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Peri-implantitis

1-definition
2-implant failures
3-Peri-implantitis
4-diagnosis of Peri-implantitis
5-histology of implantitis
6-microbiology of implantitis
7-contributing factors
8-management

    1-definition

1-Osseintegration:is the direct attachement between the bone and the surface of implant with present of osteoblast that grow on implant surface in addition to high fibrous epithelial attachment between gingiva and implant surface above the central bone and then the implant must resist the displacement and dissipate the occlusal loads

2-Re-osseointegratio:the formation of new bone in contact with the previously contaminated titanium surface. 

2-implant failures

1-Early implant failures

are the result of events that  may  jeopardize or prevent osseointegration from occurring and include among others:

1. Improper preparation of the recipient site which in under hard tissue damage such as necrosis of the bone

2. Bacterial contamination and extensive inflammation of the wound that may delay healing of the soft and hard tissues

3. Improper mechanical stability of the implant following its insertion

4. Premature loading of the implant

2-Late implant failures

occur in situations during which osseointegration of a previously stable  and properly functioning implant is lost

such late failures are often the result of

1- excessive load

2- infection

inflammatory process that (1) affects the tissues around an osseointegrated implant in function, and (2) results in loss of supporting bone

4-Diagnosis of implantitis

 A-clinically

By observation of the following signs and syptoms

1-formation of peri-implant pocket(>4mm)

2-bleeding or suppuration after gently probing

3-tissue tenderness and swelling

4-mobility

B-Radiographically

By the  evidence of vertical destruction of creastal bone often(saucer shaped)

5-histology of PERI-IMPLANTITIS

(A)Light  microscope:including the following findings:

1-distinct proliferation & acanthosis of sulcular epithelium.

2-increase of density of mono &polymorpho nuclear cell in epithelium.

3-infiltration of mononuclear & plasma cells in connective tissue.

4-the proportion of inflammatory  cell infiltrate(ICT)of C.T in diseased sits 65.5% 

 while in healthy site 8.2%.

5-subsulcular C.T from healthy sits of mucosa contain scare ICT & mature collagen

fibers.

6-ICT reached to the crest of alveolar bone& extentd to bone marrow.

(B)Electronic microscope:including the following findings:

1-intercelcular spaces of sulcular epithelium found to harbour bacteria in close apposition to desmosomal junctions.

2-progressing deeper to the epithelium and connective tissue.

3-increasingly replace the fibroblast & collagen fibers by ICT often plasma cells & lymphocytes dominating.

4-alteration the morphology of blood vessels with evidence of engorgement & conjestion.

6- microbiology of PERI-IMPLANTITIS

*Bacterial infection is most often described in relation to biofilms that defined as one or more communities of M.O embedded in glycocalyx of aqueous solutes attached to roughened surface of implant.

*Build up of bacterial plaque is allowed on dental implant causing inflammatory changes to the adjacent soft tissue and subsequent progression to involve the bone that is not clarified in peri-implantitis.

*microbiology of peri- implantitis significantly different from healthy implant & tooth sits in same or between the individuals.

*microorganisms found in failing site of implant including:

1-Gram –ve anaerrobic rods.

2-spirochaetes.

3-fusiform bacteria.

7-c0ntributing factors to PERI-IMPLANTITIS

1-Microbiology plays an important role in the etiology of peri-implantitis.

2-clear proportional relationship between surface roughness & the rate of bacterial colonization.

3-no significant difference in disease progression between titanium plasma-sprayed ,hydroxy apatite-coated ,acid-etched& commercially titanium implants.

4-smoking is increase risk of implant loss.

5-the peri-implant sulcus in healthy is deeper than that found in natural teeth.

6-lack of keratinized gingiva around implants may increase the susceptibility to plaque induced peri-implantitis.

7-other factors: heavy occlusal force , trauma , &host immune response.

8-management of PERI-IMPLANTITIS

*Mombelli(2002), suggests five consideration in the therapy of peri-implantitis:

1-the disturbance &\or removal of the bacterial biofilm in the peri-implant pocket.

2-decotamination & conditioning of the surface of the implant

3-correction via reduction or elimination of sites that cann’t be adequately maintained by oral hygiene measures.

4-establishment of an effective plaque control regime.

5-Re-osseoitegration.

Decision tree for Cumulative Interceptive Supportive Therapy (CIST). Depending on the mucosal condition and probing depth, either regime A or regime A+B, regime A+B+C or regime A+B+C+D are performed. A: Mechanical debridement; B: Antiseptic cleansing; C: Antibiotic therapy; D: Resective or regenerative surgery

Four , osseointegrated implantitis used for retention of an overdenture in an edentulous lower jaw.

A submerged regenerative therapy was initiated by removal of the abutments 6 months before surgery

Elevated flap showing bone loss around three of the four implantitis

Two membranes placed over the peri-implant bone defects , allowing a blood clot to form underneath.

After an uneventful healing period of 4 month, the surgical sites are exposed and membranes removed.

Postoperative clinical evaluation 11/2 years later.