osseointegration
TRANSCRIPT
- 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.