osseointegration

- DEFINITION- MICRO & MACRO EXPLANATION - MICROSEAL

OSSEOINTEGRATION

Sunil Gurram

INTRODUCTION

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

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

Evolution of Osseo integration concept:

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

The term “Osseointegration” was coined

by Dr Per-Ingvar Branemark (Fig-1),

Professor at the Institute for Applied

Biotechnology, University of Goteborg,

Sweden in the year 1985 to describe the

direct connection between a living bone

and load-carrying endosseous implant at

the light microscopic level.

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

DEFINITIONS

According to Branemark, Zarb, and Albrektsson (1985)

Osseointegration is the direct structural

and functional connection between

ordered, living bone and the surface of a

load–carrying implant.

According to Branemark’s histologic point of view: (1985)

Osseointegration is a direct connection

between a living bone and load-carrying

endosseous implant at the light

microscopic level

According to Glossary of Prosthodontic terms (J Prosthet Dent 2005; 94: p58)

Osseointegration is defined as 1: the apparent direct attachment or connection of osseous tissue to an inert, alloplastic material without intervening connective tissue 2: the process and resultant apparent direct connection of an exogenous material’s surface and the host bone tissues, without intervening fibrous connective tissue present 3: the interface between alloplastic materials and bone.

According to the American Academy of Implants Dentistry (1986)

Osseointegration is the contact established without interposition of non-bone tissue between normal remodeled bone and an implant entailing a sustained transfer and distribution of load from the implant to and within the bone tissue.

According to Zarb and Albrektsson

(1991)

Osseointegration is a time-dependent

healing process whereby clinically

asymptomatic rigid fixation of alloplastic

materials is achieved, and maintained, in

bone during functional loading.

BONE HEALING:An injured bone heals either by primary or

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

Hence to duplicate this healing process, the surgery should be performed on healthy bone, free from infection or necrotic tissue.

Secondary healing occurs when a large defect or large fracture site precludes close approximation of the two sites. This type of healing is prolonged due to infection and granulation tissue formation. This type of healing may result in fibrous tissue formation, which is undesirable in case of implants.

Bone healing around an inserted implant

Three phases1st phase – injury phase – starts

immediately after insertion of implant2nd phase – granulation phase – 3-2 weeks

after implantation. Formation of new local connective tissue, new capillaries and new supporting cells.

3rd phase – callus phase – 4-6 weeks after injury – evidence of new bone formation

BONE REMODELING: Osseointegration requires new bone

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

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

FOREIGN BODY REACTION:

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

An antigen-antibody reaction is the process of

formation of an antibody in response to the

foreign body. An antigen is formed after a latent

period as a protective mechanism. This reaction

occurs in the presence of protein, but with

implant materials devoid of protein, there is no

antigen-antibody reaction.

CONDITIONS AFFECTING BONE REPAIR AT AN IMPLANT SITE: (CELLULAR BACKGROUND)

In principle, bone may react in three different ways as a response to the necrosis

1. Fibrous tissue formation may occur.2. Dead bone may remain as sequester

without repair.3. New bone healing or Osseointegration

(bone formation = bone resorption)

Bone repair of the necrotic implant cortex

will depend on the presence of

1. Adequate cells

2. Adequate nutrition to these cells

3. Adequate stimulus for bone repair.

In case of bone healing, the adequate

stimulus has been regarded by various

authors as based on a cell-to-cell contact,

soluble matrix molecules or stress-

generated electric potentials.

Tissue-implant biological seal

The concept of the role of the gingival

epithelium in forming a biologic seal is one

of the great importance in implant dentistry

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

This permucosal passage creates a “weak link” between the prosthetic attachment and the predicted bony support of the implant .

This is the area where intial tissue break down begins that can result in eventual tissue necrosis and destruction around the implant

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

if seal is violated

Adjacent tissue will become inflamed

Osteoclastic activity is stimulated

Chronic resorption of supporting bone

Discrepency will fill with granulation tissue and implant becomes mobile

Percolation of bacteria and toxins

Acute suppurative inflammation

Excessive mobile.

Support of dental prosthesis impractical

Removal of implant

Decrease support of other new implants to place or any restorative procedure.

So how is this seal formed Implant surgery

attached gingiva regenerates around

the implant

epithelial cuff /free gingivalmargin(more appropriate term)

regenerating epithelium forms the free gingival margin & a gingival sulcus

epithelium regenerate into the sulcus

Non keratinized sulcular (crevicular) epithelium & a zone of epithelial cells at the base of the sulcus that interface the implant surface.

Series of biologic attachment structures

Formation of a basal lamina collagenous structure (type IV)

attachment

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

Biologic structures creating biologic seal following surgical placement of an implant

Epithelial cell with cell membrane Basal lamina outside cell membrane lamina lucida lamina densa sublamina lucida Hemidesmosomes on cell membrane peripheral densities pyramidal particles fine filaments Linear body on the implant face

THEORIES ON BONE TO IMPLANT INTERFACE

There are two basic theories regarding the

bone-implant interface.

a) Fibro-osseous integration (Linkow

1970, James 1975, and Weiss 1986)

b) Osseointegration (supported by

Branemark, Zarb, and Albrektsson 1985)

A. FIBRO-OSSEOUS INTEGRATION:

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

In 1986, the American Academy of

Implants Dentistry (AAID) defined fibrous

integration as “tissue-to-implant contact

with healthy dense collagenous tissue

between the implant and bone”

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

Failure of fibro-osseous theory

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

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

B. THEORY OF OSSEOINTEGRATION

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

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

The temperature during drilling should be

controlled by copious irrigation, if not can

inhibit alkaline calcium synthesis there by

preventing osseointegration.

The first month after fixture insertion is

the critical time period for initial healing

period. When loads are applied to the

fixture during this period primary fixation is

destroyed.

Osseointegration Vs Biointegration:

. In 1985, DePutter et al. observed that

there are two ways of implant anchorage

or retention; mechanical and bioactive.

Mechanical retention basically refers to the

metallic substrate systems such as

titanium or titanium alloy. The retention is

based on undercut forms such as vents,

slots, dimples, screws, and so forth and

involves direct contact between the

dioxide layer on the base metal and bone

with no chemical bonding.

Bioactive retention is achieved with

bioactive materials such as hydroxyapatite

(HA), which bond directly to bone, similar

to ankylosis of natural teeth. Bone matrix

is deposited on the HA layer as a result of

some type of physiochemical interaction

between the collagen of bone and the HA

crystals of the implant.

MECHANISM OF OSSEOINTEGRATION(BONE TISSUE RESPONSE)

MECHANISM OF INTEGRATION: (Davies

- 1998)

MECHANISM OF INTEGRATION:

(Osborn and Newesley – 1980)

MECHANISM OF INTEGRATION: (Osborn and Newesley – 1980)The terms “Distance and Contact

osteogenesis” were first described by Osborn and Newesley in 1980 and it refers to the relationship between forming bone and the surface of an implanted material. Their terms described essentially two distinctly different phenomena by which bone can become juxtaposed to an implant surface.

a. Distance osteogenesis:

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

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

b. Contact osteogenesis: In contact osteogenesis, new bone forms

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

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

MECHANISM OF INTEGRATION: (Davies - 1998) Davies divided the contact osteogenesis

into two distinct early phases of osteogenic cell migration (Osteoconduction) and de novo bone formation and a third tissue response that consist of bone remodeling at discrete sites.

a. Osteoconduction:

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

In this case, as in fracture healing,

migration of the connective tissue cells will

occur through the fibrin that forms during

clot resolution. Fibrin, the reaction product

of thrombin and fibrinogen released into

the healing site can be expected to adhere

to almost all surfaces. It is via this that the

osteogenic cells get migrated.

The migration of cells through a

temporary matrix such as fibrin will cause

retraction of the fibrin scaffold. Thus, the

ability of an implant surface to retain fibrin

attachment during this wound contraction

phase of healing is critical in determining if

the migrating cells will reach the former.

The phenomenon of osteoconduction

relies on the migration of differentiating

osteogenic cells to the implant surface.

Implant design can have a profound

influence on osteoconduction by

maintaining the anchorage of the

temporary scaffold through which these

cells reach the implant surface

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

b. De novo bone formation:

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

Two noncollagenous bone proteins

Osteopontin and bone Sialoprotein has

been identified in this initial organic phase,

but no collagen. Calcium phosphate

crystal growth follows nucleation, and

concomitant with crystal growth at the

developing interface, there will be initiation

of collagen fiber assembly.

Finally, calcification of the collagen

compartment will occur both in association

with individual collagen fibers or in the

interfiber compartment. Thus, in this

process of de novo bone formation, the

collagen compartment of bone will be

separated from the underlying substratum

by a collagen-free calcified tissue layer

containing non-collagenous bone proteins.

Bone bonding in de novo bone formation: Bonding of de novo bone will occur by the

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

Bone remodeling:

During the long-term phase of peri-implant

healing, it is only through those

remodeling osteons that actually impinge

on the implant surface that de novo bone

formation will occur at these specific sites

on the transcortical implant

The remainder of the transcortical portion of the implant will be occupied by old, dead bone or connective tissue space created by peri-implant necrosis and lysis of bone tissue. Although trabecular remodeling occurs this is not vital to implant stability.

Calcium phosphates accelerate early peri-implant bone healing by potentiating osteoconduction through structural protein adsorption and retention during early healing.

In this view it is possible to envision that

biologic design strategies for dental

implants have surfaces that are replaced

by bone during normal tissue remodeling.

Moreover, it is also seen that calcium

phosphate coating (Fig-22) can be site-

specifically resorbed by osteoclasts.

STAGES OF OSSEOINTEGRATION

According to Misch there are two stages (Fig-23) in osseointegration, each stage been again divided into two substages. They are:

Surface modeling Stage 1: Woven callus (0-6 weeks) Stage 2: Lamellar compaction (6-18 weeks)

Remodeling, Maturation Stage 3: Interface remodeling (6-18 weeks) Stage 4: Compacta maturation (18-54 weeks)

STAGE 1: (Woven callus)

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

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

STAGE 2: (Lamellar compaction)

This stage starts from 6th week of

implantation and continues till 18th week.

During this stage the woven callus

matures as it is replaced by lamellar bone.

This stage helps in achieving sufficient

strength for loading.

STAGE 3: (Interface remodeling)

This stage begins at the same time when

woven callus is completing lamellar

compaction. During this stage callus starts

to resorb, and remodeling of devitalized

interface begins. The interface remodeling

helps in establishing a viable interface

between the implant and original bone.

Remodeling of non-vital interface is

achieved by cutting/filling cones

emanating from the endosteal surface.

The mechanism is similar to typical cortical

remodeling except that many of the

cutting/filling cones are oriented

perpendicular to the usual pathway.

STAGE 4: (Compacta maturation)

This occurs form 18th week of implantation and continues till the 54th week. During this stage compacta matures by series of modeling and remodeling processes. The callus volume is decreased and interface remodeling continues.

It was previously believed that maturation

involved two physiologic transients.

a. Regional acceleratory phenomenon

(RAP)

b. Secondary mineralization of newly

formed bone

According to this a new bone get

strengthened only after 12 months through

secondary mineralization process. But

now it is thought that because of rapid

remodeling at the impact site, bone

mineralization could occur faster.

Osseointegration, once looked upon with skepticism, is

now even regarded by some investigators as a frequently

occurring, primitive foreign body reaction to an implanted

material. A biomechanical factor alone is thought to

determine whether a fibrous encapsulation or a bone

covering will develop around an implanted device

Conclusion

New developments of oral implants have,

generally, been focused on changes in the

hardware of the implant, i.e. new

materials, designs or surfaces have been

introduced with simultaneous claims of

these been superior to those used in the

past.

The future of oral implants will mean a

greater understanding of the important

contributions by the responsible surgeon

and prosthodontist.