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Online Dental Magazine

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Welcome To Guident

Welcome To Guident

Welcome to Guident our online dental magazine. Guident is a globally well-known online international dental journal/publication that is circulated in India as well as globally. The journal is designed to help dentists to build long-term dentistry career success by providing them knowledge to optimize their practice performance during changing times. The field of dentistry has gone through a phase of transformation from in the last century with many new advances and technologies coming up. The complete dental profession is on the verge of many new innovations. To keep all the people associated with this profession we provide our dental magazine ‘Guident’. Our magazine upgrades the knowledge of professionals with information about the latest achievements and advances in the field. Our journal is an online international dental journal which is internationally indexed. The Journal is globally acclaimed in terms of dentistry Knowledge and information; it has been reviewed by many professional dentists of all over the world. Despite the advances in healthcare segments, the Indian population continues to be affected by numerous oral diseases. These dental problems have encouraged people to search and opt for professional dental healthcare services including Endodontic, Prosthodontics, Orthodontic, Periodontics, Implantology, Pedodontics, and Cosmetic dental services etc. Young professionals and experienced dentists skilled in these and many more advanced dentistry services need to constantly keep themselves updated in order to deliver the best treatment to the seekers of such facilities. GUIDENT Indexed by globally known hosts like ProQuest, EBSCO Host and Ulrichsweb Global Series Directory, the journal has been reviewed by numerous professional dentists practicing across the world. This rich storehouse of dental data is easy to access and can be referred to any minute, even when you are mobile. Serving as your ready reckoner, Guident aims to bring the global dental information at your fingertip to add an ultra-modern touch to your dental practice so that you can help your patients smile forever.

Implantology

Author : Dr. Kuts Pavel

Case Report:

A 36-year-old patient turned to the clinic with the complaints of absence of teeth and impaired chewing function.

Diagnosis:

root caries of 15, 23, 38, 48, 31, 32, 41 and 42 teeth. Adentia of 12, 14, 16, 22, 25, 36, 37, 46 and 47 teeth (Photos 1 and 2).

Plan of treatment:

Extraction of roots of 15, 23, 38, 48, 31, 32, 41 and 42 teeth with placement of Alpha Deny Implants in the area of 12, 14, 16, 22, 25, 36, 37, 46 and 47 teeth.

A temporary removable dental prosthesis was made at the stage of preparation for the operation (Photo 3).

Fig 1. Initial clinical situation.


Course of operation:

Removal of 15, 23, 31, 32, 38, 41, 42, 48 teeth and curettage of alveolar sockets were performed under infiltration anesthesia. The mucous membrane was cut along the alveolar crest in the area of 16, 14, 12, 22, 25, 36, 37, 46 and 47 teeth. Exfoliation of periosteal mucosal graft. Formation of bone bed. Placement of Alpha Dent Implants in the area of 12, 14, 16, 22, 25, 36, 37, 46 and 47 teeth (Photo 5). The implants are covered with screw-type plug. Suture of mucous membrane. Adjustment of temporary removable dental prosthesis. Administrations: antibiotic therapy, removal of stitches in seven days.

Fig 2. Patient’s orthopantomogram at the stage of planning. Fig 3. Temporary removable dental prosthesis after extraction of teeth. Fig 4. Single-stage extraction of 15, 23, 31, 32, 38, 41, 42 and 48 roots of teeth. Fig 5.Control orthopantomogram after operation
Fig 6. Individual mandibular abutments Fig 7. Individual maxillary abutments Fig 8. Individual mandibular spoon Fig 9. Individual maxillary spoon.
Fig 10. Fixation of central occlusion with the wax rolls. Fig 11. Temporary plastic maxillary bridge. Fig 12. Temporary plastic mandibular bridge. Fig 13. Temporary plastic prostheses after placement of implants.This was done in order to eliminate gingival reduction around the implants as well as to determine the real height of bite, horizontal line of cutting edge, location of central incisor midline and their compliance with the implants.
 
Fig 14. Metal-ceramic bridge prosthesis. Fig 15. Finished fixed orthopedic constructions in the oral cavity.

The doctors set to orthopedic part of treatment in six months. Opening of implants and placement of the gingiva formers were followed by correction and insertion of immediate prosthesis being already available. The individual abutments were made (Photos 6 and 7). The imprints were taken with individual spoons (Photos 8 and 9). Then removable orthopedic construction was replaced by fixed one – temporary plastic bridge prosthesis was made (Photos 11, 12 and 13).

Then the metal-ceramic bridge prostheses were made (Photo 14).

Result: There was complete and total rehabilitation attained with insertion of maxillary and mandibular metal-ceramic bridge prostheses. The chewing and aesthetic functions were restored (Photo 15).

COVER SCREW EXPOSURE OVER AN IMPLANT FIXTURE- AN OVERVIEW

The early exposure of a part of dental implant fixture through surrounding soft tissue might lead to a serious complication during the initial healing phase,

Early full or partial exposure of the cover screws can be considered a foci for plaque accumulation. If left untreated this may result in inflammation, damage to the peri- implant mucosa, and possible bone loss.( BARBOZA AND CAULA 2002).

COVER SCREW EXPOSURE MIGHT OCCUR DUE TO:

  • Over-tightened sutures.
  • Flap closure under tension.
  • A decreased amount of keratinized tissue.
  • Torn wound edges or a lacerated flap.
  • Muscle pull along the wound edges.
  • Oral habits like smoking and alcohol.

CLASSIFICATIONS:

TAL CLASSIFICATION( 1999):

CLASS O: Mucosa covering the implant is intact
CLASS 1: The cover screw can be detected by a periodontal probe
CLASS 2: Borders of perforation’s aperture do not reach or overlap borders of the cover screw at any point
CLASS 3: Cover screw is visible
CLASS 4: cover screw is completely visible

BARBOZA AND CAULA CLASSIFICATION (2002):

CLASS I: Cover screw spontaneous early partial exposure-a communication betwe3en the cover screw and oral cavity, with a fenestrated mucosa still partially covering the cover screw.

CLASS II: Cover screw spontaneous early total exposure-the fenestration reveals the cover screw completely.

Subdivisions are proposed based on clinical signs of healthy, inflammation, and suppuration. They are as follows:



BARBOZA TREATMENT MODALITIES:-

Treatment Modality No.1: includes professional cleaning of cover screw if plaque or calculus is detected. The cover screw shold be mechanically cleaned using specific curettes, abrasive air, rubber cup, polishing paste, oral hygiene instructions reinforcement, and rinses with chlorhexidine digluconate 0.12%. Shortened recall periods for if inflammation signs are present. Radiographs are indicated to evaluate peri- implant bone morphology.

Treatment Modality No.2: includes identification of microorganisms and antibiotic therapy. In the presence of purulent exudates, specific microbial information is indispensable. Microbiological samples must be collected to identify the putative pathogens. If the patient presents localized peri-implant problem, a topical antibiotic therapy can be considered.

Treatment Modality No.3: includes surgical exposure of cover screw and adaptation of a healing abutment to avoid mucosa regrowth and facilitate patient oral hygiene.

Treatment Modality No.4: includes typical peri-implantitis treatment .

Conclusion :

Post operative soft tissue complications can be devastating to the implant’s overall success. Unfortunately, the factors that influence soft tissue healing are numerous. The potential threat of dehiscence is bacterial colonization that could occur between the implant surface and the oral environment. If left untreated, there could be damage to the peri- implant mucosa, and possible bone loss. Thus, it is important to detect these exposures early to avoid more serious complications.

References:

  • BARBOZA,E. and A. CAULA. 2002 diagnosis, clinical classification, and proposed treatment of spontaneous early exposure of submerged implants. Implant dent,11, pp 331-337
  • Bengazi, F.,J.L. Wennstrom, and u. lekholm. 1996. Recession of the soft tissue margin at oral implants. Clin oral iplant res, (7), pp. 303-310
  • EL ASKARY, A.S., R.M. Meffert, and T. Griffin 1999a and b WHY DO IMPLANTS FAIL,PART 1 AND 2.
  • Nemkovsky, C., and Z. ARTZI. 2002. Comparative study of buccal dehiscence defects in immediate,delayed and late maxillary implant placement with collagen membranes: clinical healing between placement and secont stage surgery, J Periodontol, 73, pp. 753-761
  • Textbook on FUNDAMENTALS OF ESTHETIS IMPLANT DENTISTRY by EL ASKARY.
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.

Authors : Dr. Saloni Gupta, Dr. Nikhil wazir

Abstract
Implant dentistry has seen the most significant growth in the dental field in the last 20 years .There have been great strides in the area of evidence-based research regarding dental implantology. Understanding of implant histology, biomechanics, occlusion, peri implantology and esthetics has allowed service with extremely long lasting results. There have been advances in dental implants regarding computer aided placement and CAD-CAM technology..In this review article various advances in dental implants have been described.

Key words implants,,CAD-CAM, Cone Beam Scanning,surgical guide,3 D imaging

Introduction
While dental implants have been around for decades, recent advances in technology and treatment protocols have made treatment more convenient, more effective, and more affordable; making implants the treatment of choice for missing teeth.
Computer guided implant surgery represents a giant step forward in the replacement of teeth with dental implants. With Computerized Tomography (CT) Scan techniques and 3-D imaging, we can now visualize the placement of dental implants in three dimensions. This eliminates the guesswork involved determining what parts of the jawbone offer the best sites for dental implant placement.

CAD/CAM (computer-aided design/computer aided manufacturing) systems have evolved over the last two decades and have been used by dental health professionals for over twenty years . In 1971, Francois Duret introduced CAD/CAM in restorative dentistry and, in 1983, the first dental CAD/CAM restoration was manufactured.1 Nowadays there is a greater interest in the CAD/CAM systems for implant-supported prosthesis, as they have been used for the manufacture of implant abutments) and diagnostic templates in implant dentistry .In this review article ,various developments in implant dentistry have being discussed.

CAD/CAM abutments in Implant Dentistry
Custom abutments created with CAD/CAM technology have the potential to provide the advantages of both stock and laboratory processed custom abutments without the disadvantages. First, like laboratory-made abutments, CAD/CAM abutments are specific for each patient , however the results are much more consistent.. The virtually designed abutment is electronically transferred to a CAM milling apparatus that creates the abutment from a block of the selected abutment material. 2 Most of the inherent dimensional inaccuracies of waxing, investing and casting are eliminated. Therefore, CAD/CAM abutments have the potential to provide the most accurate fit of any abutment type.

Commercially available CAD/CAM abutments systems-
1.Cercon
Comprised of the Cercon Eye scanner, Cercon Art CAD design software, Cercon Brain milling unit, and Cercon Heat sintering furnace (figure no-1)
Figure no-1-Cercon CAD CAM System
2.CAD BLU Restoration System
The CAD BLU Restoration System(figure no-2) features the MDX-40ATC wax milling unit, which is capable of milling a single coping in less than 6 minutes using a 98-mm wax disk.
Figure no-2-.CAD BLU CAD CAM system
3.DentalMill
The Digital Dental Lab CAD/CAM system(figure no-3) unites scanning and design software from 3shape, DentMILL CAM software, and the DentalMill milling machine. The DentalMill milling unit comes with an automatic tool measurement, integrated vacuum system, three-button PC interface, touch-screen monitor.
Figure no-3-DentaMill CAD CAM system
Advantages of CAD-CAM systems-
1. CAD/CAM technology applied to implant surgery allows the production of high resistance and high density crowns3
2. A custom design, a perfect fit and a higher resistance are the main characteristics of CAD/CAM implant abutments.
3. CAD/CAM surgical templates allow to transfer the software planning to the surgical field. CAD/CAM surgical guides
Placement of dental implants requires precise planning that accounts for anatomic limitations and restorative goals. Diagnosis can be made with the assistance of computerized tomographic scanning, but transfer of planning to the surgical field is limited.
Recently,novel CAD/CAM techniques such as stereolithographic rapid prototyping have been developed to build surgical guides(Figure no-4) in an attempt to improve precision of implant placement . As a result of this technology, the surgical guide permits accurate and consistent position and orientation of the implants .
Sarment et al. showed the advantage of this technique in a case-control study that compared the distances between planned implants and actual osteotomies using a conventional surgical guide and a stereolithographic surgical guide.5
Figure no-4-CAD CAM generated surgical template
Computer Aided Implant Placement
Inserting a dental implant is a tricky affair which requires a fair degree of accuracy. It is a highly skilled procedure which requires the dentist to know beforehand the exact position for the implant However, advances in dental technology such as computer aided implant placement have made this much easier to do. Technologies such as Cone Beam Scanning, 3D imaging software and Surgical Guides can achieve extremely high levels of precision that were unheard of a few years ago. 6

Cone Beam Scanning (Cone Beam CT)
Cone Beam Computerised Tomography differs from conventional scanning in that it emits a ‘cone beam’ of radiation that captures an entire image, as it revolves around the patient in a single rotation.
Figure no-5- Cone beam scanner generated image showing anatomic landmarks

High resolution 3D images of the teeth and jaw are produced via a series of algorithms. These representations are very accurate and help with implant placement. With cone beam imaging anatomic landmarks (figure no-5) such as foramina and the mandibular canal can be precisely marked, and cross-sectional views accurately show the width and length of available bone,7 Another feature of this scanner is that the patient sits up for the procedure rather than lying down as with the conventional scanner. Lying down tends to result in a collapse of the soft tissues of the mouth which is not the case with the Cone Beam scanner hence the more precise representations.

3D Imaging Software
Imaging software is a very useful tool when planning a course of dental treatment. It shows a highly realistic 3D representation of the patient’s jaw which can be explored from all angles. The dentist can also place ‘virtual’ implants which enable him/her to check the positioning and make adjustments if necessary.
The implant placement model will consist of precise measurements and positioning which is based upon an individual patient’s anatomical structure.This model is saved and then exported as an email attachment to a dental laboratory. The laboratory will then use this to produce a surgical guide for the actual implant procedure. .

Summary and conclusions
There are an array of recent advances which are making the dental implant procedure easier and more successful. The use of CAD-CAM dental abutments is one such method. This procedure is extensively used in the manufacturing world to produce intricate and complex components which would otherwise be hard to produce using more traditional methods. New CAD-CAM procedures are making it easier for dentists to build a dental implant abutment which is customized to each of their patients
The Cone Beam CT Scanner is a new dawn in dentistry. From the 3-D images, we can construct exact models of a patient’s jaw and perform surgery on the model prior to performing the surgery on the patient. The result is more accurate planning and surgical treatment. This method reduces the overall time of the implant procedure, minimizes post-operative discomfort, and makes the outcome more accurate and predictable.

REFERENCES
  1. Christensen GJ. New Directions in Dentistry. Dentistry Today. 2006 Feb; 108-15.
  2. Ángeles FM , Albalat ES. CAD / CAM dental systems in implant dentistry: Update. Med Oral. 2009 Mar 1;14 (3)
  3. Grossmann Y, Pasciuta M. A novel technique using a coded healing abutment for the fabrication of a CAD/CAM titanium abutment for an implant-supported restoration. J Prosthet Dent. 2006;95:258-61.
  4. Drago CJ. Two new clinical/laboratory protocols for CAD/CAM implant restorations. J Am Dent Assoc. 2006;137:794-800.
  5. Sarment DP, Sukovic P. Accuracy of implant placement with a stereolithographic surgical guide. Int J Oral Maxillofac Implants. 2003;18:571-
  6. Strub JR, Rekow ED. Computer-aided design and fabrication of dental restorations: current systems and future possibilities. J Am Dent Assoc. 2006;137:1289-96
  7. Kopp KC, Koslow AH. Predictable implant placement with a diagnostic/surgical template and advanced radiographic imaging. J Prosthet Dent. 2003;89(6):611-615.

First author : Yashpal Singha,Reader,Subharti Dental College, Meerut
Co-Authors : Monika Sainib,Reader,Subharti Dental College, Meerut
Suraj Suvarnac,Associate Professor,SBB Dental College, Ghaziabad

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
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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
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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,
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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;
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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

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