PERI-IMPLANTITIS

INTRODUCTION Developing artificial replacements for missing teeth has been an elusive goal for more than 1500 years. The present surge in the use of implants was initiated in 1952 by Branemark Branemark & associates described the relationship b/n titanium & bone for which they coined the term Osseointegration, as the direct structural & functional connection b/n ordered ,living bone & the surface of a load carrying implant.

PERI IMPLANT MUCOSA The mucosal tissues around intraosseous implants form a tightly adherent band consisting of a collagenous lamina propria covered by stratified squamous keratinised epithelium.

The implant epithelium junction is analogous to the junctional epithelium around natural teeth, in that the epithelial cells attach to the titanium implant by means of hemidesmosomes and basal lamina.

Clinically normal gingival mucosa next to 2 implants. Normal epithelium lining the implant after removal of the cover screw.

A sulcus forms around the implant lined with a sulcular epithelium. Capillary loops in the CT under the junctional & sulcular epithelia appear to be anatomically similar to those found in the normal periodontium

-The depth of a normal noninflamed or minimally inflamed sulcus around an intraosseous implant has not been accurately determined but is assumed to be between 1.5 to 2.0 mm. -Collagen fibers are nonattached & run parallel to the implant surface owing to the lack of cementum. -This is an important difference between peri implant & periodontal tissues.

IMPLANT-BONE INTERFACE The relationship b/n endosseous implants & bone consists of one of 3 mechanisms. 1) Osseointegration where the bone is in intimate but not ultra structural contact with the implant 2) Fibrosseous integration in which soft tissues such as fibers & /or cells are interposed b/n the 2 surfaces 3) Biointegration, which denotes a direct biochemical bond of the bone to the surface of an implant at the electron microscopic level & is independent of any mechanical inter locking system. [eg: Bonding of HA to bone].

The osseointegration concept proposed by Branemark et al & called functional ankylosis by Schroeder states that there is absence of CT or any tissue in the interface b/n the implant & the bone. It is important to note that osseointegration refers to the direct contact of bone & implant at the light microscopic level.

Successful cases have b/n 30% & 95% of the implant surface, as measured by light microscopy , in contact with bone.

CRITERIA FOR IMPLANT SUCCESS INCLUDE 1) Absence of signs/symptoms such as pain, infection, neuropathies, parathesia & violation of vital structures 2) Implant immobility 3) No continuous peri implant radiolucency 4) Negligible progressive bone loss(less than 0.2mm annually) after physiologic remodelling during the first year of function 5) Patient/dentist satisfaction with implant supported restoration.

PERI IMPLANT DISEASE Despite the long-term predictability of Osseointegrated implants, biologic, biomechanical & esthetic complication can occur in a small percentage of cases.

Pathologic changes of the peri-implant tissues can be placed in the general category of periimplant disease.

Peri-implant mucositis- Inflammatory changes that are confined to the soft tissue surrounding an implant.

Peri implantitis is defined as an inflammatory process affecting the tissues around an osseointegrated implant in function, resulting in loss of supporting bone. Progressive peri implant bone loss in conjunction with a soft tissue inflammatory lesion is termed peri implantitis.

Early implant failures are the result of events that may jeopardize or prevent Osseointegration from occurring & include: 1) Improper preparation of the recipient site, which results in undue hard tissue damage such as necrosis of the bone. 2) Bacterial contamination & extensive inflammation of the wound that may delay healing of the soft & hard tissues. 3) Improper mechanical stability of the implant following its insertion. 4) Premature loading of the implant.

Late failures occur in situations during which osseointegration of a previously stable & properly functioning implant is lost.
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that late failures are the result of excessive load & /or infection.

ETIOLOGY OF PERI IMPLANTITIS - Bacterial infection - Biomechanical factors. 1) Bacterial infection - If plaque accumulates on the implant surfaces, the sub epithelial connective tissue becomes infiltrated by large number of inflammatory cells & the epithelium appears ulcerated & loosely adherent. - When the plaque front continues to migrate apically, the clinical & radiographic signs of tissue destruction are seen around both implants & teeth; however the size of the soft tissue inflammatory lesion & the bone loss is larger around implants.

One reason for the increased inflammation around an implant might be the low-vascularity soft tissue band and the difference in collagen/fibroblast ratio of gingival tissues, which affects the defense mechanisms around an implant as compared with those seen in tissues around teeth with a periodontal ligament.

BIOMECHANICAL FACTORS - excessive biomechanical forces may lead to high stress or micro-fractures in the coronal bone to implant contact & thus lead to loss of osseointegration around the neck of the implant.

The role of overloading is likely to increase in four clinical situations: 1. The implant is placed in poor quality bone. 2. The implants position or the total amount of implants placed does not favor ideal load transmission over the implant surface. 3. The patient has a pattern of heavy occlusal function associated with parafunction. 4. The prosthetic superstructure does not fit the implants precisely. Other etiological factors traumatic surgical procedures, smoking, inadequate amount of bone at placement, compromised host response can act as co-factors in the development of peri implant disease.

FEATURES AND FREQUENCY The following signs & symptoms are typical for peri-implantitis lesions: -There is radiological evidence for vertical destruction of the crestal bone. The defect usually assumes the shape of a saucer around the implant while the bottom part of the implant retains perfect osseointegration. In some instances wedge-shaped defects develop along the implant. Whether specific patterns of marginal bone loss indicate a specific underlying cause is not known. Bone destruction may proceed without any notable signs of implant mobility until osseointegration is completely lost. A continuous periimplant radiolucency indicates implant failure

-Vertical bone destruction is associated with the formation of a peri-implant pocket. -There is bleeding after gentle probing with a blunt instrument and there may be suppuration from the pocket. -Tissues may or may not be swollen. Hyperplasia is frequently seen if implants are located in an area with nonkeratinized mucosa or if the suprastructure is an overdenture. -Pain is not a typical feature of peri-implantitis.

Diagnosis of Peri implant tissue breakdown 1) Peri implant probing -To diagnose a compromised implant site, soft tissue measurements using manual or automated probes have been suggested. (measure of soft tissue hyperplasia or recession) - Bleeding after probing & - Exudation & suppuration from the peri-implant space

2) MOBILITY
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Implant mobility is an indication for lack of osseointegration

Even if disease conditions in the peri-implant tissues have progressed relatively far, implants may still appear immobile due to some remaining direct bone to implant contact. Thus mobility is insensitive in detecting the early stages of peri-implant disease. The parameter serves to diagnose the final stage of osseodisintegration & may help to decide that an implant has to be removed .

- Implant mobility indicates the final stage of peri-implant

disease, characterized by complete loss of the direct bone to implant interface.
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For interpretation of low degrees of mobility an electronic device has been designed to measure the damping characteristics of the periodontium of natural teethPeriotest

3) SUPPURATION

Suppuration is associated with disease activity & indicates a need for anti-infective therapy.

4) CLINICAL INDICES
Swelling & redness of the marginal tissues have been reported form peri-implant infections in addition to pocket formation, suppuration & bleeding.

5) PERI IMPLANT RADIOGRAPHY

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For accurate assessments of bone level changes , longitudinal series of standardized radiographs are required. Detection of minute changes of bone level or density requires a reproducible projection geometry for the x- ray beam ,provided by an appropriate aiming device.

6) MICROBIOLOGY - Bacterial culture, DNA probes, polymerase chain reaction, monoclonal antibody & enzyme assays to monitor the sub gingival flora have been proposed to determine an elevated risk for periodontal disease or peri-implantitis.

INITIAL PHASE OF PERI IMPLANTITIS TREATMENT Occlusal therapy - When occlusal forces are considered the main etiologic factor for periimplant bone loss, treatment involves an analysis of the fit of the prosthesis, the number & position of the implants & an occlusal evaluation. Prosthesis design changes, improvement of implant number & position & occlusal equilibration can contribute to arrest the progression of peri implant tissue breakdown.

NON SURGICAL THERAPY

Indications
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Mucosal inflammation detected by clinical signs Radiographic bone level stable.

Involves 1) the local removal of plaque deposits with plastic instruments & polishing of all accessible surfaces with pumice, 2) sub-gingival irrigation of all peri implant pockets with a 0.12% Chlorhexidine, 3) systemic antimicrobial therapy for 10 consecutive days & 4) improved patient compliance with oral hygiene until a healthy peri implant site is established.

Mechanical devices
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Mechanical instrumentation may damage the implant surface if performed with metal instruments harder than titanium.
The method of choice involves the use of a high- pressure air powder abrasive (mixture of sodium bicarbonate & sterile water). This method removes microbial deposits completely, does not change the surface topography & does not adversely affect the cell adhesion.

Chemo therapeutic agents

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Use of a supersaturated solution of citric acid for 30-60 seconds has the highest potential for removal of endotoxins from both Hydroxy apatite- & titanium implant surfaces.
Irradiation with a soft laser for elimination of bacteria associated with Peri implantitis has also shown promising results in the destruction of bacterial cells.

SURGICAL TECHNIQUES Once the inflammatory process in the periimplant tissues is under control, an attempt may be made to improve or reestablish osseointergration. The surgical techniques advocated to control periimplant lesions are modified from techniques used to treat bone defects around teeth.

ADVANCED TYPE IV BONE LOSS AROUND IMPLANTS

The regenerative therapy is also used to reduce pockets with the ultimate goal of regeneration of lost bone tissue

To accomplish regeneration of lost bone tissue & reosseointegration, Guided bone regeneration & bone graft techniques have been suggested.
The GBR principle using a non-resorbable e PTFE membrane has been used for healing of bone defects seen at the time of implant placement & around failing implants.

IMPLANT MAINTENANCE
CUMULATIVE INTERCEPTIVE SUPPORTIVE THERAPY The principle of this method is to detect periimplant infections as early as possible & to intercept the problems with appropriate therapy. The basis for this system is a regular recall of the implant patient & the repeated assessment of the following key parameters around each implant. a) The presence of plaque b) The bleeding tendency of the periimplant tissues c) Suppuration d) Presence of periimplant pockets e) Radiological evidence of bone loss.