INTRODUCTION :

Since tooth loss from disease and trauma has always been a feature of
mankinds 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. he 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 :
!mplants 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. !n most cases, loading leads to gradual widening
of fibrous tissue layer and loosening of implant, with conse"uent implant
failure. !n contrast to periodontal ligament, a fibrous tissue sheath is a
poorly differentiated layer of scar tissue.
#r. $er !ngvar %ranemark, an anatomist is credited as the person who
has coined the term &osseointegration'. %ranemark along with his team was
working in the laboratory of the vital microscopy ()*+,-, laboratory of
experimental %iology, .niversity of /oteberg Sweden, ()*01-, !nstitute of
2pplied biotechnology, /oteberg ()*34-. he main study of his group was
to understand the mechanism of bone healing and bone response to the
thermal, mechanical, chemical in5uries by using vital microscopy.
6ital microscopy, is a type of the miniature microscope, which is
introduced in to the living organisms. E.g. 7abbit in their study the titanium
(i- chambers were used for placing the vital microscope into the rabbits
fibula. 2fter 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. 8hile recovering %ranemark observed that the i chambers were
firmly adherent to the bone. %y this observation they concluded that the
titanium was firmly integrated to the bone and later they used i screws and
i bars for reconstruction of the long bones and mandibles of the dogs.
2fter ensuring the favourable bone response to the i, the team tried
to replace the teeth for the dogs. he i implants also showed good response
for the mucosa and skin penetrating implants. he implants, which used for
replacement of the teeth in the dogs showed good integration upto )1 years
and the implants could bear the load of upto )11 9gs without failure at the
bone:implant interface. %y observing this property the integration between
the bone and i screws was termed as &osseointegration'.
he i vital microscopic chambers were used to analyze
microcirculation in the healthy and diabetic human volunteers without any
signs of inflammation around the i chamber. !n )*0+, first human
edentulous patient was treated by using the i screws (implants- by
reconstruction of resorbed edentulous arches using autologus tibial bone
grafts.
The salient features of Branemar an! his team"s #or
2bout more than +1 designs of i screws (!mplants- were tested
and used.
he surgical protocol followed was ; two stage surgery, which was
proved beneficial.
<inimal trauma during the surgery results in bone regeneration
rather than bone repair at the implant site.
=on:contaminated implants (sterile and clean implants- proved
good integration.
$rosthesis and abutments were screw attached for more technical
flexibility.
here were more mechanical failures at the interface rather than
biological failures.
<r. 6ictor 9uikka helped in designing the hardware parts in this
study. !n the longitudinal study of the i implants from )*0+ to )*3>
showed a success rate of **? in mandibles and 4*? in maxilla.
!n the mean time Schroeder et al. ()*31-, the members of the
international team for development of oral implants (!..!- studied the i
plasma sprayed @p i cylindrical implants in <onkey models and achieved
the firm integration between the implant and the tissues. !n their study the
bone was 5oined to implant by fine bridges of fibrous tissue. hey termed
this union as functional ankylosis.
DEFINITION AND OTHER TER$INO%OGIES :
Osseointe&ration :
%ranemark defined it &as a direct contact between the bone and
metallic implants, without interposed soft tissues layers' ()*0*-.
Aater it is modified &as a direct structural and functional connection
between ordered, living bone and the surface of a load carrying implant'
()*33-. BStructurally oriented definitionC
Ameri'an A'a!em( of Im)lant Dentistr( *+,-./ :
@ontact 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.
<effert et al. ()*43- Subdivided into
A!a)ti0e Osseointe&ration : Dsseous tissue approximating the surface of
the implant without apparent soft tissue interface at light microscopic level.
Biointe&ration : !s a direct biochemical bone surface attachment confirmed
at electron microscopic level.
1ar2 an! T3 Al2retsson *+,,+/ : !t is a process whereby clinically
asymptomatic rigid fixation of alloplastic materials is achieved and
maintained, in bone during functional loading.
S'hroe!er et al *+,45"s/ ; @oined the term &Functional 2nkylosis'.
Bhe Swiss 2cademyC
Other Terminolo&ies :
Osteo)reser0ation *Stallar! R3E3/ :
!t 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. !t limits the
further bone resorption.
.sed in case of plateEblade form endosseous implants and endodontic
stabilizers.
6eriosteal inte&ration :
!t 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.
$ECHANIS$ OF OSSEOINTEGRATION :
2fter the surgical placement of implants into endosteal location, the
traumatized bone around these implants begins the process of wound
healing. 2s mentioned previously, it can be separated into the inflammatory
phase, the proliferative phase, and the maturation phase. his is summarized
in able along with some of the specific aspects of bone healing during
these stages.
6hase one inflammator( )hase :
he placement of implants into bone involves the creation of an
osseous defects with the subse"uent 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.
!n 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. 8hen the implant is
exposed to the surgical site, it comes to contact with extracellular fluid and
cells. his 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.
$latelet 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. %lood 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. 2ctivation of the clotting cascade also leads
to the formation of bradykinin, which is a strong mediator of vasodilation
and endothelial permeability.
#uring this initial implant host interaction, numerous cytokines
(growth factors- are release from the local cellular elements. hese
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. able >., lists some of the cystokines
believed to be important in tissue implant integration. hese 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.
he next events noted to occur during this phase of wound healing
consist of a cellular inflammatory response. !nitially, it is nonspecific in
nature and consists mainly of neutrophil emigration into the area of
damaged tissue. !ts duration is variable but generally peaks during the first F
to > days following surgery. he role of this cell is primarily phagocytosis
and digestion of debris and damaged tissue. =eutrophils are accompanied by
smaller numbers of eosinophils. Eosinophils have a similar phagocytic
function and they can also digest antigen antibody complexes. hese 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. =eutrophils and eosinophils are end state cells and
thus further division is not possible. hey act as a type of first stage cellular
defence and their duties are later augmented by the lymphocyte and the
monocyte.
oward the end of the first week, the generalized inflammatory
response becomes more specific in nature. !ncreasing numbers of thymus
dependent lymphocytes ( cells- bursa e"uivalent lymphocytes (% cells-,
killer (9- cells, natural killer (=9- cells and macrophages are found in the
wound at this time. hese cells respond to foreign antigens such as bacteria
and pla"ue debris that have been introduced into the area during the surgical
procedure. hese antigens are processed and presented to the % and cell
populations by macrophages. Four functionally distinct cell populations
respond and perform regulatory, inflammatory, cytotoxic and augumentary
functions resulting in a variety of effector modalities. @ellular
intercommunication is essential for effective immunoregulatory function
and this is accomplished with the release of soluble signal molecules called
lymphokines. Aymphokines are specific cytokines released from local
cellular elements that effect immunologic function.
<acrophages are the predominant phagocytic cell found in the wound
by the fifth to sixth postoperative day. hese cells are derived from
circulating monocytes, which originate from the bone marrow via
monoblast differentiation. <acrophages have the ability to ingest
immunologic and non:immunologic particles by phagocytosis and attempt
to digest these particles with lysosomal enzymes. hey have cell surface
receptors that are instrumental in the killing of bacteria, fungi, and tumor
cells. 2s mentioned previously, macrophages also process and present
foreign antigens to lymphocytes as part of the cellular immune response. !n
contrast to the neutrophil, this cell is not an end state cell and thus has the
ability to undergo mitosis. <acrophages cal also fuse to form multinuclear
foreign body giant cells to ingest larger particles. he 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. !n 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.
he reaction of macrophages on exposure to foreign materials
depends on the physical and chemical nature of the material. !n 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
(A#G-. !n contrast, particles of cobalt, nickel and cobalt:chromium alloy
cause marked changes in cellular morphology and release of A#G. Some
materials act directly on the macrophage, whereas other materials act
through the immunologic involvement of lymphocytes. he 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.
.ltimately the reaction of macrophages to an implant governs the global
tissue reaction to the material. 2 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.
6hase T#o 6roliferati0e 6hase :
Shortly after the implant is inserted into bone, the proliferative phase of
implant healing is initiated. #uring this phase, vascular ingrowth occurs
from the surrounding vital tissues, a process called neovascularization. !n
addition, cellular differentiation, proliferation and activation occur during
this phase, resulting in the production of an immature connective tissue
matrix that is eventually remodeled. 2s noted previously, this phase of bone
repair begins while the inflammatory phase is still active.
#uring the placement of implants into their endosseous locations,
interruption of the local microcirculation occurs in the surgical areas.
7egeneration of this circulation must eventually occur if wound healing is
to begin as early as the third postoperative day. <etabolism of the local
inflammatory cells, fibroblasts, progenitor cells and other local cells creates
an area of relative hypoxia in the wound area. his results in the
development of an oxygen gradient with the lowest oxygen tension near the
wound edges. his hypoxic state combined with certain cytokines, such as
basic fibroblast growth factor (bF/F- and platelet derived growth factor
($#/F- is responsible for simulating this angiogenesis. bF/F seems to
activate hydrolytic enzymes, such as collagenase and plasminogen, which
help to dissolve the basement membranes of local blood vessels. his
initiates the process of endothelial budding, which progresses along the
established chemotactic gradient. Dnce 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. !n addition, the new circulation provides
the delivery of nutrients and oxygen necessary for connective tissue
regeneration.
Aocal 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. hese
cells begin to lay down an extracellular matrix composed of collagen,
glycosaminoglycans, glycoproteins and glycolipids. he 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. Dssification
centers begin within secretory vesicles that are liberated from the local
osteoblasts. hese vesicles called matrix vesicles, are rich in phosphate and
calcium ions and also contain the enzymes alkaline phosphatase and
phospholipase 2,. his callus transformation is aided by improved oxygen
tension and enhanced nutrient delivery that occurs with improvement of
local circulation. he initial bone laid down is randomly arranged (8oven
type- bone that is eventually remodeled.
!n 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. hey have
revealed that vascular ingrowth precedes ossification. @apillary ingrowth
appears initially and it matures to be a more developed vascular network
during the first three weeks after implant insertion. Dssification 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. Aong term
follow up (H ) year- of these unloaded implants reveals little change from
the picture seen at the 0 to 4 week period with only some condensation of
bone and some reorientation of the vascular pattern.
6hase Three $aturation 6hase :
he 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. 2ppositional woven bone is laid down on the scaffold
of dead bone trabeculae by differentiated mesenchymal cells in the
advancing granulation tissue mass. his 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.
raditional 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. 8hen the superstructure is fabricated,
loading of the implants can be initiated. %one remodeling occurs around
an implant in response to a load transmitted through the implant to the
surrounding bone. !n a histopathologic comparison of loaded and
unloaded implants, #onath 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. Aoaded implants
were surrounded by a more compact type of bone with only small bone
free areas near the haversian canals. he 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. he load
dependent remodeling of bone follows the same principles that govern
fracture healing.
.nder normal circumstances, healing of implants is usually associated
with a reduction in the height of alveolar marginal bone. 2pproximately
1.+ to ).+ mm of vertical bone loss occurs during the first year after
implant insertion. 2fter this point, a steady state is reached and normal
bone loss occurs at a rate of approximately 1.) mm per year. he 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. he 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. !n a prospective review of
hydroxylapatite (G2- coated implants %lock and 9ent found that the
presence of keratinized gingiva in the peri:implant region strongly
correlated to bone maintenance in the posterior mandibular region.
hus, if excessive losses of marginal bone are noted, one must consider
the possibility of inappropriate loading of the implant or the presence of
peri:implant inflammation and step should be taken to rectify the
problem before excessive implant support is lost.
$UCO6ERIOSTEA% HEA%ING :
!mplants are placed into their endosteal position through incisions in the
mucoperiosteum. hey can be placed using a one stage techni"ue, in
which the endosteal and transmucosal portions of he implant are
allowed to heal as a single unit, or a two staged techni"ue, in which the
endosteal component is placed initially followed some time later by the
placement of the transmucosal portion after a period of healing. Gealing
of the mucoperiosteal complex around implants is of paramount
importance for the longevity of prosthetic reconstructions. 2n
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. 2s in the
previous section on bone healing, there are also three phases of wound
healing in soft tissue wounds ; inflammatory, proliferative and
maturation phases. !n addition, there is also significant overlap between
these phases as they pertain to mucoperiosteal wound healing.
6hase one inflammator( )hase :
he inflammatory phase of wound healing for the mucoperiosteal
complex is essentially the same as that mentioned in the previous
section on bone healing. !t involves an initial vascular response followed
by platelet aggregation and activation, the clotting cascade and then an
initial non:specific cellular inflammatory response consisting of
infiltrates of predominantly neutrophils. his is followed shortly
thereafter by a more specific cellular inflammatory response consisting
of infiltrates of predominantly neutrophils. his is followed shortly
thereafter by a more specific cellular inflammatory response marked by
increased number of lymphocytes and macrophages. @ytokines also play
an important role in the healing of soft tissue wounds.
6hase t#o )roliferati0e )hase :
he proliferative phase of wound healing begins within hours of the
in5ury 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. <igration and proliferation of epithelial
cells is seen within the first ,> to >4 hours of wound healing. he 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. 2 watertight seal is usually established within the
first ,> hours after primary wound closure, but little structural strength is
provided by the seal.
he main connective tissue cell involved in the proliferative phase of
soft tissue wound healing is the fibroblast. #ifferentiation 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.
=eovascularization provides the foundation for fibroblastic proliferation by
supplying the local area with the nutritional support re"uired to maintain
this enhanced metabolic state. Fibroblasts produce ground substance,
collagen and elastic fibers. he ma5or components of ground substance are
proteoglycans and glycoproteins. /lycoproteins are adhesive
macromolecules. hey interact with cells and constituents of the
extracellular matrix that interact with cells to promote adhesion, migration
and proliferation and alter gene expression. $roteoglycans are large
molecules composed of protein cores to which are attached side chains of
glycosaminoglycans, which are polysaccharide chains formed from
repeating disaccharide units. $roteoglycans are classified according to their
dominant disaccharide unit and include hyaluronate, chondroitin, dermatan,
keratin and heparin. hese molecules retain water and form bulky gels that
fill most of the extracellular space. he ma5or proteoglycan in connective
tissues early in inflammation is hyaluronic acid. !ts concentrations decrease
after the fifth day simultaneously with an increase in concentrations of other
proteoglycans, dermatan sulfate and chondroitin:> 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.
@ollagen and elastic fibers, the ma5or protein structures in connective
tissues are also produced by the fibroblast. @ollagen formation is
microscopically detected between the fourth and sixth days, but biochemical
evidence of collagen formation is noted between the second and fourth days.
#uring the formation of collagen, three polypeptide chains are produced and
hydroxylated which occurs under the influence of propyl hydroxylase,
which is an enzyme that re"uires vitamin @, molecular oxygen, ferrous iron
and : ketoglutarate as cofactors for proper function. hese molecules and
the combined to form a triple helix called procollagen. 2fter glycosylation,
procollagen is secreted from a triple helix called procollagen. 2fter
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. he resultant molecule, tropocollagen
combines with other tropocollagen molecules to form collagen fibrils and
the collagen fibrils are then combined to form collagen fibers. hese
structures are stabilized by intermolecular and intramolecular cross linkages.
Elastic fibers are also produced in a similar fashion. ropoelastin 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.
he proliferative phase of wound healing is marked by cellular
proliferation and synthetic activity. @ollagen 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.
ermination of this phase of wound healing marked by an increase in local
collagen content and a decrease in the number of local fibroblasts. @ollagen
content of the wound rises rapidly between the 0
th
and the )3
th
day but
increases only slightly between the )3
th
day and the >,
nd
day. 2t the
beginning of this phase, the tensile strength of the wound is provided by
epithelialization, blood vessel growth and aggregation of proteins. @ollagen
deposition increases the tensile strength significantly during this phase and
the magnitude is proportional to the collagen content of the tissues.
6hase three maturation )hase :
#uring the final phase of wound healing, maturation of the deposited
collagen occurs. here 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.
@ollagen 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 F weeks of wound healing, the
bursting strength of the wound in on about )+? of the normal skin level
at this time. 2s time proceeds however, the unorganized fibrils are
replaced larger, thicker and better organized fibers, with the final result
being one of Ilacing' the wound edges together with a three dimensional
weave. his is made possible by the continuous turnover of collagen by
fibroblasts with balanced synthesis and degradation. !mprovement in
strength of the wound is thus possible without an increase in total
collagen content. he bursting strength of the wound is noted to
improve dramatically from F to * weeks, reaching a level of 31? of
normal skin by the end of this period. %y 0 months, the bursting strength
of the wound is approximately *1? of the level of normal skin. !t 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.
I$6%ANT TISSUE INTERFACE :
!t consists of implant and bone interface.
!mplant and connective tissue interface.
!mplant and epithelium interface.
Im)lant an! 2one interfa'e :
Dn observing the implant and bone interface at the light microscopic
level ()11J- it shows that close adaptation of the regularly organized
bone next to the i implants.
Scanning electron microscopic study of the interface shows that parallel
alignment of the lamellae of haversian system of the bone next to the i
implants. =o connective tissue or dead space was observed at the
interface. .ltra microscopic study of the interface (+11 to )111J- 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.
$e'hanism of atta'hment :
2s a general rule cells do not bind directly to the foreign materials. he
cells binds to each other or any other foreign materials by a layer of
extracellular macro molecules (glycoproteins-.
he glycoprotein layer in between the cells or in between the tissues
will be at a thickness of )1 to ,1 nm ()11 to ,11 2
1
-.
2t the interface the glycoprotein layer of normal thickness ()1:,1 nm- is
adsorbed on the implant surface within the help of adhesive
macromolecules like Fibronectin, Aaminin, Epibiolin, Epinectin,
6itronectin (serum spreading factor-, Dsteopontin, thrombospodin and
others. 2t the molecular level the macromolecules contains ri:peptides
made up of 2rginin:glycin:2spertic acid (7/#-. he cells like
fibroblasts and other connective tissue cells contain binding elements
called as &integrins'. he integrins recognizes the 7/#s and bind to
them.
he macromolecules are adherent more firmly to the metallic oxide
layer on the i implants. he mode of attachment between the oxide
layer and the macromolecules may be of covalent bonds, ionic bonds or
van:der:walls bonding.
Im)lant 'onne'ti0e tissue interfa'e :
he connective tissue above the bone attaches to the implant surface in
the similar manner as that of the implant bone interface. he supra
crestal connective tissue fibers will be arranged parallel to the surface of
the implant. %ecause 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. %ut the implant connective tissue
interface is strong enough to withstand the occlusal forces and microbial
invasions.
Im)lant e)ithelial interfa'e :
he implant epithelial interface is considered as %iologic seal by many
authors. 2t this interface the glycoprotein layer is adherent to the
implant surface to which hemidesomosomes are attached. he
hemidesmosomes connect the interface to the plasma membrane of the
epithelial cells. %ecause of this attachment the implant epithelial
interface is almost similar to the 5unctional epithelium. For the
endosseous implants the sulcus depth varies from F to >mm.
Fa'tors of im)ortan'e to ensure a relia2le 2one an'hora&e of an
im)lante! !e0i'e :
!n most cases whenever an implant is inserted in bone, healing will
dependent on the conditions like ade"uate cells, nutrition to these cells
and ade"uate stimuli for repair. Gowever, bone tissue is different from
soft tissue in some aspects. !n 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. his 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. he 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. <any authors claim that the one cell will need the other
to be in an active state. his 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. Dn the contrary, there are several
reasons for primary as well as secondary failure of osseointegration.
hese failures may be attributed to an inade"uate control of the six
different factors known to be important for the establishment of a
reliable, long:term osseous anchorage of an implanted device. hese
factors are ;
). !mplant biocompatibility
,. #esign characteristics
F. Surface characteristics
>. he state of the host bed
+. he surgical techni"ue and
0. he loading conditions
here is a need to control these factors more or less simultaneously
to achieve the desirable goal of a direct bone anchorage.
I$6%ANT BIOCO$6ATIBI%ITY :
8ith respect to metals, commercially pure (c.p- titanium, niobium and
possibly tantalum are known to be most well accepted in bone tissue. !n
the case of c.p. titanium, there is likewise a documented positive long
term function. he 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.
8hereas 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. Dther 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. 2 significantly impaired interfacial bone formation compared
to c.p. titanium has been found with titanium:0 aluminium:> vanadium
alloy, probably dependent on a less good biocompatibility of the alloy.
Dne concern with metal alloys is that one alloy component may leak out
in concentrations high enough to cause local or systemic side effects.
@eramics such as the calcium phosphate hydroxyapatite (G2- 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. 8ith respect to G2, the available literature points
to at least a short term (K)1 weeks- enhanced interfacial bone formation
in comparison to various reference metals. his represents a potential
clinical benefit of G2, whereas the risk or coat loosening with
subse"uent problems represents a potential risk.
I$6%ANT DESIGN *$ACRO STRUCTURE/ :
here 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. Gowever, 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. 8ith currently used cylindrical implants,
many authors reported more severe bone resorption than would have
been expected with certain screw designs. !t must be observed that there
are other unthreaded implant designs that may give an excellent long
term clinical result.
he threaded implants provide more functional area for stress
distribution than the cylindrical implants. he design of the threads may
also influence the long term osseointegration. For e.g. 6:shaped thread
transfer the vertical forces in a angulated path, may not be efficient in
stress distribution as that of the s"uare shaped threads.
I$6%ANT SURFACE *$ICRO STRUCTURE7 SURFACE
TO6OGRA6HY/ :
8ith 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. @linical 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. 8ith a gradual increase of the surface topographical
irregularities, problems due to an increased ionic leakage are prone to
occur. 8ith plasma sprayed titanium surfaces for instance, more than
)011 ppm titanium has been reported in implant ad5acent haversian
systems, probable resulting in an impairment of osteogenesis.
2nother 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. Dne practical way of increasing the
surface energy is the use of glow discharge (plasma cleaning-. Gowever,
published reports have not been able to confirm the superiority of so
artificially enhanced implant energy levels. Dne 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.
<any researchers recommended various procedures for improving the
surface energy or surface characteristics of the implants to improve the
osseointegration. Stefini @.<. et al. (,111- recommended to apply
platelet derived growth factor and insulin like growth factors on the
implant surface before placing into the cervical bed. 2ccording to their
results this method showed better wound healing and rapid integration.
<usthafa 9. et al (,111- reported to sand blast the titanium implants
with titanium oxide particles (>+:*1- to achieve higher rate of cell
attachment.
Dther authors like Aima L.M. et al. (,11)- and Drsini N. et al. (,111-
reported to perform acid etching of the titanium implants by
hydrofluoric acid, a"ueous nitric acid and sodium hydroxide to reduce
the contact angle less than )1
1
for better cell attachment and utilization
of )? hydrofluoric acid O F1? nitric acid to clean the implant surface
and to remove the alumina particles after sand blasting which improves
the osseointegration.
=ishiguchi S. et al (,11)- reported to provide alkali O heat treatment to
improve the amount of bone bonding, i.e. + molElt =aDG at 01
1
@ for ,>
hours and 011
1
@ for ) hour (#og study-.
7ich and Garris presented some of the salient features of fibroblasts
during healing i.e. 7ugophalia; attracted towards rough surfaces,
Gaptotaxis; the directional cell movement that depends upon adhesive
gradients on the substratum, @ontact guidance ; the tendency of the cells
to be guided in their direction of locomotion by the shape of substratum.
hese properties denotes that the implant fixture with rough surface
topography and more surface energy promotes faster and complete
osseointegration.
STATE OF THE HOST BED :
!f available, the ideal host bed is healthy and with an ade"uate bone
stock. Gowever, in the clinical reality, the host bed may suffer from
previous irradiation, ridge height resorption and osteoporosis, to
mention some undesirable states for implantation. $revious irradiation
need not be an absolute contraindication for the insertion of oral
implants. Gowever, it is preferable that some delay is allowed before
an implant is inserted into a previously irradiated bed. Furthermore,
some )1:)+? poorer clinical results must be anticipated after a
therapeutical dose of irradiation. he explanation for less satisfactory
clinical outcome found in irradiated beds could be vascular damage, at
least in part. Dne 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. his 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.
Dther common clinical host bed problems involve osteoporosis and
resorbed alveolar ridge. Such clinical states may constitute an
indication for ridge augmentation with bone grafts. Gowever, present
clinical techni"ue for bone grafting are under debate and it appears that
0:year success of oral implants in the 3+? range is a realistic outcome
after most such procedures. his figure is slightly alarming seen
against the fact that, at least in the maxilla, )1:,1? 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. Dn the contrary, if the
bone "uality and "uantity in the maxilla is controlled, the expected
outcome of an oral implantation procedure is similar to that of the
mandible.
2s stated by %ranemark et al. and <isch, the bones with #) and #,
bone densities shows good initial stability and better osseointegration.
he bone densities #F and #> shows poor prognosis. <any authors
have recommended to select suitable implants depending upon the
"uality and "uantity of the available bone, i.e., G2 coated or i plasma
coated implants are better for #F and #> and conventional threaded
implants for #) and #, bone "ualities.
SURGICA% CONSIDERATIONS :
he 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. !f too violent a surgical techni"ue 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. %one
tissue is more sensitive to heat than previously believed. !n the past the
critical temperature was regarded to be in the +0
1
@ range, as this
temperature will cause denaturation of one of the bone enzymes,
alkaline phosphatase. Gowever, the critical time E temperature
relationship for bone tissue necrosis is around >3
1
@ applied for one
minute. 2t a temperature of +1
1
@ applied for more than one minute we
are coming close to a critical level where bone repair becomes severely
and permanently disturbed. his critical temperature should be seen
against observed frictional heat at surgical interventions. !n the
orthopaedic field, despite ade"uate cooling, temperatures of *1
1
@ have
been measured. Gigh drilling temperatures in the dental field are to be
expected when drilling, particularly in the dense mandible.
Erickson 7.2. recommended the importance of using well sharpened
drills, slow drill speeds, a graded series of drills (avoid making, for
instance, a >mm hole in one step- and ade"uate cooling by profuse
irrigation. %y using such a controlled techni"ue it has been
demonstrated in clinical studies that overheating may be totally
avoided. he mechanical in5ury will of course remain and is "uite
sufficient to trigger a proper healing response. Erickson also
recommended bone cutting speed of less than ,111 rpm and tapping at
a speed of )+ rpm with irrigation.
Gence, the surgical preparation se"uences as well as the instruments
depend upon the "uality of the bone as shown in the diagram.
2nother surgical parameter of relevance is the power used at implant
insertion. oo strong a hand will use in bone tension and a resorption
response will be stimulated. his means that the holding power of the
implant will fall to dangerous levels after a strong insertion tor"ue. 2
moderate power at the screwing home of an implant is therefore
recommended. 8ith other implant designs there may be a need for
implantation of the implant at insertion and other rules may apply.
Sur&i'al fit of the fi8ture : he accurate fit consists of more surface
contact, less dead space and thus better healing.
%OADING 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. his 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. !n essence, the
situation is similar to that of a fracture. Aoading of an unstabilized
fracture will result in soft tissue healing and poor function, whereas
stabilization with plates or plaster of $aris will ensure a satisfying
rigidity leading to bone healing of the fracture. he case of an implant
is, in principle, very similar. $remature 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. he length of time loading should be
avoided is dependent on the implantation site as well as on the bone
bed "uality. 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.
%ranemark with his controlled implant system advocated the use of a F
month loading delay in the mandible and a >:0 month delay in the
healthy maxilla where the bone is, as a rule, more cancellous in
character. Gowever, 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 techni"ue
for functional braces in fracture healing. !n the similar way <isch et al.
recommended progressive loading criteria or staged loading and
implant protective occlusion for better maturation of the bone
surrounding the implants. he problem in the case of oral implants is
how properly to define to the patient how a gradual increase of load
should be controlled P a complicated task not the least since the
appropriate loading pattern also depends on individual patients factors.
7ecently, many authors are reporting the results of immediate loading
of the endosseous implants. 2ccording to them the physiological loading of
the healing implants promotes better osseointegration.
Sagara et al ()**F- also showed evidence of osseointegration when
titanium screw implants were immediately loaded with a unilateral
prosthesis. heir 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 ()**+- 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. %oth the patients
were followed from F3 to >1 months after implant placement and immediate
loading. 2ll implants osseointegrated and were restored with a fixed
prosthesis.
%abbush and co:workers ()*40- showed implant success rate of 44?
to *3? over + to )F years with immediate loading implants.
Aederman and colleagues ()**4- histologically confirmed
osseointegration with 31? to 41? bone to implant contact in a mandibular
symphysis necropsy specimen after ), years of implant and prosthesis
function in a *+ year old patient.
$eitelli and colleagues ()**3- found significantly greater bone:to:
implant contact in ,> immediately loaded mandibular implants compared
with ,> unloaded.
THE SUCCESS CRITERIA *A%BER9TSSON ET A%/ :
)- he individual unattached implant should be immobile when tested
clinically.
,- he radiographic evaluation should not show any evidence of
radiolucency.
F- he vertical bone loss around the fixtures should be less than 1., mm
per year after first year of implant loading.
>- he implant should not show any signs of pain, infection,
neuropathies, parasthesia, violation of mandible canals and sinus
drainage.
+- he success rate of 4+? at the end of + year and 41? at the end of )1
service.
$ETHODS OF E:A%UATION OF OSSEOINTEGRATION :
In0asi0e metho!s :
)- Gistological sections ()1 microns sections-.
,- Gistomorphometric Q to know the percentage of bone contact.
F- ransmission electron microscopy
>- %y using tor"ue gauges
+- $ull out tests.
he invasive methods are usually used in the animal experiments.
Non;in0asi0e metho!s :
)- apping with a metallic instruments ; he fixture produces ringing
sound, it osseointegrated, produces dull sound if fibrous integration.
,- he radiographs
F- $erio test ; @hecks mobility and damping system.
=ormal values ; :+ to O + $6
>- #ental fine tester ; evaluates the mobility, should be less than +.
+- 7everse tor"ue test with ,1 = cm.
0- 7esonance fre"uency analysis ; this method gives the idea of amount,
rate of osseointegration. his method can be utilized for healing or
failing implants.
SCO6E OF THE OSSEOINTEGRATION :
he osseointegrated endosseous implants are utilized for providing
the prosthesis or stabilizing the various structure of the body. 2 schematic
representation of the scope of the osseointegration is depicted in the
diagram.
CONC%USION :
he <osseointe&ration= is a multifactorial entity. 2chieving the
osseointegration of the endosteal dental implants needs understanding of the
many clinical parameters.
BIB%IOGRA6HY :
)- Dsseointegration in clinical dentistry Q %ranemark, Narb, 2lbrektsson
,- Dsseointegration and occlusal rehabilitation Q Sumiya Gobo
F- @ontemporary !mplant #entistry Q @arl. <isch
>- Endosseous implants for <axillofacial reconstruction Q %lock and
9ent
+- !mplants in #entistry Q%lock and 9ent
0- #ental and <axillofacial !mplantology Q Mohn. 2. Gobkrik, 7oger
8atson
3- Endosseous !mplant ; Scientific and @linical 2spects Q /eorge
8atzak
4- Dptimal !mplant $ositioning and Soft issue management Q $atrik
$allaci
*- Dsseointegration in craniofacial reconstruction. . 2lbrektssson.
)1- Dsseointegration in dentistry ; an introduction ; $hilip 8orthington,
%rein. 7. Aang, 8.E. Aavelle.
))- Effect of implant surface topography on behaviour of cells Q#.<.
%runette !MD<! )*44 P F ; ,F):,>0
),- !mplant stability assessment Q =eil <. !M$, )**4 P + ; >*):+11.
)F- Dsseointegration and its experimental background. $.!. %ranemark.
M$#, )*4F, +1 ; F**:>)1.
)>- #.@.=.2., )*40 P )1:F>, )+):)01
)+- #.@.=.2., )**, P F0, ):)3
)0- Structural aspects of the interface between tissue and itanium
implants. 9.2. Ganson, . 2lbrektsson. M$#, )*4F P +1 ; )14:))F.
)3- %iocompatibility of itanium !mplants. %. 9asemo. M$#, )*4FP
+1;4F,:F3.
)4- #irect %one 2nchorage. . 2lbrektsson et al. !M$, )**1 P F ; F1:>).
)*- <echanism of Dsseointegration. M.E. #avis. !M$, )**4 P )) ;F*):>1).
,1- he attachment mechanism of epithelial cells. .7.A. /ould. M. $erio.
7est )*4) P )0 ; 0)):0)0.
,)- he effects of early occlusal loading on one stage titanium alloy
implants in beagle dogs ; 2 pilot study ; Sagara. <, 2hagawa L, =ikai.
G, suru. G, M$# )**F P 0* ; ,4):,44.
,,- !mmediate loading of bilaterally splinted titanium root form implants
in fixed prosthodontics ; Salama.9, 7ose EF, Salama.<, %etts. =.M P !nt
M. $eriodont 7est #ent )**+ P )+ ; F>+:F0).
,F- itanium plasma sprayed screw implants for reconstruction of the
edentulous mandible ; %ubbush @.2, 9ent M.=, 8islik #M P M Dral
<axillofac Surg. )*40 P )>> ; ,3>:,4,.
,>- Aong:lasting osseointegration of immediate located, bar:connected
$S screws after ), years of function ; 2 histologic case report of a *+:
year old patient ; Aedermann $# P !nt M $eriodont 7estorative #ent
)**4 P )4 ; ++F:+0F.
,+- !mmediate loading of titanium plasma sprayed screw:shaped implants
in man ; 2 clinical and histological report of two cases; $eattelli 2,
@origliano <, Scrano 2 P M $eriodontal )**3 P 04 ; +*):+*3.
CONTENTS
INTRODUCTION
HISTORY OF OSSEOINTEGRATION
DEFINITIONS AND OTHER TER$INO%OGIES
$ECHANIS$ OF OSSEOINTEGRATION
INF%A$$ATORY 6HASE
6RO%IFERATI:E 6HASE
$ATURATI:E 6HASE
FACTORS RES6ONSIB%E FOR OSSEOINTEGRATION
$ATERIA% BIOCO$6ATIBI%ITY
I$6%ANT DESIGN : $ACRO STRUCTURE
I$6%ANT SURFACE : $ICRO STRUCTURE
STATE OF HOST BED
SURGICA% CONSIDERATIONS
%OADING CONDITIONS
C%INICA% E:A%UATION OF OSSEOINTEGRATION
SCO6E OF OSSEOINTEGRATION
CONC%USION
REFERENCES
#E$27<E= DF $7DSGD#D=!@S
!=@A.#!=/ @7D8= 2=# %7!#/E
CO%%EGE OF DENTA% SCIENCES
DA:ANGERE
SE<!=27 D=
OSSEOINTEGRATION
$resented %y
#7. =!!= /2.2<
*>55+ ? >55>/