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Peri-implant
diseases and
its management
Definition
 Peri-implant disease- Peri-implant disease is a collective
term for inflammatory processes in the tissues surrounding
an implant - Albrektsson & Isidor 1993, 1st EWP, Switzerland.
 Definition of Mombelli A, Lang N.P 1998- pathological
inflammatory changes that take place in the tissue
surrounding a load bearing implant
Normal v/s peri-implant tissues
Periodontal Peri-implant
Difference in probing and
clinical condition
Peri-implant mucositis
 Albrektsson & Isidor (1994) reversible inflammatory reactions in
the soft tissues surrounding a functioning implant.
 According to Kostovillis (2008) Inflammatory changes which are
confined to the soft tissue surrounding an implant with no signs of
loss of supporting bone.
 Roos-Jansaker AM et al. prevalence is 48% of implants followed
from 9 to 14 years
Clinical features
• Probing depth > 4mm
• BOP or suppuration
Histopathology
 Response to early plaque formation
 Pontoriero et al. (1994)- Inflammation and probing
depth change over a period of 3 weeks
 Zitzmann et al. (2001) also concluded that at the end
of 3 weeks of plaque built-up, increase in size of
peri-implant mucosa from 0.03 mm2 at baseline to
0.2 mm2
 Proportions of neutrophills increased in CT
 Response to long standing plaque formation
 Ericsson et al.- Inflammatory response same
 In gingival tissues amount of tissue breakdown that
occurs during the 3 month interval is more or less
fully compensated by the tissue built up during the
subsequent phases of repair.
 In the lesion within the peri-implant mucosa, the
tissue breakdown is not fully recovered by reparative
events. (reduced tissue built up)
Histopathology
Concluding remark
 Shares similarity with gingivitis in terms of host
response and development of clinical signs.
 it represents an obvious precursor to peri-implantitis.
 Early detection is essential.
Peri-implantitis
 The term “Peri-implantitis” was introduced in the late
1980s (Mombelli et al. 1987) and was subsequently
defined as “an inflammatory process affecting the
soft and hard tissues around a functioning
osseointegrated implant, resulting in loss of
supporting bone” (Albrektsson & Isidor 1994).
 In the consensus report from the 6th European
Workshop on Periodontology- peri-implant
mucositis was an inflammatory lesion that resides
in the mucosa, while peri-implantitis also affects
the supporting bone”. (Lindhe & Meyle 2008,
Zitzmann & Berglundh 2008).
 Peri-implantitis- progressive loss of supporting
bone beyond biological bone remodeling.
Consensus report of Working Group JCP 2012
Retrograde peri-implantitis
• First described by McAllister and colleagues.
Etiopathogenesis
 Biofilm formation
 Staph. Aureus for initiation and host response is
overwhelmed by gram –ve bacteria.
 The connective exhibit B-lymphocytes and plasma
cell infiltration
Etiopath…
 The rate of disease progression and the severity of
inflammatory signs different than periodontitis
 The increased susceptibility for bone loss around
implants may be related to the absence of inserting
collagen fibers into the implant
 spontaneous continuous progression of the disease
with additional bone loss
Risk factors
 Previous periodontal disease
 Residual cement
 Smoking
 Genetic factors
 Diabetes mellitus
 Occlusal overload
Emerging Risk factors
 Rheumatoid arthritis
 Premature loading
 Alcohol consumption
Clinical features
Classification
 Newman and Flemming (1992) have proposed a
classification of non successful implants, based on the
severity of peri-implantitis:
1. “Compromised successful implant” characterized by
inflammation, hyperplasia, fistula formation occurring
near an otherwise fully osseointegrated implant.
2. “Failing implant” characterized by progressive bone
resorption, but the implant remains functional.
3. “Failed implant” in which infection persists around an
implant whose function is compromised.
Classifications
 Based on the % of bone loss
 Froum SJ, Rosen PS, 2012
 Based on radiographic presentation of peri-
implant bone loss as 5 main types:
Zhang L, Geraets W, Zhou Y, et al, 2014
Diagnosis of peri-implantitis
 The examination of peri-implant tissues should
include:-
1. Evaluation of oral hygiene standard.
 Modified plaque index- Mombelli et al.
2. Evaluation of peri-implant marginal tissues.
 Probing, bleeding and suppuration
3. Evaluation of bone-implant interface
 Radiographs and mobility
Probing around implants
 Initial probing immediately before installing final
restoration using 0.25N probing force
 Gentle probing resulting in bleeding suggests the
presence of soft tissue inflammation
 presence of suppuration/exudate indicates
pathological changes
 Increasing probing depth and bleeding are
indicators for additional radiographic examination
Radiographs
 IOPA following placement and then following the
prosthesis installation should function as the
baseline
 Bone loss can have a number of nonbacterial
causes including surgical technique, implant
design, implant position, crestal thickness of bone,
loose prosthesis/abutment, and excessive occlusal
force
Treatment
approaches
Treatment
 Objectives in the therapy of peri-implantitis:
1. The removal of bacterial plaque within the peri-
implant pocket.
2. The decontamination and conditioning of the
implant surface.
3. Elimination of the sites that cannot be maintained
plaque-free by oral-hygiene procedures.
4. The establishment of an effective maintenance
program.
CIST
 Cummulative interceptive and supportive therapy
 Cumulative therapy depending on the clinical and
radiographic diagnosis
Nonsurgical approach
1. Mechanical debridement
 Hand Instruments coated with titanium, carbon fiber,
polytetrafluoroethylene, plastic, polyetheretherketone,
or silicon.
 Ultrasonic tips or polishing cups coated with carbon
fiber or plastic
 Air abrasive systems that use low abrasive amino acid,
glycine powder
2. Occlusal therapy
 An analysis of the fit of the prosthesis
 Prosthesis design changes, improvement in
implant number and occlusal equilibration can
contribute to the arrest of peri-implant tissue
breakdown progression
3. Antimicrobial therapy
 Systemic antibiotic
 Amoxicillin-CV 625mg BID
 Metronidazole 200mg TID
 Local antimicrobial
 Minocycline microspheres (1mg Arestin)
 doxycycline hyclate gel
 Tetracycline fiber (Actisite)
 Implant surface decontamination:
 Saline, citric acid,
 hydrogen peroxide, EDTA
Laser
• The commonly used lasers for the decontamination of
the implant surface are:
 Nd:YAG (1064 nm),
 Erbium:yttrium-aluminium garnet(Er:YAG)(2940 nm),
 Diode (660 nm), and
 Carbon dioxide (10600 nm) lasers
• Er:YAG laser could remove the bacterial-contaminated
titanium oxide layer, thus promoting reosseointegration
Nevins M, Nevins ML, Yamamoto A, et al. 2014
Photodynamic therapy
• The activation of these dyes, such as toluidine
blue-O, using specific wavelength of light
(630– 700 nm) causes the release of oxygen
radicals that will decimate periodontal
pathogens.
 Konopka K, Goslinski T. 2007
Surgical interventions
1. ACCESS FLAP
 The objective of the access flap is to gain
access to submucosal implant surface for
debridement and decontamination
2. Implantoplasty
• Clinical trial reported that implants treated with implantoplasty had
a higher implant survival rate compared with those that were treated
with an apically positioned flap only
Romeo E, Ghisolfi M, Murgolo N, et al, 2005
• 2 gm amox 1 hr prior to surgery
• FTF to expose the area
• Debride the defect with titanium or plastic curettes
• Air powder abrasive (Bicarbonate powder) for 60 Sec
• 60 sec irrigation with sterile saline
• 60 sec application of tetracycline
• Defect filled with Bone Graft
• Membranes are placed to cover all surfaces
• Flap released and coronally advanced and sutured.
REGENERATIVE APPROACH
• The effectiveness of 4 surgical procedures (access
flap and debridement alone, Surgical resection,
regeneration with bone grafts, and guided bone
regeneration) were studied in a systematic review
and meta-analysis
• Each of the 4 procedures yielded roughly 2 to 3
mm PD reduction
• 2-mm increase in bone height was associated with
the regenerative procedures in a systematic review
Chan HL, Lin GH, Suarez F, et al 2014
MAINTENANCE
Needs to be individually determined
Needs to be enforced by doctor and Hygienist
Patient need to assume responsibility
Low Risk Patients
-Highly motivated
-Excellent oral hygiene
-One or two implants
-No associative risk
factors
Moderate Risk
Patients
-Loss of motivation
-Fair oral hygiene
-3-6 implants
-Moderate smoker
(half pack)
-Controlled medical
issues
High Risk Patients
-Unmotivated
-Poor oral hygiene
-Previous periodontitis
->6 implants
-Smokers more than
half pack
-Poorly controlled
systemic diseases
 There is no single superior antiinfective method available.
 Surgical interventions achieved greater probing depth
reduction and clinical attachment gain compared with
nonsurgical
 Access flap surgery shows resolution in only 58% of the
lesions.
 The combination of resective and regenerative surgical
techniques seemed to have favorable treatment outcomes in
the management of periimplantitis.
 Reosseointegration of a previously contaminated implant
surface is possible but highly variable and unpredictable.
Summery & Conclusion
 Similarity between periodontal and peri-implant
diseases
 Early diagnosis of peri-implantitis is imperative
 Several risk factors exist for the development of peri-
implantitis, which can guide patient selection and
treatment planning.
 Treatment of peri-implantitis should be tailored to the
severity of the lesion (as outlined by the CIST
protocol), which ranges from non surgical to surgical
approach
Refrences
1. Rosen P, Clem D, Cochran D, et al. Peri-implant mucositis and peri-
implantitis: a current understanding of their diagnoses and clinical
implications. J Periodontol 2013;84(4):436–43.
2. Froum SJ, Rosen PS. A proposed classification for peri-implantitis.
Int J Periodontics Restorative Dent 2012;32(5):533–40.
3. Schwarz F, Herten M, Sager M, et al. Comparison of naturally
occurring and ligature-induced peri-implantitis bone defects in
humans and dogs. Clin Oral Implants Res 2007;18(2):161–70.
4. Zhang L, Geraets W, Zhou Y, et al. A new classification of peri-
implant bone morphology: a radiographic study of patients with
lower implant-supported mandibular overdentures. Clin Oral
Implants Res 2014;25(8):905–9.
5. Padial-Molina M, Suarez F, Rios HF, et al. Guidelines for the
diagnosis and treatment of peri-implant diseases. Int J
Periodontics Restorative Dent 2014;34(6):e102–11.
5. Saaby M, Karring E, Schou S, et al. Factors influencing severity
of peri-implantitis. Clin Oral Implants Res 2014.
6. Heitz-Mayfield LJ. Peri-implant diseases: diagnosis and risk
indicators. J Clin Periodontol 2008;35(8 Suppl):292–304.
7. Jia-Hui Fu, Hom-Lay Wang. Can Periimplantitis Be Treated?
Dent Clin N Am.2015:59;951–980.
Peri implant Diseases and its management

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Peri implant Diseases and its management

  • 2. Definition  Peri-implant disease- Peri-implant disease is a collective term for inflammatory processes in the tissues surrounding an implant - Albrektsson & Isidor 1993, 1st EWP, Switzerland.  Definition of Mombelli A, Lang N.P 1998- pathological inflammatory changes that take place in the tissue surrounding a load bearing implant
  • 3. Normal v/s peri-implant tissues Periodontal Peri-implant
  • 4. Difference in probing and clinical condition
  • 5. Peri-implant mucositis  Albrektsson & Isidor (1994) reversible inflammatory reactions in the soft tissues surrounding a functioning implant.  According to Kostovillis (2008) Inflammatory changes which are confined to the soft tissue surrounding an implant with no signs of loss of supporting bone.  Roos-Jansaker AM et al. prevalence is 48% of implants followed from 9 to 14 years
  • 6. Clinical features • Probing depth > 4mm • BOP or suppuration
  • 7. Histopathology  Response to early plaque formation  Pontoriero et al. (1994)- Inflammation and probing depth change over a period of 3 weeks  Zitzmann et al. (2001) also concluded that at the end of 3 weeks of plaque built-up, increase in size of peri-implant mucosa from 0.03 mm2 at baseline to 0.2 mm2  Proportions of neutrophills increased in CT
  • 8.  Response to long standing plaque formation  Ericsson et al.- Inflammatory response same  In gingival tissues amount of tissue breakdown that occurs during the 3 month interval is more or less fully compensated by the tissue built up during the subsequent phases of repair.  In the lesion within the peri-implant mucosa, the tissue breakdown is not fully recovered by reparative events. (reduced tissue built up) Histopathology
  • 9. Concluding remark  Shares similarity with gingivitis in terms of host response and development of clinical signs.  it represents an obvious precursor to peri-implantitis.  Early detection is essential.
  • 10. Peri-implantitis  The term “Peri-implantitis” was introduced in the late 1980s (Mombelli et al. 1987) and was subsequently defined as “an inflammatory process affecting the soft and hard tissues around a functioning osseointegrated implant, resulting in loss of supporting bone” (Albrektsson & Isidor 1994).
  • 11.  In the consensus report from the 6th European Workshop on Periodontology- peri-implant mucositis was an inflammatory lesion that resides in the mucosa, while peri-implantitis also affects the supporting bone”. (Lindhe & Meyle 2008, Zitzmann & Berglundh 2008).  Peri-implantitis- progressive loss of supporting bone beyond biological bone remodeling. Consensus report of Working Group JCP 2012
  • 12. Retrograde peri-implantitis • First described by McAllister and colleagues.
  • 13. Etiopathogenesis  Biofilm formation  Staph. Aureus for initiation and host response is overwhelmed by gram –ve bacteria.  The connective exhibit B-lymphocytes and plasma cell infiltration
  • 14. Etiopath…  The rate of disease progression and the severity of inflammatory signs different than periodontitis  The increased susceptibility for bone loss around implants may be related to the absence of inserting collagen fibers into the implant  spontaneous continuous progression of the disease with additional bone loss
  • 15. Risk factors  Previous periodontal disease  Residual cement  Smoking  Genetic factors  Diabetes mellitus  Occlusal overload Emerging Risk factors  Rheumatoid arthritis  Premature loading  Alcohol consumption
  • 17. Classification  Newman and Flemming (1992) have proposed a classification of non successful implants, based on the severity of peri-implantitis: 1. “Compromised successful implant” characterized by inflammation, hyperplasia, fistula formation occurring near an otherwise fully osseointegrated implant. 2. “Failing implant” characterized by progressive bone resorption, but the implant remains functional. 3. “Failed implant” in which infection persists around an implant whose function is compromised.
  • 18. Classifications  Based on the % of bone loss  Froum SJ, Rosen PS, 2012
  • 19.  Based on radiographic presentation of peri- implant bone loss as 5 main types: Zhang L, Geraets W, Zhou Y, et al, 2014
  • 20. Diagnosis of peri-implantitis  The examination of peri-implant tissues should include:- 1. Evaluation of oral hygiene standard.  Modified plaque index- Mombelli et al. 2. Evaluation of peri-implant marginal tissues.  Probing, bleeding and suppuration 3. Evaluation of bone-implant interface  Radiographs and mobility
  • 21. Probing around implants  Initial probing immediately before installing final restoration using 0.25N probing force  Gentle probing resulting in bleeding suggests the presence of soft tissue inflammation  presence of suppuration/exudate indicates pathological changes  Increasing probing depth and bleeding are indicators for additional radiographic examination
  • 22. Radiographs  IOPA following placement and then following the prosthesis installation should function as the baseline  Bone loss can have a number of nonbacterial causes including surgical technique, implant design, implant position, crestal thickness of bone, loose prosthesis/abutment, and excessive occlusal force
  • 24. Treatment  Objectives in the therapy of peri-implantitis: 1. The removal of bacterial plaque within the peri- implant pocket. 2. The decontamination and conditioning of the implant surface. 3. Elimination of the sites that cannot be maintained plaque-free by oral-hygiene procedures. 4. The establishment of an effective maintenance program.
  • 25. CIST  Cummulative interceptive and supportive therapy  Cumulative therapy depending on the clinical and radiographic diagnosis
  • 26. Nonsurgical approach 1. Mechanical debridement  Hand Instruments coated with titanium, carbon fiber, polytetrafluoroethylene, plastic, polyetheretherketone, or silicon.  Ultrasonic tips or polishing cups coated with carbon fiber or plastic  Air abrasive systems that use low abrasive amino acid, glycine powder
  • 27. 2. Occlusal therapy  An analysis of the fit of the prosthesis  Prosthesis design changes, improvement in implant number and occlusal equilibration can contribute to the arrest of peri-implant tissue breakdown progression
  • 28. 3. Antimicrobial therapy  Systemic antibiotic  Amoxicillin-CV 625mg BID  Metronidazole 200mg TID  Local antimicrobial  Minocycline microspheres (1mg Arestin)  doxycycline hyclate gel  Tetracycline fiber (Actisite)  Implant surface decontamination:  Saline, citric acid,  hydrogen peroxide, EDTA
  • 29. Laser • The commonly used lasers for the decontamination of the implant surface are:  Nd:YAG (1064 nm),  Erbium:yttrium-aluminium garnet(Er:YAG)(2940 nm),  Diode (660 nm), and  Carbon dioxide (10600 nm) lasers • Er:YAG laser could remove the bacterial-contaminated titanium oxide layer, thus promoting reosseointegration Nevins M, Nevins ML, Yamamoto A, et al. 2014
  • 30. Photodynamic therapy • The activation of these dyes, such as toluidine blue-O, using specific wavelength of light (630– 700 nm) causes the release of oxygen radicals that will decimate periodontal pathogens.  Konopka K, Goslinski T. 2007
  • 31. Surgical interventions 1. ACCESS FLAP  The objective of the access flap is to gain access to submucosal implant surface for debridement and decontamination
  • 32. 2. Implantoplasty • Clinical trial reported that implants treated with implantoplasty had a higher implant survival rate compared with those that were treated with an apically positioned flap only Romeo E, Ghisolfi M, Murgolo N, et al, 2005
  • 33. • 2 gm amox 1 hr prior to surgery • FTF to expose the area • Debride the defect with titanium or plastic curettes • Air powder abrasive (Bicarbonate powder) for 60 Sec • 60 sec irrigation with sterile saline • 60 sec application of tetracycline • Defect filled with Bone Graft • Membranes are placed to cover all surfaces • Flap released and coronally advanced and sutured. REGENERATIVE APPROACH
  • 34.
  • 35. • The effectiveness of 4 surgical procedures (access flap and debridement alone, Surgical resection, regeneration with bone grafts, and guided bone regeneration) were studied in a systematic review and meta-analysis • Each of the 4 procedures yielded roughly 2 to 3 mm PD reduction • 2-mm increase in bone height was associated with the regenerative procedures in a systematic review Chan HL, Lin GH, Suarez F, et al 2014
  • 36. MAINTENANCE Needs to be individually determined Needs to be enforced by doctor and Hygienist Patient need to assume responsibility Low Risk Patients -Highly motivated -Excellent oral hygiene -One or two implants -No associative risk factors Moderate Risk Patients -Loss of motivation -Fair oral hygiene -3-6 implants -Moderate smoker (half pack) -Controlled medical issues High Risk Patients -Unmotivated -Poor oral hygiene -Previous periodontitis ->6 implants -Smokers more than half pack -Poorly controlled systemic diseases
  • 37.
  • 38.  There is no single superior antiinfective method available.  Surgical interventions achieved greater probing depth reduction and clinical attachment gain compared with nonsurgical  Access flap surgery shows resolution in only 58% of the lesions.  The combination of resective and regenerative surgical techniques seemed to have favorable treatment outcomes in the management of periimplantitis.  Reosseointegration of a previously contaminated implant surface is possible but highly variable and unpredictable.
  • 39. Summery & Conclusion  Similarity between periodontal and peri-implant diseases  Early diagnosis of peri-implantitis is imperative  Several risk factors exist for the development of peri- implantitis, which can guide patient selection and treatment planning.  Treatment of peri-implantitis should be tailored to the severity of the lesion (as outlined by the CIST protocol), which ranges from non surgical to surgical approach
  • 40.
  • 41.
  • 42. Refrences 1. Rosen P, Clem D, Cochran D, et al. Peri-implant mucositis and peri- implantitis: a current understanding of their diagnoses and clinical implications. J Periodontol 2013;84(4):436–43. 2. Froum SJ, Rosen PS. A proposed classification for peri-implantitis. Int J Periodontics Restorative Dent 2012;32(5):533–40. 3. Schwarz F, Herten M, Sager M, et al. Comparison of naturally occurring and ligature-induced peri-implantitis bone defects in humans and dogs. Clin Oral Implants Res 2007;18(2):161–70. 4. Zhang L, Geraets W, Zhou Y, et al. A new classification of peri- implant bone morphology: a radiographic study of patients with lower implant-supported mandibular overdentures. Clin Oral Implants Res 2014;25(8):905–9.
  • 43. 5. Padial-Molina M, Suarez F, Rios HF, et al. Guidelines for the diagnosis and treatment of peri-implant diseases. Int J Periodontics Restorative Dent 2014;34(6):e102–11. 5. Saaby M, Karring E, Schou S, et al. Factors influencing severity of peri-implantitis. Clin Oral Implants Res 2014. 6. Heitz-Mayfield LJ. Peri-implant diseases: diagnosis and risk indicators. J Clin Periodontol 2008;35(8 Suppl):292–304. 7. Jia-Hui Fu, Hom-Lay Wang. Can Periimplantitis Be Treated? Dent Clin N Am.2015:59;951–980.

Editor's Notes

  1. Retrograde peri-implantitis is defined as a radiographically diagnosed, periapical, lucent lesion that is symptomatic and that develops shortly after implant placement.
  2. self-limiting” process existing in the tissues
  3. Boneloss on the buccal and lingual surfaces of implant
  4. Protocol of access flap Elevation of full thickness flap Debridement of the implant surface Decontamination Postoperative antimicrobial and antiseptic mouth rinses.
  5. Increase in bone height may not be reosseointegrated bone but merely bone filling a space. Even nonosseointegrated bone in a treated lesion could be an achievable treatment goal that would provide for more favorable maintenance, esthetics, and implant stability compared with a lack of new bone.