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Implantology

Abstract
Peri-implantitis is unarguably one of the most significant risk factor associated with implants. It is a multifactorial disease which if not diagnosed at early stage, could lead to implant mobility and ultimately failure of the implant. The treatment of the disease is primarily determined by the stage at which it is diagnosed. Extensive research has been done for earliest diagnosis and comprehensive treatment of the disease.
This paper reviews all the aspects of per-implantitis including etio-pathogenesis, diagnosis and management.

Introduction
Peri-implantitis has been a matter of concern since the inception of implants. It may cause bone loss around implants leading to mobility and ultimately failure of implant. The infection may begin to affect during the initial phase of Osseo-integration and may also spread in to well-Osseo integrated implant at later stage. Peri-implantitis affects 5% to 10% of implant patients, and is a major cause of late implant failure.   Diagnosis at initial stage and comprehensive treatment of disease is still an enigma to the dentists.

Definition
According to the 1st European Workshop on periodontology (Albrektsson Isidor 1994), peri-implantitis is defined as the "term for inflammatory reactions with loss of supporting bone in the tissues surrounding a functioning implant1".
Zitzmann & Berglund in 2008 defined it as presence of inflammation in the mucosa and loss of supporting bone at an implant.

A peri-implant disease is a descriptive term used to describe a non specific inflammatory
reaction in the host tissues. “Peri-implantitis” should be distinguished from “peri-implant
mucositis” in that the former is defined as, “an inflammatory reaction with loss of supporting bone in the tissues surrounding a functioning implant”, while the latter involves a reversible inflammation localized to the soft tissues only.

Etio-pathogenesis
The pathogenesis of peri-implantitis may be: the traditional pathway; infective peri-implatitis; (from soft tissue apically to bone), with dental plaque causing gingivitis, progressing to peri-implantitis with resultant bone loss; or retrograde peri-implantitis (from bone to soft tissue), with bone loss occurring at crest due to micro fractures in the bone from overloading, loading too soon, lateral forces or occlusal factor.

Histology
(a) Light microscope
The histological picture portrayed in peri-implantitis lesions are clearly very different to that seen around retrieved functioning implants4. The microscopic findings of peri-implantitis lesions have been consistently described in the literature. Sanz et al. 5found a distinct pattern of proliferation and acanthosis of the sulcular epithelium. There was an increased density of mononuclear and polymorphonuclear cells (PMN) in the epithelium, while the connective tissue contained a mononuclear and plasma cell infiltrate, not seen in the healthy specimens. The proportion of inflammatory cell infiltrate (ICT) in the connective tissue of diseased sites were 65.5% while that of the healthy sites were 8.2% (p<0.001).
 
The mucosa from healthy sites showed a subsulcular connective tissue with a scarce ICT and mature collagen fibres.Ligature induced peri-implantitis carried out in beagle dogs over a 6 week period, found the ICT reached the bone crest and extended into the bone marrow 6. This was in stark contrast to the ligature induced lesions around natural teeth, which consistently displayed a zone of intact tissue between the apical termination of the ICT and crest of bone. These observations may reflect the nature of the implant- soft tissue interface, whereby orientation of the collagen fibres are vertical in nature with an obvious lack of cementum and periodontal ligament, providing an environment perhaps less resistant to the ingress of bacteria in an apical direction.

(b) Electron Microscope ultra structural investigations closely correlate with findings of light microscopy.
 
The intercellular spaces of the sulcular epithelium in peri-implantitis lesions are found to harbor bacteria in close apposition with desmosomal junctions. Progressing deeper into the epithelial and connective tissues, collagen fibres and fibroblasts are increasingly replaced by an ICT often with plasma cells and lymphocytes dominating. The morphology of blood vessels is additionally altered, with evidence of engorgement and congestion. Results are suggestive of that which is seen around teeth in periodontal disease and may indicate a similar host immune reaction to bacterial agents7.

Microbiology
The evidence concurs that the microbiology at peri-implantitis sites is significantly different to that of healthy implant and tooth sites in the same individual and between individuals. Forty-one percent of the cultivated organisms were gram-negative anaerobic rods in the samples of the failing sites. Gram negative anaerobic rods, spirochaetes and fusiform bacteria were found in higher proportions at peri-implantitis sites as compared with healthy sites, which were predominantly composed of coccoid forms.

Traditional periodontal pathogens such as Porphyromonas gingivalis (Pg), Actinomyces actinomycetemcomitans (Aa) and Prevotella intermedia (Pi) have been shown to colonize the peri-implant sulcus from 1 to 3 months after exposure to the oral environment.
This number was significantly higher than that of the successful sites, where the group of facultative cocci was predominating. Failing sites harbored significantly elevated numbers of P.intermedia and Fusobacterium spp.These sites included putative periodontal pathogens such as P.intermedia and Fusobacterium, but not P.gingivalis. Another study reported on peri-implantitis lesions that exhibited a higher proportion of staphylococci (15.1%) than were present in gingivitis (0.06%) or periodontitis (1.2%) lesions, suggesting that the staphylococci may be of greater etiological significance than was previously assumed12.

The black pigmented, anaerobic bacteria present in peri-implantitis are known to produce endotoxins such as collagenase, hyaluronidase and chondroitin sulphates in identifiable amounts and that has been shown to initiate an acute inflammatory response in addition to producing bone destruction, whether tooth or dental implant.

Immunology
Various studies strengthen the belief that the local host response to this peri-implant infection is biochemically similar to the response seen in periodontitis The significant elevation of PGE2 and IL-1B, in both failing implant sites and in mouth stable implant sites, demonstrate that an increased local response is measurable on the patient level as well as at local sites of inflammation. Inflammatory mediators, such as prostaglandin E2 (PGE2), interleukin-1B (IL-1B), and possibly interleukin-6 (IL-6) produced by the chronic inflammatory cells of the periodontal tissues initiate pathways that stimulate osteoclastic bone resorption.

Elevated levels of PGE2 was found  associated with disease progression.Gingival crevicular fluid IL-1B levels of diseased implants was found to be elevated three folds as compared to clinically healthy site.

Post-implantation interleukin analysis will certainly provide information on whether the local inflammatory process was the cause of widespread immune stimulation and of the associated peripheral cytokine release or whether a systemic immune regulatory defect was manifested in the periodontium or peri-implant area as the location of higher antigen density. Interleukin analysis seems to be a promising diagnostic approach for detecting periodontal or peri-implant inflammation at an early stage and thus in time to initiate appropriate treatment.

Contributing Factors
There seems to be a clear proportional relationship between surface roughness and the rate of bacterial colonization in regards to both supragingival and subgingival plaque. The subgingival plaque associated with rough abutments displayed up to twenty five times more bacteria than smooth abutments. Following on from this, it may be surmised that roughened implant surfaces would provide a greater surface area for bacterial invasion and that once this surface becomes exposed to the oral environment, control of infection is difficult.14
Smoking is an established risk factor for chronic periodontitis and undoubtedly contributes to an increased risk of implant loss. The incidence of peri-implantitis in patients who smoke, in addition to having a history of chronic periodontitis is still largely unknown16.

Lack of keratinized gingiva around implants may increase the susceptibility to plaque-induced peri-implantitis. There is a lack of long term human clinical trials to corroborate these findings.

Other factors such as residual cement in the peri-implant sulcus, oral hygiene habits and occlusal loading have been suggested to contribute to the initiation or progression of peri-implantitis.

Retrograde Peri-Implantitis
A condition known as retrograde peri-implantitis may also be associated with implant failure. Retrograde implant failure may be due to bone micro fractures caused by premature implant loading or overloading, other trauma, or occlusal factors .Implant failures from retrograde peri-implantitis are characterized by periapical radiographic bone loss without, at least initially, gingival inflammation. The distinction between implant failure due to infection with periodontal pathogens (infective failure) and implant failure associated with retrograde peri-implantitis (traumatic failure) is also reflected in the microflora. Rosenberg et al (1991) demonstrated that, in failing implants with a primarily infectious etiology, 42% of the subgingival flora consists of 42% Peptostreptococcus sp., Fusobacterium sp., and enteric Gram-negative rods implants with a traumatic etiology have a microflora more consistent with gingival health and composed primarily of streptococci19. Peri-implant tissues do not accommodate increased biomechanical stresses, due to the fact that: (1) implants move minimally in bone compared with their natural tooth counterparts; (2) with overload, microfracturing of the bone occurs, and this is irreversible, even with control of the overload; and (3) a reduced area of support exists in the root-form implant compared with that of natural teeth. In contrast, (1) the periodontal ligament hypertrophies with increased function, allowing for greater movement in bone; (2) with overload, mineralized bone volume may be reduced around natural teeth, but in the absence of inflammation, periodontal disease, the situation is reversible once the overload is eliminated or reduced; and (3) the periodontal ligament is attached to a natural tooth with greater surface area and allows for off-axis loading.

Partially Edentulous mouth v/s fully Edentulous mouth
Research shows that the implants in a partially edentulous case are probably more at risk than those in a fully edentulous case, due to the bacteria being more pathogenic, which can provide a seeding mechanism from the tooth pocket to the implant crevice found few differences in the microflora between implant and teeth in partially edentulous patients, with a marked difference (decrease) in the number of periodontal pathogens in implant crevice in the fully edentulous implant case. From studies it has been proposed that the implant in a partially edentulous mouth, with a non-existent connective tissue attachment and a non-predictable perimucosal seal, is at more risk for peri-implantitis than one in a fully edentulous case.

Peri-implantitis v/s Periodontitis
A periodontitis-like process, peri-implantitis, can affect dental implants and since untreated periodontitis may ultimately lead to the loss of natural teeth, peri-implantitis can result in the loss of dental implants.

It is apparent that periodontitis = peri-implantitis in etiology and therapy.

The bacteria are the same (black pigmented bacteriodes and others).The infective process is the same i.e. progressing from gingivitis or soft tissue involvement to the osseous structures The osseous defect topography is similar to  crater or cup like defect at crest around the implant fixture, progressing apically. The response of the soft tissue around implants and teeth is the same when exposed to dental plaque, that is , when home care is instituted and effective, the tissues respond.

The response to therapy is the same, applied to implants and teeth i.e. after teeth / implants are detoxified and osseous defects grafted, repair will usually take place.
In fact, the implant is more subject to breakdown than the natural tooth.

  1. There is no periodontal or peri-implant ligament allowing for shock absorbing or stress absorbing.
  2. There is no connective tissue attachment.
  3. The design of the superstructure on dental implants renders it less conducive to optimum home care
Diagnosis
The well advanced peri-implantitis lesion may be clearly identifiable via evidence of radiographic bone loss, mobility and clinical signs of infection. It is the early lesion that poses the greatest challenge to the clinician and is undoubtedly of greatest value in order to avoid further bone resorption and subsequent loss of the implant. Diagnosis of peri-implantitis relies on crude parameters commonly used for the diagnosis of periodontal diseases. Typical signs and symptoms of peri-implantitis include;

  1. Evidence of vertical destruction of the crestal bone, often “saucer shaped”
  2. Formation of a peri-implant pocket (> 4mm),
  3. Bleeding or suppuration after gently probing,
  4. Tissue redness and swelling
  5. Mobility (insensitive in detecting early implant failure).
Clinical signs of peri-implantitis may not always be evident. Standardized radiographs are suggested one year after fixture placement and every alternate year thereafter.

Six levels of peri-implantitis:

  1. BOP(bleeding on probing) + PPD(pocket probing depth) ≥ 4 mm + ≥ 2.0 mm bone loss
  2. BOP + PPD ≥ 6 mm + ≥ 2.0 mm bone loss
  3. BOP + PPD ≥ 4 mm + ≥ 2.5 mm bone loss
  4. BOP + PPD ≥ 6 mm + ≥ 2.5 mm bone loss
  5. BOP + PPD ≥ 4 mm + ≥ 3.0 mm bone loss
  6. BOP + PPD ≥ 6 mm + ≥ 3.0 mm bone loss
Decision process for peri-implantitis can be summarized through following flow-chart.

Management
When the dental implant is pathologically involved such as in terms of gingival changes (inflammation, swelling, purulence) or radiographic changes, in terms of bone loss, it is important to determine whether the implant is ailing, failing or failed.
The ailing implant is the one with radiographic bone loss but no clinical inflammation.
The failing implant is the one with radiographic bone loss, and with signs of inflammation(bleeding, purulence, redness, etc.) with no clinical mobility. This implant can usually be treated successfully if the etiology and cause of the problem is identified. The failed implant is the one with clinical mobility, along with the above signs of radiographic bone loss and clinical inflammation. This implant should be removed
Mombelli (2002) suggests five considerations in the therapy of peri-implantitis22:

  1. The disturbance and/or removal of the bacterial biofilm in the peri-implant pocket
  2. “Decontamination” and conditioning of the surface of the implant
  3. Correction via reduction or elimination of sites that cannot be adequately maintained by oral hygiene measures
  4. Establishment of an effective plaque control regime
  5. Re-osseointegration.
One strategy, the “cumulative interceptive supportive therapy”(CIST) suggests a protocol for the monitoring of healthy implants and the interception of peri-implant diseases (Fig.1). The principle of this method is to detect peri-implant infections as early as possible and to intercept the problems with appropriate therapy. The basis for this system is a regular recall of the implant patient and the repeated assessment of the following key parameters around each implant.The parameters are the presence of plaque, the bleeding tendency of the peri-implant tissues, suppuration, the presence of peri-implant pockets and radiological evidence of bone loss. This protocol relies on PPD(pocket probing depth), BOP(bleeding on probing) and radiographic evidence of bone loss. As each parameter becomes more severe, more complex treatment is introduced, with subsequent treatment incorporating that of the previous. For example, according to this protocol, if a PPD of 6mm is displayed, positive for BOP and greater than 2mm bone loss,combination therapy of A + B + C + D is instituted. The goal of this cumulative treatment approach is to intercept peri-implant tissue destruction as early as possible and to avoid explantation (E) due to loss of osseointegration.

Recent Modalities

Photo-Dynamic Therapy
According to Joerg Neugebauer PDT involves the use of a non-toxic dye (a photosensitizer) and low-intensity laser light, which combine to create singlet oxygen molecules that are lethal to certain bacteria25. Neugebauer notes that Laser treatment is best combined with surgical opening of the implant site for cleaning and disinfecting the local defect. In this way, photodynamic therapy can be used successfully to decontaminate the implant surface. Photodynamic therapy has been defined as “the light induced inactivation of cells, microorganisms, or molecules.” Antimicrobial photo-dynamic therapy involves a process of staining infectious bacteria with a photosensitizing dye, followed by bacterial destruction via tissue exposure to a light of appropriate wavelength and intensity (690 nm for 60 seconds). The activation of the photosensitive dye (Toluidine blue) by the laser causes a build up of singlet oxygen, resulting in the oxidation of membrane lipids and enzymes in the pathogenic bacteria, leaving healthy cells unharmed.

Titanium granules for treating peri implantitis
Advanced peri-implant osseous defect were treated with PTG (porous titanium granules) implants. PTG treated defects healed uneventfully with improvement in the clinical and sub-clinical parameters.

Conclusions
Periimplantitis is an inflammatory process affecting tissues surrounding osseointegrated dental implants. It seems to be very similar to periodontitis in all aspects, but severity of infection is more in case of perimplantitis. Peri-implantitis has higher incidence in partially edentulous patients as compared to fully edentulous patients.
Diagnosis at the intial stage is the key to success for control of the infection. Facultative anaerobes i.e. Fusiform bacteria, spirochaetes are largely responsible for the infection. Diagnostic signs may include periapcal radiographic bone loss, peri-implant pocket> 3mm, bleeding, suppuration, redness swelling and mobility.
Treatment may range from cleaning and debriding exposed implant surface and pocket around implants to resective/regenerative surgical procedure depending on the stage at which the infection is diagnosed.
Factors which initiate or expedite the infection should be intercepted at the right time to completely eliminate the infection.

References:
1 Albrektsson T, Isidor F. Consensus report of session IV. In: Lang N, Karring T, Eds.
Proceedings of the 1st European Workshop on Periodontology. London: Quintessence; 1994. p. 365-369.

2 Boucher CO, ed. Current Clinical Dental Terminology; A Glossary of Accepted terms in All Disciplines of Dentistry. St. Louis, Mo: Mosby; 1963:273.

3 Meffert R.M What causes peri-implantitis. CDA-Journal 1991;19:53-59

4 Berglundh T, Lindhe J, Ericsson I, Marinello CP, Liljenberg B, Thomsen P. The soft
tissue barrier at implants and teeth. Clin Oral Impl Res 1991; 2:81-90.

5 Sanz M, Alandez J, Lazaro P, Calvo JL, Quirynen M, Van Steenberghe D. Histop-pathologic characteristics of peri-implant soft tissues in Branemark implants with 2 distinct clinical and radiological patterns. A histometric and ultrastructural study. Clin Oral Impl Res 1991; 2:128-134.

6 Lindhe J, Berglundh T, Ericsson I, Liljenberg B, Marinello CP. Experimental
breakdown of peri-implant and periodontal tissues. A study in the beagle dog. Clin Oral
Impl Res 1992; 3:9-16.

7. Page RC, Schroeder HC. Pathogenesis of inflammatory periodontal disease. A
summary of current work. Lab Invest 1976; 33(3):235-249.

8. Mombelli A, Van Oosten MAC, Schurch E, Lang NP. The microbiota associated with
successful or failing osseointegrated titanium implants. Oral Microbiol Immunol 1987;
2:145-151.

9. Mombelli A, Marxer M, Gaberthuel T, Grunder U, Lang NP. The microbiota of
osseointegrated implants in patients with a history of periodontal disease. J Clin Periodontol 1995; 22:124-130.

10. Meffert R.M. How to treat ailing and failing implants. Implant Dent 1992;1:25-33.

11. Mombelli A, Lang NP, Microbial aspects of implant dentistry. Periodontology 2000,
1994;4:74-80

12 Rams TE, Feik D, Slots I (1990). Staphylococci in human periodontal diseases. Oral Microbiol Immunol 5:29-32.

13. Salcetti JM, Moriarty D, Cooper LF, Collins JG, Socransky SS, Offenbacher S. The Clinical, Microbial, and Host Response Characteristics of the Failing Implant. Int J Oral Maxillofac Implants 1997;12:32-42.

14. Quirynen M, Van Der Mei HC, Bollen CML, Schotte A, Marechal M, Doornbusch GI, et al. An in vivo study of the influence of the surface roughness of implants in microbiology of supra- and subgingival plaque. J Dent Res 1993; 72(9):1304-1309.

15. Albandar JM, Streckfuss CF, Adesanya MR, Winn DM. Cigar, pipe and cigarette
smoking as risk factors for periodontal disease and tooth loss. J Periodontol 2000;
71(12):1874-1881.

16. Bergstrom J. Cigarette smoking as risk factor in chronic periodontal disease.
Community Dent Oral Epidemiol 1989; 17:245-247.

17.  Quirynen M, De Soete M, Van Steenberghe D. Infectious risks for oral implants; a
review of the literature. Clin Oral Impl Res 2002; 13:1-19.

18  Misch CE (1990). Effect on treatment plans, surgical approach, healing and progressive loading. Int J Oral Implant 6:23-31.

19. Rosenberg ES, Torosian IP, Slots I (1991). Microbial differences in two clinically distinct types of failures of osseointegrated implants. Clin Oral Implant Res 2:135-144.
 
20. Meffert R.M. Periodontitis vs. peri-implantitis: The Same Disease? The Same Treatment? Crit Rev Oral Biol Med 1996;7:278-291.

21. Mombelli A. Etiology, diagnosis, and treatment considerations in peri-implantitis. Curr Opin Periodontol 1997; 4:127-136.

22. Mombelli A, Lang NP. The diagnosis and treatment of peri-implantitis. Periodontol 2000 1998; 17:63-76.

23. Mombelli A. Microbiology and antimicrobial therapy of peri-implantitis. Periodontol
2000 2002; 28:177-189.

24. Lang NP, Lindhe J. Maintenance of the implant patient. In: Lindhe J, Karring T, Lang
N, Eds. Clinical Periodontology and Implant Dentistry. 4th ed. Oxford: Blackwell
Munksgaard; 2003. p.

25  Neugebauer J, Jozsa M,Kubler A. Antimicrobial photodynamic therapy for prevention of alveolar ostitis and postextraction pain [in German]. Mund KieferGesichtschir 2004; 8:350-355.

26. Hamblin MR, Hasan T.Photodynamic therapy: A new antimicrobial approach to infectious disease?Photochem Photobiol Sci 2004; 3:436-450.

Legends

Fig.1

Cumulative Interceptive Supportive Therapy Decision Tree.