegration is to occur. Branemark with his controlled
implant system advocated the use of a 3 month loading delay in the
mandible and a 4-6 month delay in the healthy maxilla where the bone is, as
a rule, more cancellous in character. However, these precise unloaded times
are empirically based and to the knowledge of the author there are no
published studies comparing different unloaded periods and relating this to
implant success. Furthermore, from a bone biologic point of view a more
suitable design would be to have the implant unloaded and then gradually
increase the load in the manner of the Sarmiento technique for functional
braces in fracture healing. In the similar way Misch et al. recommended
progressive loading criteria or staged loading and implant protective
occlusion for better maturation of the bone surrounding the implants. The
problem in the case of oral implants is how properly to define to the patient
how a gradual increase of load should be controlled ; a complicated task not
the least since the appropriate loading pattern also depends on individual
patients factors.
Recently, many authors are reporting the results of immediate loading
of the endosseous implants. According to them the physiological loading of
the healing implants promotes better osseointegration.
Sagara et al (1993) also showed evidence of osseointegration when
titanium screw implants were immediately loaded with a unilateral
prosthesis. Their findings showed that osseointegration did occur, although
the immediately loaded implants exhibited less direct bone contact than with
the delayed loading which were used as controls.
Salama et al (1995) reported on two patients in whom titanium root
form implants were immediately loaded and successfully utilized to support
provisional fixed restoration in the maxilla and mandible. Both the patients

were followed from 37 to 40 months after implant placement and immediate
loading. All implants osseointegrated and were restored with a fixed
prosthesis.
Babbush and co-workers (1986) showed implant success rate of 88%
to 97% over 5 to 13 years with immediate loading implants.
Lederman

and

colleagues

(1998)

histologically

confirmed

osseointegration with 70% to 80% bone to implant contact in a mandibular
symphysis necropsy specimen after 12 years of implant and prosthesis
function in a 95 year old patient.
Peitelli and colleagues (1997) found significantly greater bone-toimplant contact in 24 immediately loaded mandibular implants compared
with 24 unloaded.
THE SUCCESS CRITERIA (ALBERKTSSON ET AL) :
1) The individual unattached implant should be immobile when tested
clinically.
2) The radiographic evaluation should not show any evidence of
radiolucency.
3) The vertical bone loss around the fixtures should be less than 0.2 mm per
year after first year of implant loading.
4) The implant should not show any signs of pain, infection, neuropathies,
parasthesia, violation of mandible canals and sinus drainage.
5) The success rate of 85% at the end of 5 year and 80% at the end of 10
service.
METHODS OF EVALUATION OF OSSEOINTEGRATION :
Invasive methods :
1) Histological sections (10 microns sections).
2) Histomorphometric – to know the percentage of bone contact.
3) Transmission electron microscopy
4) By using torque gauges

5) Pull out tests.
The invasive methods are usually used in the animal experiments.
Non-invasive methods :
1) Tapping with a metallic instruments : The fixture produces ringing
sound, it osseointegrated, produces dull sound if fibrous integration.
2) The radiographs
3) Perio test : Checks mobility and damping system.
Normal values : -5 to + 5 PTV
4) Dental fine tester : evaluates the mobility, should be less than 5.
5) Reverse torque test with 20 N cm.
6) Resonance frequency analysis : this method gives the idea of amount,
rate of osseointegration. This method can be utilized for healing or
failing implants.
SCOPE OF THE OSSEOINTEGRATION :
The osseointegrated endosseous implants are utilized for providing
the prosthesis or stabilizing the various structure of the body. A schematic
representation of the scope of the osseointegration is depicted in the
diagram.

CONCLUSION :
The “osseointegration” is a multifactorial entity. Achieving the
osseointegration of the endosteal dental implants needs understanding of the
many clinical parameters.

BIBLIOGRAPHY :
1)

Osseointegration in clinical dentistry – Branemark, Zarb, Albrektsson

2)

Osseointegration and occlusal rehabilitation – Sumiya Hobo

3)

Contemporary Implant Dentistry – Carl. Misch

4)

Endosseous implants for Maxillofacial reconstruction – Block and Kent

5)

Implants in Dentistry –Block and Kent

6)

Dental and Maxillofacial Implantology – John. A. Hobkrik, Roger
Watson

7)

Endosseous Implant : Scientific and Clinical Aspects – George Watzak

8)

Optimal Implant Positioning and Soft Tissue management – Patrik
Pallaci

9)

Osseointegration in craniofacial reconstruction. T. Albrektssson.

10) Osseointegration in dentistry : an introduction : Philip Worthington,
Brein. R. Lang, W.E. Lavelle.
11) Effect of implant surface topography on behaviour of cells –D.M.
Brunette IJOMI 1988 ; 3 : 231-246
12) Implant stability assessment – Neil M. IJP, 1998 ; 5 : 491-500.
13) Osseointegration and its experimental background. P.I. Branemark.
JPD, 1983, 50 : 399-410.
14) D.C.N.A., 1986 ; 10-34, 151-160
15) D.C.N.A., 1992 ; 36, 1-17
16) Structural aspects of the interface between tissue and Titanium
implants. K.A. Hanson, T. Albrektsson. JPD, 1983 ; 50 : 108-113.
17) Biocompatibility of Titanium Implants. B. Kasemo. JPD, 1983;
50:832-37.
18) Direct Bone Anchorage. T. Albrektsson et al. IJP, 1990 ; 3 : 30-41.
19) Mechanism of Osseointegration. J.E. Davis. IJP, 1998 ; 11 :391-401.
20) The attachment mechanism of epithelial cells. T.R.L. Gould. J. Perio.
Rest 1981 ; 16 : 611-616.

21) The effects of early occlusal loading on one stage titanium alloy
implants in beagle dogs : A pilot study : Sagara. M, Ahagawa Y, Nikai.
H, Tsuru. H, JPD 1993 ; 69 : 281-288.
22) Immediate loading of bilaterally splinted titanium root form implants in
fixed prosthodontics : Salama.K, Rose EF, Salama.M, Betts. N.J ; Int J.
Periodont Rest Dent 1995 ; 15 : 345-361.
23) Titanium plasma sprayed screw implants for reconstruction of the
edentulous mandible : Bubbush C.A, Kent J.N, Wislik DJ ; J Oral
Maxillofac Surg. 1986 ; 144 : 274-282.
24) Long-lasting osseointegration of immediate located, bar-connected TPS
screws after 12 years of function : A histologic case report of a 95- year
old patient : Ledermann PD ; Int J Periodont Restorative Dent 1998 ;
18 : 553-563.
25) Immediate loading of titanium plasma sprayed screw-shaped implants
in man : A clinical and histological report of two cases: Peattelli A,
Corigliano M, Scrano A ; J Periodontal 1997 ; 68 : 591-597.

CONTENTS
 INTRODUCTION
 HISTORY OF OSSEOINTEGRATION
 DEFINITIONS AND OTHER TERMINOLOGIES
 MECHANISM OF OSSEOINTEGRATION
 INFLAMMATORY PHASE
 PROLIFERATIVE PHASE
 MATURATIVE PHASE
 FACTORS RESPONSIBLE FOR OSSEOINTEGRATION
 MATERIAL BIOCOMPATIBILITY
 IMPLANT DESIGN : MACRO STRUCTURE
 IMPLANT SURFACE : MICRO STRUCTURE
 STATE OF HOST BED
 SURGICAL CONSIDERATIONS
 LOADING CONDITIONS
 CLINICAL EVALUATION OF OSSEOINTEGRATION
 SCOPE OF OSSEOINTEGRATION
 CONCLUSION
 REFERENCES

DEPARTMENT OF PROSTHODONTICS
INCLUDING CROWN AND BRIDGE
COLLEGE OF DENTAL SCIENCES
DAVANGERE

SEMINAR ON

OSSEOINTEGRATION

Presented By
DR. NITIN GAUTAM
(2001 – 2002)

Copy of osseointegration/certified fixed orthodontic courses by Indian dental academy

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