Peri-implant diseases are inflammatory conditions that develop around dental implants and affect the surrounding tissues and bone. The two main types are peri-implant mucositis, which is a reversible inflammation of soft tissues, and peri-implantitis, which involves both soft tissue inflammation and bone loss. Diagnosis involves assessing bleeding, probing depth, suppuration and radiographic bone levels. Treatment may include non-surgical approaches like debridement and antimicrobials or surgical therapies to correct bone defects and decontaminate implant surfaces. Maintaining strict plaque control is important to prevent disease progression and bone loss.

1. PERI-IMPLANT
DISEASES

2. TABLE OF CONTENTS
PERI-IMPLANT DISEASES
PERI-IMPLANT MUCOSITIS
PERI-IMPLANTITIS
DIAGNOSTIC PROCESS
TREATMENT
CUMULATIVE INTERCEPTIVE SUPPORTIVE
THERAPY(C.I.S.T)
MAINTENANCE
CONCLUSION
REFERENCES

3. PERI-IMPLANT DISEASES
• Complications that develop in an implant site involving the periodontium are
collectively termed as peri-implant diseases.
• Peri-implant diseases can be defined as
“Inflammatory process in the tissues surrounding an implant (Albrektsson and Isidor,
1994)”
• The two main complications are
1. Peri-implant mucositis
2. Peri-implantitis

4. PERI-IMPLANT MUCOSITIS
• DEFINITION:
“Reversible inflammatory process in the soft tissues surrounding a
functioning implant (Lindhe)”

5. ETIOLOGY
 The main etiological factor is plaque formation.
 A baseline examination needs to be done including
assessments of plaque, soft tissue inflammation, PPD,
soft tissue recession and composition of oral biofilm.
CLINICAL FEATURES
 They are similar to gingivitis of teeth in many respects
and include classical symptoms of inflammation, such
as swelling and redness.
 Assessment of peri-implant mucositis must therefore
always include assessment of bleeding following
probing.
 BoP is a good discriminating indicator.

6. PERI-IMPLANTITIS
• DEFINITION:
“Inflammatory process additionally characterized by loss of peri -implant bone
(Lindhe)”

8. ETIOLOGY:
• It is multi-factorial peri-implant condition. The factors involved are
1. Microbial factors – bacterial factors
Gram –ve anaerobes, fusobacterium, spirochetes and black pigmented organisms such
as Intermedia.
2. Biological factors – host factors
• Implant rejection
• Systemic status of patient
• Habits of patient
• Improper adaptation of implant to the bone
3. Mechanical factors – implant factors
• Heavy occlusal forces
• Abutment in traumatic occlusion
• Improper selection ,design and placement of implant

9. Class 1: Slight horizontal bone loss
with marginal peri implant defects
Moderate horizontal bone loss with
isolated vertical defect
Moderate to advanced horizontal
bone loss with, broad circular bone
defects.
Advanced horizontal bone loss, with
broad circumferential vertical
defects, as well as the loss of the oral
and/or vestibular bony wall.
Froum and Rosen (IJPRD 2012)
Jovanovic (1990) Spiekermann (1991)

10. CLINICAL FEATURES:
• It includes the presence of
1. An inflammatory lesion in the peri-implant mucosa
2. Loss of peri-implant bone
• The diagnosis must consequently require the detection of both bleeding on probing (bop) as well as bone loss in
radiographs.
• It initially affects marginal part of peri-implant tissues and implant may remain stable and in function for
varying periods of time.
• Crater formed defects around implants are frequently found in radiographs
• Bone loss in such sites appear to be symmetric i.e. Similar amount of bone loss occurs at mesial, buccal, distal
and lingual surfaces.

11. DIAGNOSTIC PROCESS
 Examination of soft tissue measurements using
manual or automated probes have been suggested to
diagnose a compromised implant site.
 Factors to be examined are
1. Bleeding on Probing (BoP)
2. Suppuration
3. Probing depth
4. Radiographic bone loss
5. Implant mobility
6. Microbial monitoring
 Assessment of BoP, suppuration and PPD must be
done at 4 surfaces while radiographic evaluation
related to only mesial and distal aspects.

13. TREATMENT :
• Decision on treatment strategies is based on diagnostics and severity of lesions.
• The goal is to stop the progression of bone loss by controlling bacterial infection and peri-implant
tissue inflammation.
• Mombelli (2002) has given 5 aspects in the treatment of peri-implantitis:
1. Removal of bacterial plaque
2. Decontamination and conditioning of implant surface
3. Reduction or elimination of sites that cannot be maintained plaque free by oral hygiene
procedures.
4. Establishment of an efficient plaque control regimen.
5. Regeneration of bone.
• Treatment of peri-implant diseases can be done by 2 therapies
1. Non-surgical therapy
2. Surgical therapy

14. 1. NON-SURGICAL THERAPY:
• Involves local removal of plaque deposits with plastic instruments and polishing of all accessible surfaces with
pumice, sub-gingival irrigation of all peri implant pockets with a 0.12% chlorhexidine, systemic antimicrobial
therapy for 10 consecutive days
• IMPLANT SURFACE PREPARATION:
A. Mechanical devices
B. Chemotherapeutics
A. MECHANICAL DEVICES:
• 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.
B. CHEMO THERAPEUTIC AGENTS:
• Use of a supersaturated solution of citric acid for 30-60 seconds has the highest potential for removal of endotoxins from
both hydroxyapatite- and 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.

16. 2. SURGICAL THERAPY:
• The surgical techniques advocated to control peri-implant lesions are modified from techniques used to treat
bone defects around teeth.
• The resective therapy is used to reduce pockets; correct negative osseous architecture and rough implant
surfaces, and increase the area of keratinized gingiva if needed.
• The regenerative therapy is also used to reduce pockets with the ultimate goal of regeneration of lost bone
tissue. Removal of the
supragingival
bacterial plaque.
Detoxification of
the surface of the
implant.
Surgical access
and removal of
granulation
tissue.
Correction of
bone
architecture.
Modification of
implant surface
roughness.
Implementation
of plaque
control.

17. GUIDED BONE REGENERATION
Techniques are recommended when bone loss is severe. It includes placement of a membrane after
grafting. Prior decontamination of the implant surface is required to enable bone regeneration, and to
permit the implant to osseointegrate.

18. CUMULATIVE INTERCEPTIVE
SUPPORTIVE THERAPY (CIST)
• Principle of this method is to detect peri-implant infections as early as possible and
treat them.
• Major clinical parameters to be used are
1. Presence of biofilm.
2. Presence or absence of bop.
3. Presence or absence of suppuration.
4. Increased peri-implant probing depth.
5. Evidence and extent of radiographic alveolar bone loss.

19. MAINTENANCE
Scaler tips are designed to
fit the curvature of the
standard abutment.

20. CONCLUSION
 Peri-implant lesions may develop after several years. Patients who have lost their teeth
due to periodontal disease seem to be at greater risk. Although several anti-infective
treatment strategies have demonstrated beneficial clinical effects in humans (ex:
resolution of inflammation, decrease in probing depth and gain of bone in the defects),
there is insufficient evidence to support a specific treatment protocol.
 Available studies on the treatment of peri-implantitis have included only a small
number of subjects, and in general, the study periods have been relatively short. To
date, there is no reliable evidence that suggests which interventions could be the most
effective for treating peri-implantitis.

21. REFERENCES
 NEWMAN, TAKEI, KLOKKEVOLD, CARRANZA. CARRANZA’S CLINICAL
PERIODONTOLOGY, 10TH EDITION AND 11TH EDITION.
 LINDHE, LANG, KARRUNG. CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY,
5TH EDITION.