3. Introduction:
• Osseointegrated dental implants have become an increasingly popular modality of
treatment for the replacement of absent or lost teeth. Dental implants have high rates
of long‐term survival (≥10 years) when used to support various types of dental
prostheses.
• However, the long‐term success of dental implants is not the same or as high as their
survival, as functional implants and their restorations may be subject to mechanical
and biological complications.
• Biological complications associated with dental implants are mostly inflammatory
conditions of the soft tissues and bone surrounding implants and their restorative
components, which are induced by the accumulation of bacterial biofilm.
• Such conditions, which have been named peri‐implant mucositis and peri‐implantitis,
need to be clearly defined and differentiated from a state of peri‐implant health.
4. • Much attention has been given to the terms ‘‘ailing’’ and ‘‘failing’’
when referring to implant health.
• It has been proposed that an ‘‘ailing’’ implant demonstrates
radiographic evidence of bone loss and probing depths more than 5
mm that are stable when reevaluated at 3 to 4 months.
• A ‘‘failing’’ implant demonstrates increasing probing depths,
suppuration or bleeding when probed, and progressive bone loss. A
failed implant no longer is osseointegrated or never achieved
osseointegration
6. Peri‐implant health:
• Araujo and Lindhe also concluded that
peri‐implant health requires the absence of
clinical signs of inflammation (i.e. erythema and
swelling) including no bleeding on probing.
The diagnosis of peri‐implant health requires:
• 1. Visual inspection demonstrating the absence
of peri‐implant signs of inflammation: pink as
opposed to red, no swelling as opposed to
swollen tissues, firm as opposed to soft tissue
consistency
• 2. Lack of profuse (line or drop) bleeding on
probing
• 3. Probing pocket depths could differ depending
on the height of the soft tissue at the implant
location. An increase in probing depth over time,
however, conflicts with peri‐implant health; and
4. Absence of further bone loss following initial
healing, which should not be ≥2 mm.
7. Definitions:
• The American Academy of Periodontology has defined
peri‐implant mucositis as a disease that includes
inflammation of the soft tissues surrounding a dental
implant, without additional bone loss after the initial
bone remodeling that may occur during healing
following the surgical placement of the implant.
• Peri‐implantitis has been defined as an inflammatory
lesion of the mucosa surrounding an endosseous
implant and with progressive loss of supporting
peri‐implant bone.
8. Peri-implantitis
definition:
Peri-implantitis is defined as an inflammatory process affecting tissues
around osseointegrated implants in function there by resulting in loss
of supporting bone.(ALBERKTSSON AND LINDHE)1st European
workshop on periodontology .
6 th European workshop of periodontology defined peri-implantitis as
mucosal inflammation with loss of supporting bone
(LINDHE,MEYLE,ZITMAN AND BREGLUNDH)
7th European workshop of periodontology defined as change of
crestal bone with time and bleedingon probing with or without
deepening of probing pocket depth. (LANG AND BERGLUNDH)
8 th European workshop of periodontology by SANZ AND CHAPPLE
defined whenever baseline radiographs were unavailable a vertical
distance of 2mm from expected crestal bone level following
remodelling after implant placement .
9. World workshop 2017:
Current definition of peri‐implantitis
• Peri‐implantitis is a pathological
condition occurring in tissues around
dental implants, characterized by
inflammation in the peri‐ implant
mucosa and progressive loss of
supporting bone
10.
11. Prevalence:
Based on the Consensus Report of the Sixth European Workshop in
Periodontology, Lindhe & Meyle reported an incidence of mucositis of
up to 80% and of peri-implantitis between 28% and 56%
Systematic review in 2013- Ateih et al- estimated prevalence of
implant based and subject based peri implantitis is 9.6 % and 18.8%,
and peri implant mucositis is 30.7% and 63.4%.
Systematic review in 2015- Derks and Tomasi -The prevalence for peri-
implant mucositis was reported at 43% (range, 19% to 65%), whereas
for peri-implantitis it amounted to 22% (range, 1% to 47%;).
Systematic review in 2017- Lee et al- estimated prevalence of implant
based and subject based peri implantitis is 9.25 % and 19.83%, and
peri implant mucositis is 29.48% and 46.83%
12. Pathogenesis:
• Peri-implant disease following successful
integration of an endosseous implant is the
result of an imbalance between the
bacterial challenge and the host response.
• It was shown that bacterial colonization
occurred immediately following
transmucosal implant placement (30 min)
and was stable after 2 weeks
13. Evidence of microbiota in peri implantitis:
There are essentially five lines of evidence supporting the view that
microorganisms play a major role in causing peri-implantitis:
(i) an experiment in humans, showing that deposition of plaque on implants
can induce peri-implant mucositis,
(ii) the demonstration of distinct quantitative and qualitative differences in
the microflora associated with successful and failing implants
(iii) placement of plaque-retentive ligatures in animals leading to shifts in the
composition of the microflora and peri-implantitis
(iv) antimicrobial therapy improving the clinical status of peri-implantitis
patients, and
(v) evidence that the level of oral hygiene has an impact on the long-term
success of implant therapy
14. Induction of peri-implantitis by placement of plaque retentive ligatures
in animals (Lindhe et al 1992; Lang et al 1993)
Peri-implant microflora is established shortly after implant placement.
Successful implants experience no shifts in microbial composition over
time. (Bower et al 1989; Mombelli et al 1990)
Therapy aimed at a reduction of the peri-implant microflora improves
clinical conditions (Ericsson et al 1996; Mombelli et al 1992)
15. Microbiota associated with peri implant
disease:
• Association studies have identified a microbiota characterized by high counts and
proportions of gram-negative anaerobic bacteria around implants with clinical signs of
peri-implantitis.
• These studies have found a high prevalence of pathogens associated with periodontitis,
which included members of the red complex species (Porphyromonas gingivalis,
Treponema denticola and Tannerella forsythia) and orange complex species
(Fusobacterium sp. and Prevotella intermedia), as defined by Socransky et al.
• The presence of Aggregatibacter actinomycetemcomitans has also been reported at peri-
implantitis sites.
• A number of studies have also reported an association between the presence of
Staphylococcus aureus, enteric rods and Candida albicans, and periimplantitis
16. Histological differences between periodontitis
and peri-implantitis:
Periodontitis:
• Less number of elastases.
• Inflammatory infiltrate in mostly
confined to connective tissue.
• Chronic type of infection
showing more of interleukin-1α
Peri-implantitis:
• More number of elastases.
• Inflammatory infiltrate is in
direct contact with the bone-
predominated by T and B cells.
• Acute type of infection showing
more of TNF-α
17. Risk indicators:
Local factors:
• Oral hygiene
• Foreign body
• Periodontal health
• Soft tissue conditions
• Peri-implant pocket depth
• Roughness of transmucosal
parts
• Implant prosthesis connection
General factors:
• History of periodontitis
• Genetics
• Acquired factors( diabetes, etc)
• Environmental factors (smoing,
alcohol consumption, stress)
18. Oral hygiene
and patient
compliance:
• Outcomes of cross‐sectional clinical studies have clearly indicated
that biofilm accumulation is associated with the presence of peri‐
implant mucositis around osseointegrated dental implants.
• Outcomes of study by Roos‐Jansaker et al involving 218 patients with
999 implants in function for a period of 9 to 14 years indicated that
plaque scores were significantly associated with the presence of
peri‐implant mucositis.
• Among patients not adhering to regular supportive implant therapy
(SIT), peri‐implant mucositis was reported to be a common finding
with a prevalence of 48% during an observation period of 9 to 14
years
• In partially edentulous patients, pre‐existing peri‐implant mucositis in
conjunction with lack of adherence to SIT was associated with a
higher incidence of peri‐implantitis during a 5‐year follow‐ up study
by Costa et al. The outcomes of that study yielded a 5‐year incidence
of peri‐implantitis of 18.0% in the group of patients with SIT and of
43.9% in the group without SIT, respectively. This study showed an
odd, ratio of 5.92
19. History of periodontitis:
There is strong evidence from longitudinal and cross‐sectional studies that a history of
periodontitis constitutes a risk factor/indicator for peri‐implantitis.
In two 10‐year longitudinal studies, peri‐implantitis was assessed and correlated with a history
of periodontitis. Karoussis et al. pro‐ vided implant therapy to 45 patients without a history of
periodontitits. A total of eight patients were treated with implants after having successfully
completed periodontal therapy. The 10‐year incidence of peri‐implantitis (case definition: PD
≥5 mm, BOP+ and annual bone loss >0.2 mm) in the non‐periodontitis group was 6% (implant
level) compared to 29% in subjects with a history of periodontitis.
Roccuzzo et al. followed 101 patients provided with den‐ tal implants after having been
categorized as 1) periodontally not compromised, 2) moderately compromised and 3) severely
com‐ promised.90,91 The authors reported that both the frequency of im‐ plant sites
demonstrating PD ≥6 mm (2%, 16%, 27%, respectively) and bone loss ≥3 mm (5%, 11%, 15%,
respectively) differed signifi‐ cantly between groups. The results also showed that treatment of
peri‐implantitis was more time consuming in patients with a history of periodontitis.
20. In a follow‐up study of 80 patients presenting with mucositis at baseline, the incidence of
peri‐implantitis over 5 years was assessed by Costa et al. The authors observed an overall
incidence of peri‐implantitis of 31%. Patients suffering from periodontitis at the final
examination had significantly higher odds to also have developed peri‐implantitis when
compared to individuals without periodontitis (OR 9).
In a study including 216 patients were evaluated 9 to 14 years after implant therapy,
Roos‐Jansåker et al. reported that implants placed in patients with a history of periodontits
had significantly higher odds (OR 5) for peri‐implantitis when compared to implants in
patients without.
Koldsland et al. reported similar findings after examining 109 subjects with 1 to 16 years of
follow‐up.94,95 Thus, patients with a history of periodontitis were found to be at higher risk
for peri‐implantitis (OR 6).
21. Daubert et al. found that severe periodontitis at follow‐up was the strongest
indicator for peri‐implantitis of all variables examined, presenting with an
unadjusted risk ratio of 7.
Derks et al., in a 9‐year follow‐up including 588 patients reported an odds ratio of 4
for patients with current periodontitis.
Studies by Marrone et al. and Rokn et al. failed to demonstrate a higher risk for
peri‐implantitis in patients with current periodontitis and history of periodontitis
respectively. Disagreement between studies may be explained by differences in case
definitions for 1) (history of) periodontitis and 2) peri‐implantitis
22. • Four systematic reviews; Van der Weijden et al. (2005), Schou et al.
(2006), Karoussis et al. (2007) and Quirynen et al. (2007) showed an
increased risk for peri-implant disease.
• Metanalysis by Sgolastra et al in 2013- Strong evidence suggests that
periodontitis is a risk factor for implant loss; moderate evidence
revealed that periodontitis is a risk factor for peri‐implantitis and that
patients with periodontitis have higher implant‐bone loss.
23. In AgP:
• Systematic review by Zahrani et al 2008- Bone loss around implants in
aggressive periodontitis patients, however, appears to occur more
frequently than it does in chronic periodontitis patients or
periodontally healthy individuals.
• Systematic review by Kim et al 2012- The survival rates of implants
were between 83.3% and 96% in patients with GAP in long term
studies.
24. Remaining
teeth with
periodontitis:
• The periodontal status of remaining teeth
influences the composition of subgingival
microflora around implants because teeth
with periodontal disease may act as
reservoir for micro organisms.
• A non controlled periodontal lesion adjacent
to an implant may progress to involve the
tissues at the implant.
25. Genetics:
• Gene polymorphisms may affect gene expression, protein production
and cytokine secretion.
• Based on a cross‐sectional analysis, Gruica et al. reported that 64 out
of 180 patients revealed a positive IL‐1 composite gene
polymorphism (IL‐1α +4845; IL‐1β +3954) and a total of 34 patients
(51 implants) were associated with biological complications (unclear
case definition) at 8 to 15 years after implant therapy.141 An
association between a posi‐ tive IL‐1 composite gene polymorphism
and the occurrence of biologi‐ cal complications was, however,
observed only in a subgroup of heavy smokers (≥20 cigarettes per
day).
• In another cross‐sectional analysis, Laine et al. identified a
significantly higher prevalence of IL‐1 receptor antagonist (IL‐1RA)
polymorphisms in patients that were diagnosed with peri‐implantitis
(case definition: BOP+ and/or suppuration, bone loss >3 threads at
machined implants) when compared with patients showing healthy
control implants (57% vs. 33%; OR 3).140 Similar findings were
reported by Hamdy and Ebrahem, showing that a positive IL‐1
composite gene polymorphism (IL‐1α ‐889; IL‐1β +3954) was
significantly higher among patients suffering from peri‐implantitis.
However, this association was not confirmed in other cross‐sectional
analyses
26. Diabetes:
• There is some evidence for diabetes mellitus
as a risk indicator for peri‐implant mucositis.
• Poorly controlled diabetes mellitus (HbA1c
levels > 10.1) was shown to be associated
with increased bleeding on probing at
implants.
• Ferreira et al. recorded peri‐implantitis in
24% of individuals who either medicated for
glycaemic control or presented with fasting
blood sugar ≥126 mg/dL at the final
examination. In contrast, only 7% of
non‐diabetic patients were diagnosed
accordingly. The authors reported an OR of
1.9.
27. Smoking:
• The presence of periodontitis or cigarette
smoking increased the risk for peri-implantitis
up to 4.7-fold as reported by Wallowy et al.
Moreover, smoking has been shown to be a
predictor for implant failure.
• In a recent meta-analysis by smoking increased
the annual rate of bone loss by 0.16 mm/year
• The meta‐analyses in 2020 by Naseri et al based
on implant- and patient- related data showed a
significant increase in the RR of implant failure
in patients who smoked >20 cigarettes per day
compared with non-smokers (Implant based: P =
0.001; RR: 2.45; CI: 1.42-4.22 and Patient based:
P < 0.001; RR: 4; CI: 2.72- 5.89).
Conclusion: The risk of implant failure was
elevated with an increase in the number of
cigarettes smoked per day
29. Stress:
• Psychosocial factors and stress have not
been established as influencing peri-
implantitis but may be of importance.
• Behavioural changes due to stress may result
in poor oral hygiene and an increase in
smoking and alcohol consumption.
30. Implant surface
characteristics:
• Evidence for the influence of implant surface roughness on the
incidence of peri‐implant mucositis in humans is limited.
• A 12‐month comparative analysis by Bollen et al in humans
between machined titanium abutments (Ra = 0.2 μm) and
highly polished ceramic abutments (Ra = 0.0 6 μm) indicated
that further reduction in surface roughness had no impact on
bleeding on probing (BOP) scores.
• A study by Wennerberg in humans investigated the association
between abutment surfaces of varying roughness and the
early inflammatory response of the peri‐implant mucosa.
Although a statistically significant difference among patients
was observed with respect to biofilm accumulation on the
abutment surfaces and inflammatory cells, no association was
observed between the inflammatory response and abutment
surface roughness after an observation period of 4 weeks.
• Clinical studies showed no significant differences in BOP scores
or slightly higher BOP scores were reported around ZrO2
compared with titanium abutments
31. Type of
implant-
suprastructure
connection:
• The gap between implant and the
suprastructure offers an ideal environment
for microbial colonization.
• Microbial leakage through this gap plays an
important role in bacterial colonization in
screw-retained restorations.
• It is advised that the abutment prosthesis
interface to be supramucosal to facilitate
oral hygiene procedure
• studies have indicated that platform switch
might be an important protective factor
against peri-implant disease
32. Presence of
submucosal
foreign body:
• The so called “cementitis” may be regarded as the most important
identifiable iatrogenic risk factor since its first description by Wilson
et al. in 2009 .
• If a non radiopaque cement is used for prosthetic cemntation, it will
not be visible on radiographs and may only be detected after patient
develops an infection.
• Korsch et al. found that the removal of cement remnants led to a
decrease of the inflammatory response by almost 60%.
• Linkevizius et al. examined the manifestation of peri-implantitis in a
group of patients with present cement remnants. In those who had a
history of periodontitis, peri-implantitis was found in 100% of the
patients, whereas cement remnants in patients with no previous
periodontal disease ended up in 65% peri-implantitis manifestations.
• peri‐implant mucositis was more prevalent in patients with cemented
prostheses compared with those with screw‐retained prostheses
• Therefore, to avoid cement excess, restoration margins should be
located at or above the peri‐implant mucosal margin or restorations
should be cemented on individual‐ ized abutments allowing proper
cement removal.
33. Endodontic
infections of
proximal
tooth:
• An implant can be contaminated by a natural
tooth with endodontic lesion. It is advised
not to place and implant adjcanet to teeth
with endodontic radiolucency.
34. Presence of
keratinized
mucosa:
• The impact of keratinized gingiva around dental
implants has been controversially discussed, but
most studies emphasize the importance of an
adequate zone of keratinized tissue surrounding
implants.
• In an experimental study in monkeys, absence of
keratinized gingiva around implants has shown
increased susceptibility to plaque induced tissue
destruction.
• Several clinical studies failed to associate the lack of
a minimum amount of KM with mucosal
inflammation, while other studies suggested that
plaque build‐up and marginal inflammation were
more frequent at implant sites with < 2 mm of KM.
36. Diagnosis:
• Esposito et al concluded that radiographic
examination and mobility testing were the most
reliable parameters in determining the
prognosis of osseointegrated implants.
37. Peri‐implant mucositis
• Peri‐implant mucositis has been defined as an inflammatory lesion of
the mucosa surrounding an endosseous implant without loss of
supporting peri‐implant bone.
• The important criteria for the definition of peri‐implant mucositis are
inflammation in the peri‐implant mucosa and the absence of
continuing marginal peri‐implant bone loss.
• The clinical sign of inflammation is bleeding on probing, while
additional signs may include erythema, swelling, and suppuration
38. Peri-implantitis:
Peri-implant probing depth
(≥5mm).
Radiographic bone loss of
>3mm.
Dist. b/w soft tissue margin &
ref. pt on the implant(soft
tissue hyperplasia or
recession)
Bleeding after gentle probing
Exudation & suppuration
from peri-implant space.
Mobility
Pain
41. Probing:
• Lang et al. reported that at sites with healthy mucosa or mucositis, the tip of the probe identified
the apical border of the barrier epithelium with an error of approximately 0.2 mm, while at sites
with peri‐implantitis, the measurement error was much greater at 1.5 mm.
• It was assumed that probing the implant–mucosa interface would sever the soft tissue seal and
jeopardize the integrity of the adhesion.
• Initial probing of the implant should be done once the final restoration has been installed.
• This can be done with a periodontal probe using light force (0.25N) because of the delicate and
unique anatomy of the peri-implant mucosa.
o Probing causes separation between the surface of the implant and the junctional epithelium-this
breach completely heal within 5 days of probing.
o Successful implants have 3mm of PD.
o 5mm or more PD is a sign of peri-implantitis.
o PD should not be measured during the first 3 weeks to avoid disturbing the healing and the
establishment of soft tissue seal.
42. Suppuration:
• The presence of pus suggests the existence of a
peri-implant disease with active deep lesions.
• In a clinical study evaluation healthy status of
tissues around implants after 9-14 years of
functional loading, it was noted that the
presence of pus is an important diagnostic
element in the detection of peri-implantitis.
43. Mobility:
Mobility often indicates end stage of disease. It should be differentiated from loosening of suprastructures.
Implant mobility is an indication for lack of osseointegration. The parameter rather serves to diagnose the
final stage of osseodisintegration and may help to decide that an implant has to be removed
Periotest
• An electronic device used to measure the mobility around natural teeth.
• Recommended to monitor initial degree of implant mobility.
• Force of 12 to 18 N.
Periotest values for implants:
o - 08 to -01: Implant is well osseointegrated
o 00 to +09: Clinical examination is necessary
o +10 & higher: Suspicious alarming.
Implant is not sufficiently osseointegrated
44. Resonance frequency analysis (RFA)
• Non invasive device based on the
resonance frequency analysis
used to measure implant stability
over a period of time.
• Evaluates the stiffness of bone
implant interface by means of a
signal traducer connected to a
frequency response organizer.
45. Indices:
• It has been suggested that the absence of a
periodontal ligament around implants and
the prosthetic design makes assessments
of pocket probing depth measurements at
dental implants difficult to perform and
interpret.
• Recognizing the issue, a modified bleeding
index has been proposed using a grading
scale of the extent of bleeding at dental
implants, where a score of “0” represents
healthy conditions, and a score of “1”
representing an isolated dot of bleeding.
• Modified plaque index and modified
gingival index are used.
46. Radiographic
examination:
• Peri apical radiographs should be taken to
evaluate the marginal bone level.
• Digital substraction radiographs has shown to
be more reliable in accessing the bone loss.
47. Bone defects: 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.
Jovanovic (1990) Spiekermann (1991)
Spiekermann characterized the type of bone resorption into horizontal
(class I), key-shaped (class II), funnel- and gap-like (class III a, b) as well
as horizontal-circular (class IV) forms
Galindo- moreno and collegues
found that marginal bone loss of
0.44mm per year as an indicator
of progressive peri- implantitis
49. Shwartz et al - 2007
According to the morphology was classified as follows:
• Class I: Infraosseous defect
Class Ia: Buccal dehiscence
Class Ib: 2-3 walls defect
Class Ic: Circumferential defect
• Class II: Supracrestal/horizontal defect
• Class III: Combined defect
Class IIIa: Buccal dehiscence + horizontal bone loss
Class IIIb: 2-3 walls defect + horizontal bone loss
Class IIIc: Circumferential defect + horizontal bone loss
– Each implant was subclassified to defect severity based upon the defect
depth from the implant neck and ratio of bone loss/total implant length:
• Grade S: Slight: 3-4 mm/<25% of the implant length
• Grade M: Moderate 4-5 mm/≥25%-50% of the implant length
• Grade A: Advanced: >6 mm/>50% of the implant length
51. INFECTIVE MARKERS
• □ Bacteria are major initiators of peri-implant mucositis and
peri‐implantitis as well as of periodontal diseases.
• □ Substantial differences exist in terms of anatomy and physiology
between the implant mucosa/bone interface and the periodontium; the
bacterial profiles and the host immune responses may be quite similar.
52. Author Study Conclusion
Cortelli et al (2013) P.gingivalis, T.forsythia, C.rectus,
P.intermedia, T.denticola, and A.ac
in periimplantitis and periodontitis
Trend towards higher
bacterial frequency around
teeth than around implants
Persson et al
(2014)
T. forsythia, P. gingivalis,
T.socranskii, S.aureus,
S.anaerobius, S.intermedius,
S.mitis
Test bacteria demonstrated
four times higher occurrence
in peri-implantitis
Tsigarida et al
(2015)
Influence of smoking on the
microbiome composition in
healthy and inflamed peri‐implant
conditions
Classic periodontal pathogens
seemed to be involved in the
transition from peri‐implant
health to disease
Zheng et al (2015) Subgingival microbiome in
patients with healthy and ailing
dental implants (P. gingivalis, T.
forsythia and P. intermedia)
Mucositis comprises an
important transitional phase
in the development of
peri‐implantitis
53. Sentinel biomarkers of peri‐implantitis
Staphylococcus aureus, Staphylococcus warneri, Parvimonas micra, E. nodatum,
Streptococcus mutans
Viral etiology in peri-implantitis (Akram et al; Meta analysis, 2019)
Frequencies of the viruses were increased in patients with PI compared with
healthy non-diseased sites. However, the findings of the present study should be
interpreted with caution because of significant heterogeneity and small number
of included studies.
54. GENETIC MARKERS
Case control association analysis of candidate genes - Main
research strategy adopted for the discovery of genetic risk
factors of peri‐implantitis.
Candidate genes have been selected based on the current
knowledge of the pathogenesis of peri‐implantitis.
GENETIC
POLYMORPHISMS
Immune function
Bone growth
Regulation of gene expression
Fourmousis I, Vlachos M. Genetic risk factors for the development of periimplantitis. Implant dentistry. 2019 Apr 1;28(2):103-14.
55. Author Gene
polymorphism
Conclusion
Liao and colleagues
(Meta analysis,
2014)
IL-1A(-889) and
IL-1B(+3954)
Increased risk of implant failure
(OR 1.76) and peri‐implantitis (OR
2.34)
Mo et al (Meta
analysis, 2016)
TNF-α No support for a role of TNF‐α was
found
Coelho et al (2016) BMPs and FGF Possible role for BMP‐6 and FGF-
10 in peri‐implantitis
Costa et al (2013) MMP-8 Early implant failure
Rakic et al (2015) CD14 Single Nucleotide
Polymorphism
Considering the high level of
association observed (OR > 5),
CD14 represent a promising
marker for peri‐implantitis
diagnosis.
56. MOLECULAR MARKERS
• □ Different cytokines, enzymes, and proteases have been investigated
• □ The pro‐inflammatory IL‐1β and TNF‐α are the most investigated and
may constitute promising biomarkers for peri-implantitis
57. Ramseier et al (2016)
Biomarker evaluation at teeth and implants in hundreds of
patients 10 years after implant placement
IL‐1β and MMP-8: Elevated in inflamed peri‐implant tissues and
correlated with increased probing depths
Meta-analysis by Faot et al (2015)
IL‐1β, as well as TNF‐α, can be used as additional criteria for
diagnosis of peri‐implant infection, but cannot help to
discriminate between peri‐implant mucositis and
peri‐implantitis.
58. Goals of therapy:
1. Removal of bacterial plaque within the peri-implant
pocket.
2. The decontamination and conditioning of the implant
surface.
3. The reduction or elimination of sites that cannot be
maintained plaque-free by oral hygiene procedures.
4. The establishment of an efficient plaque control regimen
to prevent mucositis and infection of residual pockets.
5. Regeneration of bone.
59. Treatments:
Pre-surgical Protocols:
• Pre-surgical protocols were not advocated to treat peri-implantitis lesions with
nonsurgical therapy but rather to remove local contributing factors.
• Froum and coworkers established in their protocol that all periodontal
treatment should be completed at least 1 month prior to treatment of Peri-
implantitis lesions. Conversely, Stein et al. Treated both peri-implant and
periodontal conditions simultaneously with antibiotic therapy.
• Some authors prescribed antibiotic therapy as pre-medication.
• A systematic review by Esposito et al reported that 2g of amoxicillin taken 1hr
before surgery decreased the post operative complications significantly.
62. Non surgical:
• Basic manual treatment can be provided by teflon-, carbon-, plastic- and
titanium curettes.
• Persson et al. and Renvert et al. experienced significantly lower numbers
of bacteria with partial reduction of plaque and bleeding scores after
mechanical curettage, while Schwartz et al. reported 30%-40% less
residual biofilm areas by using ultrasonic methods
• Usage of dry saline soaked cotton gauze or pellets is advised as a more
conservative approach “to avoid changes on implant surface roughness”.
63. Curettes:
• Curettes of different materials have been produced for use specifically to debride implant surfaces:
• Steel curettes have an external hardness higher than titanium and accordingly are not indicated for
cleaning titanium implants. Nevertheless, they can be used on other implant surfaces, such as titanium
zirconoxide or titanium oxinitride.
• Titanium-coated curettes have a similar hardness to the titanium surface and thus do not scratch its
surface.
• Carbon-fiber curettes are softer than the implant surface and therefore remove bacterial deposits
without damaging the surface, although they break easily.
• Teflon curettes have similar properties to carbon fiber curettes and they have been proposed for use in
combination with air-abrasive systems.
• Plastic curettes are the most fragile of all curette types and have limited debriding capacity
64. Ultrasonic devices
• Ultrasonic devices with polyetheretherketone-coated tips have been used to
debride the implant surface. The polyether-etherketonecoated tip is a modified
tip made of a high-tech plastic material and has a stainless-steel core.
• It debrides the implant surface easily and is comfortable for the patient
66. Titanium brushes:
• Titanium brushes have been advocated to overcome the limitations of
exposed threaded-implant surfaces.
• Sarmiento et al. proposed to use the m on contaminated implant
surfaces for 60s.
• Cha et al. studied the efficacy of titanium brushes at an oscillating low
speed of 900 rpm upon the clinical and radiographic outcomes of
treated peri-implantitis sites. After 12 months, it was reported that
titanium-brush-treated sites display a reduction in 79% and 55% of
probing depths(PD) and bleeding on probing (BOP) respectively. Overall,
a successful treatment was noted in 66.7% when compared to non-
treated sites (23.1%).
67. Air powder polishing:
• A particular interest in glycine, erythritol, or sodium
bicarbonate powders for air-abrasive devices as
adjuncts to mechanical debridement were
observed.
• John and colleagues concluded air-abrasive devices
as a monotherapy can significantly reduce PD and
BOP scores . Similarly, Stein et al. tested the
usefulness of submucosal flexible plastic tips (Perio-
flow Nozzle™) for better subgingival access.
68. • Parma-Benfenati and coworkers experimented using both glycine and sodium
bicarbonate, separately, within the same peri-implantitis site for 1 min during
regeneration therapy and reported promising results
• The extent of re-osseointegration of titanium implants after air polishing therapy
has been reported between 39% and 46% with increased clinical implant
attachment and pocket depth reduction.
69. Chemical Detoxification:
• Hydrogen peroxide, phosphoric acid, and ethylene diamine tetra acetic acid (edta) were
frequently implemented. H2O2 is commonly used.
• Experimental in vitro models evaluating sodium hypochlorite (naocl) and citric acid for
chemical implant detoxification revealed positive effects.
• Sarmiento et al. Described using a 0.9% naocl solution intended to remove residual
hydrogen peroxide
• Pini-prato et al. Experimented with a mixture solution composed of hydrobenzenes,
sulfonate group, and sulfuric acid due to their keratolytic, hygroscopic, and denaturing
properties. All treated sites showed significant reduction of PD and BOP after 3 and 6
months of treatment with only a moderate transient discomfort that disappeared after a
2- or 3day post-treatment.
• Kotsakis and coworkers reported multiple chemical agents (20% citric acid, 24% edta, 1.5%
naocl) can produce elemental contaminants that might alter the titanium physiochemistry.
Despite their positive antimicrobial effect, chemical residues can induce a cytotoxic effect
and adversely affect the cellular response to decontaminated surfaces.
71. Mouth rinses:
• The addition of antibacterial mouth rinses (e.G., CHX, cetylpyridinium [CPC]) as
a pre-surgical, intraoperative, and post-surgical adjunct has been extensively
described .
• A significant reduction in the anaerobic microbial load was reported after 12
months of resective treatment with CHX as an adjunct.
• Antimicrobial effect of cpc has been shown to inhibit bacterial growth related
to peri-implant diseases.
• A repeated submucosal delivery of povidone-iodine (pov) solution has been
proposed as a novel non-invasive therapy for peri-implantitis. Stein and
colleagues promoted the slow release of POV for 10 s repeated three times per
implant site with an additional application after 7 days
72. Systemic and Locally Delivered Antibiotics (LDA):
• Systemic antibiotics, such as azithromycin, amoxicillin, clindamycin, and
metronidazole, used as adjuncts have revealed higher treatment success
(46.7% vs. 25.0%) and a reduced number of PD > 4 mm.
• A short-term randomized controlled trial (RCT) by Cha et al. reported that
locally delivered minocycline effectively reduced PDs, increased success rates
(66.7% vs. 36.63%), and found no traces of Porphyromonas gingivalis and
Tanerella forsythia after 6 months .
• In a review by Javed et al., summarizing nine studies, systemic and local
antibiotic applications (e.g. tetracycline, doxycycline, amoxicillin,
metronidazole, minoxicycline hydrochloride, ciprofloxacin, sulfonamides +
trimethoprim) led to significant reductions of pocket depths in a period
between one and six years
73.
74. Laser:
• A recent meta-analysis by the AAP best evidence consensus concluded
that laser therapy (limited to Er:YAG, carbon dioxide, and diode lasers)
can provide minimal benefits in PD reduction, CAL gain, recession
improvement, and Pl scores in the treatment of peri implant diseases
• Schwarz et al. reported that irradiation with an Er:YAG laser did not
affect osteoblast attachment on the titanium surfaces, whereas use of
an ultrasonic scaler with a carbon fiber tip significantly decreased it.
• Kreisler et al. reported that treatment of a P. gingivalis-contaminated
micro structured titanium surface with an Er: YAG laser resulted in
greater proliferation of fibroblasts on the surface compared with that in
untreated specimens, which was similar to that in sterile specimens.
75. antimicrobial Photodynamic Therapy (aPDT)
• Emerging evidence continues supporting the use of antimicrobial
photodynamic therapy (aPDT) as an adjunct during treatment of peri-
implant diseases.
• However, this is contradictory with current AAP best evidence
consensus which concluded that aPDT provides similar clinical outcomes
compared to conventional therapy for the treatment of both
periodontitis and peri-implantitis.
• The advantages of aPDT might be beneficial during active application of
photosensitizers and remain effective for short terms
76. Probiotics:
• Galofre et al. tested a daily use of probiotics in the form of lozenges
containing a combination of 2 strains of L.reuteri
(PerioBalance®,SunstartSuisseSA) for 30 days and a maximum follow-up
of 90 days. A significant 3-fold decrease in BOP that remained stable for
the length of the study was reported.
77. Surgical:
The surgical therapy combines the concepts of the already mentioned
non-surgical therapy with those of resective and/or regenerative
procedures.
Intervention should be performed if probing depths exceed 5 mm or
are progressive as well as under occurrence of local inflammation
signs
78.
79. Open flap debridement:
• Hallström and colleagues concluded that OFD without antibiotic therapy
is effective in approximately 25% of the cases after 12 months of
treatment using a very strict success criterion.
• Renvert at al. reported less successful outcomes (5%) with OFD when
compared to regenerative therapy.
80.
81. Apically positioned flap
• Sarmiento et al. performed an apically positioned flap(APF) in
combination with mechanical (ultrasonic and titanium curettes) and
chemical (5% hydrogen peroxide and 0.9% sodium chloride)
detoxification along with laser therapy (Er:YAG) . Reductions in PD (6.79
mm to 4.32 mm) and BOP (100% to 14.3%) were reported after a 6-
month post-operative.
82. Resective surgery:
• Resective approaches (e.g., osseous, implantoplasty) are usually considered around implants with
supra bony defects (SBD) or infrabony defects(IBD) not suitable for regenerative therapy.
• Short-term results have shown resective procedures to be effective for reductions in PD (5.86 to
3.63 mm) and BOP (100% to 0%). Conversely, Koldsland et al. found that the effect of treatment is
reduced when suppuration and bone loss exceeding 7 mm are present prior to intervention.
• Berglundh, Wennström, and Lindhe demonstrated long-term outcomes using their trademark
methodology in a 2 –11-year retrospective study. When indicated, osseous recontouring is
performed to facilitate pocket elimination followed by mechanical detoxification with titanium
curettes and saline-soaked gauze. Marked reduction in post-surgical PD and BOP and stable bone
levels were observed
• Carcuac et al., they also noted that nonmodified implant surfaces (e.g., turned) responded more
favorable to therapy than modified surfaces
83. Implantoplasty:
• Implantoplasty has been indicated as a method to remove exposed threads of SBD and
eliminate niches for further biofilm deposition.
• Removal of implant threads is performed with diamond burs of 40 μm and 15 μm grit
sizes, whereas Arkansas stones and rubber flame-shaped burs are considered for
polishing purposes.
• combination therapy (implantoplasty and GBR) might be indicated at sites with both
SBD and IBD.
• Romeo et al.2004 compared Resective treatment alone or in combination with
Implantoplasty in 17 patients with 35 implants, follow-up of 36 months. Clinical
parameters were evaluated.
Concluded that both procedures improve peri-implant health, though adj.
implantoplasty afforded better implant prognosis.
84.
85. Regenerative therapy:
• Renvert et al. demonstrated that regenerative therapy (xenograft only)
of well-contained IBD was effective in 42.9% of cases.
• Mercado and colleaguesnoteda56.6% treatment success after 3 years
when combining xenograft with a biological agent (enamel matrix
derivatives [EMD]) and doxycycline solution.
• Roccuzzo et al. reported treatment success rates of 52.1% with a
significant decrease in BOP (71.5% to 18.5%) using xenograft and
connective tissue grafts
86. • De Tapia reported radiographic bone fill of 84% and successful
treatment in 66.7% of cases by using a mixture of calcium phosphate
and hydroxyapatite .
• Guler and colleagues demonstrated comparable results using porous
titanium-derived granules as a new bone substitute interms of CAL
values(5.29mmto3.59mm) and radiographic bone fill (4.77 mm to 3.30
mm) compared to GBR with xenografts, collagen membrane, and blood-
derived membranes (e.g., platelet-rich fibrin [PRF
• the effects of EMD and PDGF revealed promising results.
87. GBR:
• Absorbable (e.G., Collagen-derived) as well as non-resorbable (e.G., Dense- or
expanded polytetrafluoroethylene [d-ptfe or e-ptfe]) membranes have been
incorporated to GBR around implants as a cell occlusive barrier.
• Parma-benfenati et al. Reported the potential of eptfe membranes for
submerged approaches, with a defect bone fill ranging between 50 and 100%
• Isler and colleagues reported that regeneration therapy (xenograft and a
collagen membrane) for peri-implant IBD yielded a significant reduction in the
gingival index (GI), BOP, PD, clinical attachment level (CAL), and vertical defect
fill of 1.99 mm after a 12-month post-operative.
88. • Long-term studies have shown GBR procedures might deteriorate over
time.
• La Monaca and coworkers reported high success rates (91%) within 1
year of treatment; yet, the 5-year outcomes revealed that these were
not sustained as success rates decreased to 59%.
• In a 10-year case series of 170 implants, Froum and colleagues
experimented with different treatment alternatives for peri-implantitis
and reported survival rates of 98.8%. GBR was performed with bone
allograft, absorbable membrane, and in some occasions, CTGs as a
multi-layer approach.18 implants required a new surgical intervention
while 10 of them were subject for a third procedure.
89. Soft tissue augmentation:
• Soft tissue augmentation around dental implants should be considered
more often for site development prior to or after implant placement.
• No available RCTs were found evaluating the individual effect of free
soft tissue graft (e.g., connective tissue graft [CTG], free gingival graft
[FGG]) or substitutes (e.g., acellular dermal matrix [ADM]) for the
treatment of peri-implantitis.
90.
91.
92. Maintenance:
• A retrospective 7-year study by Frisch et al concluded that patients
under SIT were associated with lower incidence of peri-implant
diseases. Patients without regular maintenance might exhibit a 4.25-
fold increased risk for peri-implantitis.
93. 1. Assess the clinical situation, check for inflammation and evaluate implant pockets.
2. Probe at the time of placing the implant restoration with a force of 0.25 N with a plastic probe
3. Monitor probing changes over time rather than being concerned about initial probing depth
4. Take radiographs at regular intervals (every 3 months in the first year and every six months, second year
onwards) to evaluate bony changes around the implants.
5. Check for residual cement
6. Check for occlusal overload and/or signs of inflammation every 6 months
7. Occlusal adjustment to be done periodically in case of bone loss/ inflammation of Peri-implant mucosa
8. Use WaterPik professional flosser to remove the interimplant plaque from your patients.
9. Rubber cups with pumice, air abrasion, and plastic curettes is recommended to be used since they
don'tmodify the implant surface.
10. Titanium Implant curette and disposable plastic ultrasonic points may leave gentle marks on the Titanium
implant surface but can be used without excessive pressure.
11. The plastic sleeve insertion onto the metallic ultrasonic point may provide only polishing action, leaving
plastic residues on the implant surface.
12. The clinician can also use ultrasonic implant scalers/softip ultrasonic implant inserts and special titanium
implant scalers for scaling around implants.
13. If calculus around implants is adherent, use calculus scaling gel / EDTA gel to soften the calculus before
removal
14. Use Implant Paste to polish exposed/visible implant surfaces post scaling.
94. Conclusion:
1)Peri‐implantitis is defined as a pathological condition occurring in tissues around dental implants,
characterized by inflammation in the peri‐implant connective tissue and progressive loss of sup‐
porting bone.
2) The histopathologic and clinical conditions leading to the con‐ version from peri‐implant
mucositis to peri‐implantitis are not completely understood.
3) The onset of peri‐implantitis may occur early during follow‐up and the disease progresses in a
non‐linear and accelerating pattern.
4a) Peri‐implantitis sites exhibit clinical signs of inflammation and increased probing depths
compared to baseline measurements.
4b) At the histologic level, compared to periodontitis sites, peri‐implantitis sites often have larger
inflammatory lesions.
4c) Surgical entry at peri‐implantitis sites often reveals a circumferential pattern of bone loss.
95. 5a) There is strong evidence that there is an increased risk of developing
peri‐implantitis in patients who have a history of chronic periodontitis, poor
plaque control skills and no regular maintenance care after implant therapy.
Data identifying “smoking" and “diabetes" as potential risk factors/indicators
for peri‐implantitis are inconclusive.
5b) There is some limited evidence linking peri‐implantitis to other fac‐ tors
such as: post‐restorative presence of submucosal cement, lack of
peri‐implant keratinized mucosa and positioning of implants that make it
difficult to perform oral hygiene and maintenance.
6) Evidence suggests that progressive crestal bone loss around implants in
the absence of clinical signs of soft tissue inflammation is a rare event.
97. Retrograde peri implantitis:
• A clinically symptomatic peri apical lesion that develops within the
first few weeks after implant insertion while the coronal portion of
implant sustains a normal bone to the implant interface.
• Class I- <25%
• Class II- 25-50%
• Class III- >50%
98. Bone defects
• Zhang et al based on radiographs: saucer shaped, wedge shaped, flat ,
undercut and slit like
• Based on regeneration- closed defect and open defect
100. Occlusal overload has been regarded as a
major cause of biomechanical
complications, including screw loosening,
prosthesis failure, and the fracture of
screws, veneering material, or the
implant. This is significant because these
complications can be costly, time
consuming, and some complications,
such as implant fixture fracture, can lead
to implant failure
Editor's Notes
The early aim of researchers was to detect bacterial quality and quantity differences between peri‐implant mucositis and peri‐implantitis, and between gingivitis and periodontitis. For this purpose, a limited panel of periodontal pathogenic bacteria was investigated initially but was later expanded after the development of high quality large‐scale molecular technologies. The microbiological results were more complex than previously expected and gave rise to a change in hypothesis from few specific pathogens to a dynamic microbial interaction between a variety of microbial species and host immune responses.
The human genome includes numerous sequence polymorphisms and structural variations. It was observed that implant failure risk was higher if the patient had already had one implant removed. This may suggest the existence of systemic/genetic factors affecting implant survival
The peri‐implant fluid appears to be a source of biomarkers more suitable to obtain a precise diagnosis of a specific sampling site. A broad research effort has been spent to identify biochemical markers associated with peri‐implant disease. Ideally, a diagnostic test able to evaluate molecular biomarkers in peri‐implant sulcus fluids could flank clinical and radiographic examination to monitor the health level of peri‐implant tissues
modified implant surfaces tend to respond less favorable to treatment than non-modified when associated with antibiotic therapy [10]. Overall, the addition of antibiotics failed to provide a sustained benefit in terms of BOP, PD, radiographic bone loss, and microbial load after 1 year of treatment
