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Peri-implant Diseases
Dr.Diana Abo El Ola
Peri-implant diseases
Factors Classification
Diagnosis &
Treatment Maintain OH
Excessive loading??
Infection??
Improper proximal Space
Retained cement
Improper positioning(facially) /angulation
Inadequate attached gingiva
Additional
factors
Peri-implant mucositis:
Is a Inflammatory process in the tissues surrounding the implant
Reversible infl of peri-
implant soft tissues
surrounding a functioning
implant(caused by plaque)
Inflammatory process around
implants involves loss of peri-
implant bone.(crater
formation)
Peri-implantitis:
Tooth Implant
PDL, bone and
cementum
PDL Between bone &
cementum
Absent PDL & cementum (Direct
bone-implant contact
Supracrestal fibers Run perpendicular to tooth
surface
Run parallel to implant surface
Connective tissues
within the
supracrestal region
Less collagen(60%) & more
fibroblast(5-15%)
More collagen (85% ) & less
fibroblast (1-3% ) & this is the
characteristic of scar tissue
(  collagen &  cells)
Biological width 2mm 3-4mm
Vascularization Comes from:
1. Supraperiosteal B.V.
2. BV from alv. process
3. Vascular plexus of the PDL
Comes only from the large
supraperiosteal B.V.
Soft tissues turn
over
More rapid(more nutrition &
cells)
Less rapid(few BV & fibroblasts)
Similar to gingivitis in natural
teeth
The Same Classic symptoms of
infl. like redness, swelling, BOP.
Clinical Features
Histopathological features
Teeth and implant mucosa have the same
response to plaque.(plaque will cause 
neutrophils ✚lymphocytes ✚ macrophages)
BUT
• Peri-implant mucosa is less capable to repair.
– Inflammation of peri-implant mucosa (BOP, redness & PD)
– Crater bone loss (in radiograph)
– Suppuration may be found.
– Implant is immobile and in function.
Clinical Features
Histological features
– Plaque ass. with both lesions are similar(same MO
dominating by G-ve & anaerobic species)
BUT
•  vasculature faster destruction & progression.
• Plaque invade CT infl. Cell infiltration more
severe with implants (Plasma cells ✚ Lymphocytes
✚macrophages).
• The apical part of infl. lesion in CT is in a direct contact
with bacteria in contrast with that of tooth.
N.B Progression of peri-implantitis is more in implants with
rough surface than at smooth surfaces. y???
Rough surface acts as
plaque retentive area
Formation of biofilm
Inflammatory lesion in the peri-implant mucosa
( in the C.T lateral to the barrier epi.)
If untreated
It extends apically to the bone
Compromise the osteointegration
( marginal bone loss)
Diagnosis the peri-implant diseases
• Bleeding on probing
• Suppuration.
• Probing depth around the implant.
• Radiographic evidence of bone loss.
• Mobility of the implant by??
★Absence of BOP indicates the peri-implant mucosa is healthy
and stable.
★Implant mobility indicates defect osseointegration 
implant removal.
Periotest
Progressive alv. bone loss, pocket formation,
BOP,suppuration
LOSS of
osseointegration,
mobility, or pain
Hopeless and nonfunctional
implant☛ FAILED ➨removal
FAILING Implant ➨treatment
When things go wrong!!!
Treatment of failing implants
• Resolution of inflammation
– Debridement
– Improvement of OH
– Adjunctive antibiotics
• Correction of unfavorable ST morphology
(pseudopockets➨by flap surgery / gingivectomy)
• Re-osseointegration –
Decontaminate implant surface (with citric acid or tetracycline
soln.)+ GBR
Treatment of failed implants
• Remove the implant
• GBR and subsequent placement of implant.
Case 1: Bone graft around a failing
implant
Allograft bone +membrane
Granulation tissues were removed
+ decontamination by tetracycline
Crater bone loss but stable
implant
Flap closure+ antibiotic regimen
6mm pocket +circumferential bone loss
Case 2: removal of failed implant
freeze-dried bone allograft (FDBA) + Ti-
reinforced membrane
Re-enter after 6 m New implant replacement
Cumulative Interceptive Supportive
Therapy " CIST "
The Aim :
Early detection of peri-implant infection & to intercept the
problems with proper therapy.
How?
Regular recalls ✚ repeated assessment of following parameter.
• Presence of biofilm.
• Presence or absence of BOP.
• Presence or absence of suppuration.
• Increased peri-implant PD.
• Evidence & extent of radiographic alv. bone loss.
Oral implant surrounded by healthy
periodontium
• Absence of BOP
• Absence of suppuration
• Probing depth < 3mm
NO therapeutic measurement.
Protocol A:
Mechanical Debridement
• Implant with plaque & calculus deposit.
• BOP
• PD ≤ 3mm
• No Suppuration
OHI + mech. Debridement + polishing
Protocol A+B:
Antiseptic Therapy
• Implant with plaque & calculus deposit.
• BOP
• PPD = 4-5 mm
• May or not demonstrate suppuration
CHX gel application / irrigation ✚ mw bid for 3-4 w.
Protocol A+B+C:
Antibiotic Therapy
• Implant with plaque & calculus deposit
• positive BOP
• PPD ≥ 6 mm
• Absence or presence of suppuration
• Bone loss
Mechanical ✚ antiseptic ✚ systemic antibiotic treatment against
anaerobic bacteria “ metronidazole” or combination “amoxicillin
+metronidazole” for 10 days.
Local delivery devices : tetracycline fibers & minocycline microspheres
Protocol A+B+C+D:
Regenerative or Resective Therapy
• After peri-implant infection is under control
• Depending on the extent & severity of local bone loss
Surgical options: regenerative (bone graft, membrane)or resective
(osteoplasty or ostectomy ,implantoplasty with ADF)
Regenerative therapy
After removing granulation tissues
Membrane
Pre- operative
Bone graft Postoperative
of " CIST "
PD< 3 PD=4-5 PD≥6
Presence
of plaque
+ BOP
Absence of
plaque
No BOP
BOP +
No bone
loss
BOP+ bone
loss ≤2mm
BOP+ bone
loss ≥ 2mm
No
Rx
Mechanical
RX
Antisepti
c RX Antibiotic
RX
Surgical
RX
+ + +A C D
+ + +
Peri-implant diseases and their treatment.

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Peri-implant diseases and their treatment.

  • 4. Improper proximal Space Retained cement Improper positioning(facially) /angulation Inadequate attached gingiva Additional factors
  • 5. Peri-implant mucositis: Is a Inflammatory process in the tissues surrounding the implant Reversible infl of peri- implant soft tissues surrounding a functioning implant(caused by plaque) Inflammatory process around implants involves loss of peri- implant bone.(crater formation) Peri-implantitis:
  • 6. Tooth Implant PDL, bone and cementum PDL Between bone & cementum Absent PDL & cementum (Direct bone-implant contact Supracrestal fibers Run perpendicular to tooth surface Run parallel to implant surface Connective tissues within the supracrestal region Less collagen(60%) & more fibroblast(5-15%) More collagen (85% ) & less fibroblast (1-3% ) & this is the characteristic of scar tissue (  collagen &  cells) Biological width 2mm 3-4mm Vascularization Comes from: 1. Supraperiosteal B.V. 2. BV from alv. process 3. Vascular plexus of the PDL Comes only from the large supraperiosteal B.V. Soft tissues turn over More rapid(more nutrition & cells) Less rapid(few BV & fibroblasts)
  • 7.
  • 8. Similar to gingivitis in natural teeth The Same Classic symptoms of infl. like redness, swelling, BOP. Clinical Features Histopathological features Teeth and implant mucosa have the same response to plaque.(plaque will cause  neutrophils ✚lymphocytes ✚ macrophages) BUT • Peri-implant mucosa is less capable to repair.
  • 9. – Inflammation of peri-implant mucosa (BOP, redness & PD) – Crater bone loss (in radiograph) – Suppuration may be found. – Implant is immobile and in function. Clinical Features
  • 10. Histological features – Plaque ass. with both lesions are similar(same MO dominating by G-ve & anaerobic species) BUT •  vasculature faster destruction & progression. • Plaque invade CT infl. Cell infiltration more severe with implants (Plasma cells ✚ Lymphocytes ✚macrophages). • The apical part of infl. lesion in CT is in a direct contact with bacteria in contrast with that of tooth. N.B Progression of peri-implantitis is more in implants with rough surface than at smooth surfaces. y??? Rough surface acts as plaque retentive area
  • 11. Formation of biofilm Inflammatory lesion in the peri-implant mucosa ( in the C.T lateral to the barrier epi.) If untreated It extends apically to the bone Compromise the osteointegration ( marginal bone loss)
  • 13. • Bleeding on probing • Suppuration. • Probing depth around the implant. • Radiographic evidence of bone loss. • Mobility of the implant by?? ★Absence of BOP indicates the peri-implant mucosa is healthy and stable. ★Implant mobility indicates defect osseointegration  implant removal. Periotest
  • 14. Progressive alv. bone loss, pocket formation, BOP,suppuration LOSS of osseointegration, mobility, or pain Hopeless and nonfunctional implant☛ FAILED ➨removal FAILING Implant ➨treatment When things go wrong!!!
  • 15. Treatment of failing implants • Resolution of inflammation – Debridement – Improvement of OH – Adjunctive antibiotics • Correction of unfavorable ST morphology (pseudopockets➨by flap surgery / gingivectomy) • Re-osseointegration – Decontaminate implant surface (with citric acid or tetracycline soln.)+ GBR Treatment of failed implants • Remove the implant • GBR and subsequent placement of implant.
  • 16. Case 1: Bone graft around a failing implant Allograft bone +membrane Granulation tissues were removed + decontamination by tetracycline Crater bone loss but stable implant Flap closure+ antibiotic regimen
  • 17. 6mm pocket +circumferential bone loss Case 2: removal of failed implant freeze-dried bone allograft (FDBA) + Ti- reinforced membrane Re-enter after 6 m New implant replacement
  • 19. The Aim : Early detection of peri-implant infection & to intercept the problems with proper therapy. How? Regular recalls ✚ repeated assessment of following parameter. • Presence of biofilm. • Presence or absence of BOP. • Presence or absence of suppuration. • Increased peri-implant PD. • Evidence & extent of radiographic alv. bone loss.
  • 20. Oral implant surrounded by healthy periodontium • Absence of BOP • Absence of suppuration • Probing depth < 3mm NO therapeutic measurement.
  • 21. Protocol A: Mechanical Debridement • Implant with plaque & calculus deposit. • BOP • PD ≤ 3mm • No Suppuration OHI + mech. Debridement + polishing
  • 22. Protocol A+B: Antiseptic Therapy • Implant with plaque & calculus deposit. • BOP • PPD = 4-5 mm • May or not demonstrate suppuration CHX gel application / irrigation ✚ mw bid for 3-4 w.
  • 23. Protocol A+B+C: Antibiotic Therapy • Implant with plaque & calculus deposit • positive BOP • PPD ≥ 6 mm • Absence or presence of suppuration • Bone loss Mechanical ✚ antiseptic ✚ systemic antibiotic treatment against anaerobic bacteria “ metronidazole” or combination “amoxicillin +metronidazole” for 10 days. Local delivery devices : tetracycline fibers & minocycline microspheres
  • 24. Protocol A+B+C+D: Regenerative or Resective Therapy • After peri-implant infection is under control • Depending on the extent & severity of local bone loss Surgical options: regenerative (bone graft, membrane)or resective (osteoplasty or ostectomy ,implantoplasty with ADF)
  • 25. Regenerative therapy After removing granulation tissues Membrane Pre- operative Bone graft Postoperative
  • 26. of " CIST " PD< 3 PD=4-5 PD≥6 Presence of plaque + BOP Absence of plaque No BOP BOP + No bone loss BOP+ bone loss ≤2mm BOP+ bone loss ≥ 2mm No Rx Mechanical RX Antisepti c RX Antibiotic RX Surgical RX + + +A C D + + +