OSSEOINTEGRATION

OSSEOINTEGRATION
Goal of research and development in the field of implant materials is to achieve physical and
biological compatibility with alveolar bone. Ideally, bone should integrate with the implant
material rather than responding to the material as a foreign substance by encapsulating it with
fibrous tissue.

Per Ingvar Bränemark in 1950 accidently discovered the fusion of bone with titanium chambers
when he had placed them into the femurs of rabbits to study microcirculation in them (Fig.6). He
coined the term osseointegration for this phenomenon. Osseointegration is defined as “the
apparent direct attachment or connection of osseous tissue to an inert, alloplastic material
without intervening connective tissue.”

Fig 6: Branemark’s experiment in

rabbit femur

During osseointegration, osteoblasts and mineralized matrix contacts the implant surface even
when loads are applied. The first practical application of osseointegration was the implantation
of new titanium roots in an edentulous patient in 1965 and the first ground breaking study was
published 16 years later by Adell et al. in the International Journal of Oral Surgery. This is
considered to be the beginning of the birth of modern implantology. Since then, titanium and its
alloys have been extensively used as implant materials for over 40 years due to their excellent
biocompatibility, mechanical properties and high corrosion resistance.

Osseointegration provides a stable bone-implant connection that can support a dental prosthesis
and transfer applied loads without concentrating stresses at the interface between the bone and
the implant. Osseointegration takes place when the bone is viable and space between the bone
and implant must be less than 10 nm without any fibrous tissue. Both the aspects of

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osseointegration, maintenance of present bone (remodelling) and new bone formation

(modelling), determine the fate of implant healing and implant stability.

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Bränemark et al in 1969 showed that direct bone apposition at the implant surface was possible
and lasts under loading at the condition that implants were left to heal in a submerged way. Many
materials such as metals, polymers, ceramics and composites have been researched as potential
candidates for implants. Amongst these, dental implants made from commercially pure titanium
(CPTi) have shown excellent success rates in long-term studies. Biocompatibility of CPTi has
been demonstrated in in vitro studies as well as in vivo studies in animals and humans.

In addition, a number of systemic and local factors have been identified as being associated with
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the production of an osseointegrated interface. Albrektsson et al in 1981 suggested six factors
for the establishment of reliable osseointegration. These include type of material being
implanted, implant design, surface conditions, status of bone, surgical and implant loading
conditions.

Role of relevant cells in osseointegration:

Fig 7: Osteogenic cells including

osteoblasts, osteoclasts, osteocytes

1. Undifferentiated mesenchymal cells- they are stem cells and have the potential to
migrate, proliferate and differentiate into mature mesenchymal cells after stimulation.
Eg:osteoblasts. However, both the nature of the stimuli and the site may cause the stem
cells to alterntatively differentiate into other cell types such as chondroblasts, myoblasts,
adipocytes or fibroblasts.

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2. Osteoblasts- they originate from local mesenchymal stem cells and form preosteoblastby
osteogenic induction and then differentiate into mature osteoblasts (Fig.7).
3. Osteoclasts- bone resorbing cells of hematogenic origin formed by the union of
monocytic cells. They are multinucleated giants cells and are found in bays of resorbing
bone called Howship’s lacunae (Fig.7).
4. Osteocytes- they are cells of living bone and are formed when osteoblasts have formed
bone around them. Osteoblasts and osteoclasts function simultaneously to cause bone
remodeling (Fig.7).

Biology of wound healing following implant placement:

Wound healing involves a highly orchestrated sequence of events which is triggered by tissue
injury involving soluble mediators, blood cells, extracellular matrix and parenchymal cells.
Ultimately, it culminates in either partial or complete regeneration or repair. Fracture healing in
bone occurs in four phases which include inflammation, soft and hard callus formation, and
remodeling.

Following a fracture, blood coagulation and hematoma formation takes place. This is followed
by inflammation. Various chemical mediators such as thrombin and growth factors released by
activated leukocytes and platelets in the hematoma serve as chemotactic signals to many cell
types which play an important role in bone healing. Unlike soft tissue healing, bone healing does
not lead to scarring. Instead it leads to restoration of the bony tissue. During successful
implantation, insertion of metal implants into cortical bone eventually leads to complete healing.

Following implant placement, unlike in fracture healing, implants extend into and persist in the
marrow spaces and this may have a bearing on the healing process. Although implant healing
must to some extent adjust to the presence of the implant, ultimately, sound bony tissues will be
completely restored during wound healing. This adjustment involves imbedding the implant
surface in a layer of bone, continuous with the original bone.

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Wound healing around a dental implant placed into a prepared osteotomy follows three stages of
repair-
1. Osteophyllic phase (day 0 to 1 month)-
Initial formation of a blood clot occurs through a biochemical activation followed by a cellular
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activation and finally a cellular response (Stanford and Schneider , 2004). During surgery,
dental implant surfaces interact with blood components from ruptured blood vessels. Generalized
inflammatory response results and by the end of first week, inflammatory cells are responding to
foreign antigens.
Vascular ingrowth from the surrounding vital tissues begins by the third day. By the end of three
weeks, a mature vascular network forms. Various plasma proteins such as fibrin get adsorbed on
the material surface. Fibrinogen is converted to fibrin and the complement and kinin systems
become activated. As in fracture healing, the migration of bone cells in peri-implant healing will
occur through the fibrin of a blood clot due to the release of BMPs.

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2. Osteoconductive phase (1 month to 4 months)-

The bone cells spread along the metal surface laying down osteoid. Initially this is an immature
connective tissue matrix and the bone deposited is a thin layer of woven bone called foot plate.
Fibrocartilagenous callous is eventually remodeled into a bony callus. This process occurs at 3
months following implant placement. At the fourth month, bone covers maximum surface area.

3. Osteoadaptive phase (after 4th month)-

The final phase begins approximately 4 months after implant placement. Once loaded, implants
do not gain or lose contact but the foot plates thicken in response and some reorientation of the
vascular pattern may be seen. Grafted bone integrates to a higher degree than natural bone. The
osseointegration phase for normal bone is around 4 months but for grafted bone it is around 4 to
8 months (Fig.8, Fig.9).

Fig 8: Stages in osseointegration

with role of different cells

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MECHANISM OF OSSEOINTEGRATION:

BLOOD CLOT

CLOT TRANSFORMED BY PHAGOCYTES (1st to 3rd day)

PROCALLUS FORMATION (containing immature fibroblasts and phagocytes)

DENSE CONNECTIVE TISSUE (differentiation of osteoblasts and fibroblasts)

CALLUS FORMATION

FIBROCARTILAGENOUS CALLUS

BONY CALLUS (penetration and maturation)

Fig 9: Osseointegrated dental

implant with the surrounding bone

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