Periimplant diagnosis/ orthodontic straight wire technique


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Periimplant diagnosis/ orthodontic straight wire technique

  2. 2. INTRODUCTION Artificial replacements for missing teeth during the early 15-16th century. A fine dark stone shaped tooth was found in a Mayan skull 600A.D. Later on the development of stainless steel, vitallium titanium implants brought oral implantology to the forefront. All play essential roles in the placement and maintenance of oral implants ,However the principles of periodontal therapy play an important role in influencing the final success of treatment.
  3. 3. Pathologic alterations in the tissues that contact a dental implant fall under the definition of peri implant pathology. The development of inflammatory process that is limited to the peri-implant soft tissue can be defined as peri-implant mucosites. The progressive peri-implant bone loss occupied by inflammatory pathology in the soft tissue is refered to as peri- implantitis.
  4. 4.
  5. 5. Peri-implant tissue breakdown can be the result of microbial action as well as of biomechanical and occlusal overload. The long-term goal of the treatment of per-implant breakdown is to arrest the progression of the disease and to achieve a maintainable site for the patient. Peri-implant bony defects around functioning implants can be treated with either non-surgical or surgical.
  6. 6. NORMAL PERI-IMPLANT MUCOSA The mucosal tissues around intraosseous implants form a tightly adherent band consisting of a dense collagenous lamina propria covered by stratified squamous keratinizing epithelium. The implant-epithelium junction is analogous to the junctional epithelium around natural teeth, in that the epithelial cells attach to the titanium implant by means of hemidesmosomes and a basal lamina.
  7. 7. The Histologic examination of the sections revealed that the two soft tissues units, the gingiva and the peri-implant mucosa, have several features in common. The oral epithelium of the gingiva is well keratinized and is continuous with a smooth junctional epithelium that faces the crown of the tooth and ends at the cemento-enamel junction(arrow). The supra-alveolar connective tissue is about 1mm(arrow) high and the periodontal ligament about 0.2-0.3mm wide. The principal fibers extend from the root cementum in a fan-shaped pattern into the soft and hard tissues of the marginal periodontium.
  8. 8. The outer surface of the peri-implant mucosa is also covered by a well –keratinized oral epithelium, which in the marginal border (arrow) connects with a barrier epithelium is facing the abutment part of the implant. The barrier epithelium is only a few cell layers thick and terminates about 2 mm apical of the soft tissue margin. In a zone that is about 1-1.5mm high, between the apical level of the barrier epithelium and the alveolar bone crest, the connective tissue appears to be in direct contact with the TiO2 layer of the implant. The collagen fibres originates from the periosteum of the bone crest and extend towards the margin of the soft tissue in directions parallel to the surface of the abutment. Microphotograph of a Peri –Implant mucosa
  9. 9. Collagen fibres are nonattached and run parallel to the implant surface, woing to the lack of cementum. This is an important difference between periimplant and periodontal tissues. However some reports have suggested that microscope irregularities and porosities like those found on plasma sprayed titanium surfaces may favor the appearance of fibres oriented perpendicularly to the implant surface.
  10. 10. Peri-implant mucositis is a term used to describe reversible inflammatory reactions in the mucosa adjacent to an implant. In the lesion within the peri-implant mucosa, the tissue breakdown that occurred during the 3 months of plaque exposure was not fully recovered by reparative events. The small number of fibroblasts present in this particular lesion may simply have been unable to produce enough collagen and matrix during the reparative phase. This reduced build-up resulted in an additional propagation and spread of the inflammatory cell infiltrate in the peri-implant
  11. 11. Peri-implantitis defined as an inflammatory process that affects the tissues around an osseointegrated implant in function, and tissue in loss of supporting bone. Berglundh et al (2003) found that mucosa contained large lesions with numerous plasma cells, lymphocytes and macrophages. It was further demonstrated that the inflammatory cell infiltrate consistently extended to an area apical of the pocket epithelium and that the apical part of the soft lesion frequently reached the bone tissue. He also observed that numerous PMN cells were present in the human peri-implantitis lesion.
  12. 12. PERIODONTAL TISSUES VERSUS PERI-IMPLANT TISSUES The soft and hard tissues surrounding an osseointegrated implant show some similarities with the periodontium in the natural dentition . The absence of a periodontal ligament in the peri- implant region. The orientation of the collagen fibres of the soft tissues around the implants, which are non-attached and parallel to the implant surface, while the gingival fibres around teeth are perpendicular and attached to the root cementum.
  13. 13. The response to a pathological insult. the coronal portion of the implant and/or abutment is surrounded by a thin layer of collagen fibres arranged circumferentially and with minimal vascular structures. This low vascularity soft tissue band may affect the defense mechanisms around an implant as compared to those seen in tissues around teeth with a periodontal ligament. If plaque accumulates on the implant surface, the subepithial connective tissue is infiltrated by large numbers of inflammatory cells and the layer of epithelial cells appears ulcerated and loosely adherent..
  14. 14. A recent report comparing plaque-associated lesions around teeth and around implants showed that lesions became more pronounced and occupied a larger volume of the connective tissue around implants. If the plaque front continued to migrate apically, the clinical and radiographic signs of tissue destruction were seen around both implants and teeth however, the size of the soft tissue inflammatory lesion was larger around implants.
  15. 15. Smith and Zarb proposed the following criteria for implant success. 1. The individual unattached implant is immobile when tested clinically. 2. No evidence of peri-implant radiolucency is represent as assessed on an undistorted radiograph. 3. Mean vertical bone loss is less than 0.2mm annually after the first year of function or service.
  16. 16. 4. Three is no persistence pain, discomfort or infection attributable to the implant. 5. Implant design does not preclude placement of a crown or prosthesis with an appearance that is satisfactory to the patient and dentist. 6. There is an 85% success rate at the end of a 5 year post restorative period, with an 80% success rate at the end of 10 years postrestorative or function.
  17. 17. MICROBIOLOGIC FINDINGS IN PERIIMPLANTITIS:- Bacterial flora is associated with periodontitis and periimplantitis. It has shown that pathogens associated with periodontal disease are a gram – negative, black – pigmented anaerobic flora. Failing implants were clinically characterized by increased mobility and periimplant radiolucency and probing depths greater than 6mm where as associated with periodontal pathogenesis, including Actinobacillus actinomycetemcomitans, prevotella intermedia.
  18. 18. Becker et al has been demonstrated that the bacteria found in the implant crevice in the successful implant case are basically the same flora as found in the natural tooth crevice/sulcus in a state of health. Implants in partially edentulous cases / patients appear to be at greater risk for periimplantitis than implants in completely or fully edentulous cases/ patients. There are few qualitative differences in the microflora surrounding implants and teeth in partially edentulous patients.
  19. 19. However, there are marked quantitative decreases in the number of periodontal pathogens around implants in completely edentulous patients. It is possible that the natural teeth may serve as a reservoir for periodontal pathogens from which they may colonize implants in the same mouth.
  20. 20. Rosenberg et al. demonstrated that, in failing implants with a primarily infectious etiology, 42% of the sub gingival flora consists of Peptostreptococcus spp., Fusobacterium spp., and enteric gram – negative rods. Failing implants with a traumatic etiology have a microflora more consistent with gingival health and composed primarily of streptococci.
  21. 21. Periodontitis is the same as periimplanttitis is the study by Dharmer et al that shows that 1.There is higher enzymatic activity in teeth/implants with 3 to 4mm pocket depth than in those with 1 to 2mm pocket depth. 2. There are more motile rods in implants/teeth with 3 to 4mm pockets compared with those with 1 to 2mm pockets. 3.There are no spirochets around implants in the totally edentulous patients as compared with partially edentulous patients.
  22. 22. 4. The enzymatic tests revealed that the microflora around BRanemark implants is similar to that around natural teeth. 5. Cervicular fluid from partially edentulous cases in both healthy and inflamed sites, found no differences in periimplant crevicular fluid (PICF) and gingival crevicular fluid (GCF) in healthy Vs. inflamed sites, and they concluded that the inflammatory and immune responses were similar around tooth and implant.
  23. 23. RETROGRADE PERIIMPLANTITIS:- A condition known as retrograde periimplantitis 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 periimplantitis are characterized by periapical radiographic bone loss without, at least initially, gingival inflammation. The distinction between implant failure caused by infection with periodontal pathogens (infective failure) and implant failure associated with retrograde periimplantitis (traumatic failure) is also reflected in the
  24. 24. ETIOLOGIC FACTORS Two primary etiologic factors are acknowledged today as causative in peri-implant marginal bone loss: Bacterial infection Biomechanical overload
  25. 25. Biomechanical Overload Bone loss at the coronal aspect of implants can result form biomechanical overloading and the resultant microfractures at the coronal aspect of the implant-bone interface. The loss of osseointegration in this region results in apical down growth of epithelium and connective tissue. The speed and degree of loss of implant-bone contact depends upon the frequency and magnitude of the occlusal loading as well as superimposed bactrerial invasion.
  26. 26. While it should be obvious that occlusal loading alone cannot cause progressive bone resorption, in the presence of marginal infection is certainly an important etiologic factor, similar to the situation with natural teeth. The role of over loading is likely to increase in four clinical situations: 1. The implant is placed in poor quality bone. 2. The implant’s position or the total amount of implants placed does not favor ideal load transmisson over the implant surface.
  27. 27. 3. The patient has a pattern of heavy occlusal function associated with parafunction. 4. The prosthetic superstructure does not fit the implants precisely. other etiologic factors such as traumatic surgical techniques, smoking, inadequate amount of host bone resulting in an exposed implant surface at the time of placement and a compromised host response can act as co-factors in the development of periimplant disease.
  28. 28. BACTERIAL INFECTIONS Most authors have assumed that peri-implant diseases (mucositis, peri-implantitis) are comparable to periodontal diseases in that they are primarily plaque- induced. If plaque accumulates on the implant surface, the subepithelial connective tissue becomes infiltrated by large number inflammatory cells and the epithelium appears ulcerated and loosely adherent. When the plaque front continues to migrated apically, the clinical and radiographic signs of tissue destruction are seen around both implants and teeth. However the size of the soft tissue inflammatory lesion and the bone loss is larger around Implants.
  29. 29. In addition, the implant lesions extend into the supracrestal connective tissue and approximate/populate the bone marrow. While the lesions associated with teeth do not. These studies suggest that plaque-associated soft tissue inflammation around implants may have more serious implications than marginal inflammation around an implant might be the low-vascularity soft tissue band and the difference in collagen/fibroblast ratio of gingival tissue, which affects the defense mechanisms around teeth with a periodontal ligament.
  30. 30. In addition, different implant surface characteristics influence the amount of periimplant tissue breakdown and inflammation; specially, HA-coated implants seem to have increased bone loss when compared with titanium implants. Bacterial plaque removed from implant surfaces is very similar to that removed from natural teeth in both healthy and diseased states. Peri-implant inflammation can be successfully treated by plaque control and effective oral hygiene.
  31. 31. Additional Possible Etiologic and Modifying Factors In addition to bacterial infection and excessive biomechanical loading, other etiologic and modifying cofactors have been considered as potential initiators of peri-implant disease. Implant Shape and Implant Surface Peri-implant soft tissue attachment
  32. 32. IMPLANT SHAPE AND IMPLANT SURFACE Over the long term, users of the branemark system have generally observed peri-implant bone loss of approximately 1.5mm during the first year implant insertion and 0.1 mm per year in subsequent years. Bone resorption was reported to be exclusively horizontal in nature: vertical defects were not observed. (Adell et al. 1986, Alberktson et al. 1988).
  33. 33. with other systems (eg : IMZ, care vent) higher bone resorption rates and occasionally vertical defect have been reported very little information is available regarding whether the implant design (cylindrical ,screw type) implant surface morphology (e.g. highly polished cervical region) the technique of surgical placement, or other factors may be responsible for the various peri- implant reactions.
  34. 34. Peri-implant soft tissue attachment Several authors have proposed that the maintenance of healthy peri-implant conditions requires a collar of attached gingival around the implant neck. Furthermore, clinical and animal experimental research has demonstrated that if oral hygiene is sufficient, healthy peri-implant conditions can be maintained even if mobile oral mucosa surrounds the implants. (Krekeler et al. 1985, Adell et al. 1986, van Steenberghe 1988, Strub et al. 1991). Zone of attached gingiva as a means to prevent peri-implant disease (mucositis, peri-implantitis) is not necessary; this is comparable to the situation with natural teeth (Wennstrom et al. 1981).
  35. 35. Nevertheless, if recurrent inflammation persists around implant surrounded by mobile mucosa, it may be prudent to surgically create a peri-implant zone of attached gingiva, which will also simplify implant hygiene. In the visible, anterior segments of the mouth, the presence of keratinized gingival may be necessary for esthetic reasons (Langer et all 1980).
  36. 36. CLASSIFICATION Classification – Peri-implantitis Peri-implantitis - Class 1 Peri-implantitis - Class 2 Peri-implantitis - Class 3 Peri-implantitis - Class 4
  37. 37. Peri-implantitis - Class 1 Slight horizontal bone loss with minimal peri-implant defects
  38. 38. Peri-implantitis class 2 Moderate horizontal bone loss with isolated vertical defects.
  39. 39. Peri-implantitis class 3 Moderate to advanced horizontal bone loss with broad, circular bony defects.
  40. 40. Peri-implantitis class 4 Advanced horizontal bone loss with broad, circumferential vertical defects, as well as loss of the oral and/or vestibular bony wall.
  41. 41. DIAGNOSIS OF IMPLANT TISSUE BREAKDOWN:- To diagnose a compromised implant site, soft tissue measurements using manual or automated probes have been suggested. A probe with a tip diameter of 0.5mm was inserted into the buccal “pocket” using a standardized force of 0.5 N. Probing depth was markedly deeper than at the tooth site, namely 2.0mm. The tip of the probe was consistetly positioned deep in the connective tissue/abutment interface and apical of the barrier epithelium. The distance between the probe tip and the bone crest at the tooth sites was about 1.2mm. The corresponding distance at the implant site was
  42. 42. This means that at the implant sites, the probe almost made contact with the bone crest. From these observations, it may be concluded that the attachment between the implant surface and the mucosa was weaker than the corresponding attachment between the tooth and gingiva, and care must be exercised when data from probing depth measurements from tooth and implant sites are compared. if a light probing pressure is applied during probing, the epithelial attachment of the transmucosal tissue seal will be disrupted but will heal within 5-7days. (Etter et al 2002) This means that – as is the case in probing around teeth probing the peri-implant tissue can be performed without causing permanent damage to the integrity of the transmucosal attachment.
  43. 43. Although some reports say that probing is contraindicated, careful monitoring of probing depth and clinical attachment level over time seems useful in detecting changes of the peri -implant bone level have been shown to be useful. Standardized radiography, both with and without computerized analysis, has been documented in a number of studies. suppuration Besides pocket formation and radiographic bone destruction,, swelling, color changes, and bleeding upon gentle probing have been documented as signs of peri-implant disease. Microbial monitoring is useful in evaluating the peri implant health condition and the microbial composition of a peri–implantitis site. This information can then potentially be used to determine the etiology of the breakdown and to select a specific antiobiotic regimen.
  44. 44. MANAGEMENT Depending on the etiology of the problem, specific treatment is selected. When biomechanical forces are considered the main etiologic factors for peri – implant bone loss, treatment is undertaken into two phases. The first phase involves an analysis of the fit of the prothesis, the number and position of the implants, and an occlusal evaluation. Prosthesis design changes, improvement of implant number and position, can arrest the progression of peri – implant tissue breakdown. To eliminate deep peri – implant soft tissue pockets or to regenerate bone around the implant, surgical techniques can be employed in a second phase of treatment.
  45. 45. Peri- implant disease caused by bacterial infection is also treated in phases. The first phase controls the acute bacterial infection and reduces the inflammation present in the tissues. The treatment involves mechanical debridement, localized and/ or systemic antimicrobial therapy and improved oral hygiene until a healthy peri –implant site is established. The second phase will involve the surgical procedure.
  46. 46. INITIAL PHASE OF PERIIMPLANTITIS TREATMENT Occlusal therapy When excessive forces are considered the main etiologic factor for periimplant bone loss, treatment involves analysis of the fit of the prosthesis, the number and position of the implants, and an occlusal evaluation. Prostheses design changes, improvement of implant number and position, and occlusal equilibration can contribute to arrest the progression of periimplant tissue breakdown
  47. 47. ANTI-INFECTIVE THERAPY The non surgical treatment of periimplant bacterial infection involves the local removal of plaque deposits with plastic instruments and polishing of all accessible surfaces with pumice; subgingival irrigation of all peri-implant pockets with 0.12% chlorhexidine; systemic antimicrobial therapy for 10 consecutive days; and improved patient compliance with oral hygiene until a healthy periimplant site is established
  48. 48. The implant surface is contaminated with soft tissue cells, bacteria, and bacterial by-products. Bacterial adherence is enhanced by the micro-irregularities of implant surfaces, and as long as the contamination is present, wound healing is compromised. Therefore if regeneration of new bone and reosseointegration is to occur, the defect must first be debrided and the contaminated implant surface prepared. Reosseointegration can be defined as the growth of new bone in direct contact to the previously contaminated implant surface without an intervening band of organized connective tissue.
  49. 49. Acess may be gained via full thickness or split-thickness periodontal flap reflection. The peri-implant pocket epithelium and any granulation tissue are removed using conventional curettes. Care must be taken to avoid damaging or contaminating implant surface. Subsequently plastic curettes are used to remove plaque and calculus as thoroughly as possible from the surface of the implant. PLASTIC CURETTE
  50. 50. Prophy-Jet Device (30-60 seconds application) are used to clean the implant surface. The Prophy-Jet Device using sodium hydrocarbonate with sterile water are indicated (Bass et al. 1992). The high pressure air powder abrasive, suggest that this instrument removes microbial deposits completely from titanium implant surfaces. In addition, in vitro morphologic and statistical comparisons of gingival fibroblast interactions with titanium surfaces treated with air-powder abrasives showed these surfaces have no adverse effect on cell adhesion. Prophy - Jet Device
  51. 51. Consideration should be given to the potential for air- emphysema when using high-pressure air spray instrumentation in the surgical site. Therefore, the spray should never be directed parallel to the implant surface into the surface, but rather at an angle of atleast 450 .(Brown et al 1992) PROPHY-JET
  52. 52. The final Step in cleaning the surface of the implant consists of detoxification using citric acid (pH 1-3) 30 – 60 seconds on a soaked gauze strip around the implant surface. It has been shown that the use of citric acid provides the greatest potential to remove bacteria and endo toxins from the implant surface, in comparison with other chemical agents. (Zablowsky et al. 1992). Before closing the flap, the entire area is rinsed again using sterile saline solution. De-toxification with Citric Acid
  53. 53. SURGICAL TECHNIQUES FOR TREATMENT OF PERIIMPlANTITIS The surgical techniques presently advocated to control periimplant lesions are modified from techniques used to treat bone defects around teeth. The type and size of bone defect has to be identified before deciding on the appropriate treatment modality. Therefore prob-ing and sounding of the defects is done using local anes-thesia, and radiographs are evaluated so that the surgical treatment plan is finalized immediately prior to begin-ning the procedure. This forms the basis to determine whether the implant will be removed or a resective type of surgery or a regenerative procedure will be
  54. 54. The resective therapy is used to reduce pockets, correct nega-tive osseous architect ure and rough implant surfaces, and increase the area of keratinized gingiva if needed. The regenerative therapy is also used to reduce pockets but with the ultimate goal of regeneration of lost bone tissue. As in the treatment of certain types of periodontitis, systemic antibiotics have been advocated as a supportive regimen during the treatment phase of periimplant dis-ease. This may be especially important due to the close proximity of the inflammatory lesion to the im-plant and the bone marrow .Antibiotics frequently used without sensitivity testing are doxycycline and metronidazole.
  55. 55. PERI –IMPLANT RESECTIVE THERAPY The type of osseous defect should be identified before deciding on the treatment modality. Apically positioned flap techniques and osseous resective therapy are used to correct horizontal bone loss and moderate vertical bone defects and reduce overall pocket depth. Full-thickness or split-thickness flap management are used to access the surgical area.
  56. 56. With the flap raised, de-granulation of the osseous defect is performed. Care should be taken to avoid contact between the implant and metal instruments. An implant surface can now be prepared with chemicals and air abrasives. Implant surface preparation is performed by applying the air spray of the air-powder abrasive for a maximum of 60 seconds on the implant surface, followed by copious irrigation with saline solution. Then the application of supersaturated citric acid is applied for 30 seconds, followed again by irrigation with saline
  57. 57. IMPLANTOPLASTY Many times the effort to level the bone and apically position the soft tissues during surgical treatment for peri-implantitis leads to exposure of the rough surface of the implant. Such rough surface tend to accumulate plaque, So they should be smoothed and polished. Diamond stones with copious cooling can be used to grind away plasma-spray coatings or threads on the implant surface, with final polishing accomplished using rubber disks (Jovanovic 1990). Implantoplasty
  58. 58. This type of “implantoplasty” remains the single effective method for reducing plaque accumulation; it also makes plaque control considerably easier for the patient (Lazada et. Al 1990). If this type of implant surface treatment is necessary, it should be performed immediately after flap reflection and before any contouring of the bone. Metal particles always result from this procedure and must be removed by copious rinsing.
  59. 59. PERI – IMPLANT REGENERATIVE THERAPY: An increasing number of reports have shown successful treatment of periimplant bone defects around functioning dental implants. To accomplish regeneration of lost bone tissue and reosseointegration, guided bone regeneration (GBR) and bone graft techniques have been suggested. In several experimental and clinical studies, the GBR principle using a nonresorbable expanded poly-tetra- fluoroethylene membrane has been used for healing of bone defects seen at the time of implant placement and around failing implants
  60. 60. Regeneration of bone seems to be enhanced if the area is isolated from the oral environment. Therefore it is recommended to remove the implant prosthesis 4 to 8 weeks prior to the regenerative surgical procedure to allow optimal compliance with oral hygiene procedures and the soft tissue to collapse and heal over the implant site with a newly attached cover screw in place. Thus at the time of regenerative surgery, a more intact soft tissue flap can be helpful to seal off the peri-implant tissues during the healig period. A crestal incision is then used for the flap design.
  61. 61. The surgical therapy includes implant surface preparation by air-powder abrasive for 30 to 60 seconds and the application of an oversaturated citric acid solution for 30 to 60 seconds. Consecutively, an elaborate rinse of the surgical area is performed with saline solution. A membrane is then trimmed to extend 3 to 4 mm beyond the margins of the bone defect a hole (3mm) where punched in the rigid centre of the membrane, which permitted from attachment to the fixtures. The osseous defects were completely covered by the membrane. A space was left beneath the membrane ,If the defect is large graft material (demineralized freeze – dried bone and HA )was placed to support the membrane.
  62. 62. The surgical phase was then sutured closely to the implant neck. The surgical phase was supported by the systemic administration of 250 mg tetracycline HCL every 6 hours for 1 week. After 5 to 8 weeks, the membrane were removed and the patients placed on a strict maintenance program. The membrane was surgically removed 6 weeks later. The previous osseous defect had completely filled with regenerating tissue.
  63. 63. As the membrane is being removed and during repositioning and suturing of the flaps, care must be taken not to disturb the newly formed osteoid tissue.
  64. 64. ROLES IN IMPLANT MAINTENANCE PATIENT ROLE 1. Plaque control of 85%. 2. Use of interdental (ID) brushes,hand and motorized.(Proxa-Brush,Oral-B Brush,Rota-Dent,Sonic). 3. Dip bruses in chlorhexidine,0.12% (Peridex,Periogard). 4. Use of flosses,,tapes,dipped in chlorhexidine (Super- Floss,Perio-Floss,G-Floss) 5. If patient has tooth-colored materials,composites,sand so on, use a cotton swab dipped in chlorhexidine.
  65. 65. HYGIENIST ROLE 1. Check plaque control effectiveness (85%). 2. Check for inflammatory changes 3. IF pathology is present,probe gently with plastic probe (sensor). 4. Scale supragingivally only (or slightly subgingivally). 5. Check for problems such as loose suprastructure. 6. No need to probe if no pathology is present.
  66. 66. CLINICAL ROLE 1. Check every 3 or 4 months 2. Check for 85% plaque control effectiveness. 3. Expose radiographs every 12 to 18 months if no pathology is present and as needed pathology is present. 4. Is suprastructure is retrievable, remove and clean the ultrasonic every 10 to 24 months. 5. If implant needs it repair, degranulate, detoxify and graft with guided bone regeneration (GBR) if necessary.
  67. 67. REVIEW OF LITERATURE Mc Kinney, Atelic, koth D L (1984) defined the terms permucosal, perimucosal and transmucosal can all be used correctly to describe the unique and interesting biologic seal that occurs around a dental implant. Per means ‘through’ and peri means ‘around’. The term per-perimucosal seal is used to describe most accurately the biologic function of the division between the internal and external environments of dental implants. Permucosal designates the vertical orientation of the implant penetration though the oral mucosa and perimucosal designates the horizontal or circumferential seal of the mucosa to the biomaterial.
  68. 68. D. Van Steenberghe (1988) drew parallels between tissue attachment on teeth and permucosal implants for both epithelial and connective tissue parts. Plaque accumulates more rapidly on titanium abutments than on natural teeth. Presence of deep pockets with probing depths of 7mm have been found to occur around osseointegrated implants. It is due to the thickness of the mucoperiostium through which the abutment is installed.
  69. 69. Block M, Kent J 1990 found on follow up examinations or a non scheduled visit, recognized soft and hard tissue compromise i.e. bleeding on probing, pain, purulent drainage, discharge or progressive bone loss. Patient prosthesis were removed and cleaned of plaque. It may be modified to provide the patient easier access for maintenance. The patient was instructed regarding implant hygiene. Chlorhexidene is recommended for use on the floss, proxy brush or electric tooth brush as well as with demineralised bone graft is placed over the implant. The flap in then closed primarily. At least 4 months is allowed for consolidation of the graft where upon the implants are the re-exposed the abutment heads replaced and the restoration replaced or remade.
  70. 70. Buser Daniel, Weber H.P et al 1992 examined the soft tissue reactions to non-submerged unloaded titanium implants. A complication free tissue integration with a dense connective tissue indirect contact to the implant surface in the supracrestal area of epithelial structures similar to those around teeth.
  71. 71. Heretel R.C. et al 1993 discussed that the influence of the dimensions of implant superstructures on peri- implant bone loss is the implant position and consequently the design and dimensions of the superstructure influence the way in which occlusal forces are transmitted to the implant and surrounding bone. In certain areas these forces may reach greater level-arm action. This leads to high-stress zones and potential bone resorption. As with the natural dentition, long span fixed partial dentures should not be splinted by only a few implants.
  72. 72. Jovanovic sascha. A 1993 suggested that experimental peri-implant bone loss can be induced by plaque accumulation. Moderate tissue destruction can be arrested with careful surgical techniques. Bony defects treated with resective or regenerative surgical therapy. Detoxification of contaminated implant surface based on biological principle of GTR, a concept of bone regeneration around failing implants has been developed. Histological data shows evidence of new bone formation and ‘reosseointegration’.
  73. 73. Touhlar Richards 1998 discussed the primary difference between dentogingival and implantogingival soft tissues is the structure and arrangement of the collagen fibres. Decreased vascular supply may account for functional differences in inflammatory responses.
  74. 74. Weber Hans Peter and Cochran David 1998 reviewed the morphologic and clinical features of peri-implant soft tissues around titanium abutments or non-submerged one- stage implants. The major connective tissues fibres run parallel to the long axis of the implant. The connective tissue forms a nonvascularized circular scar type structure surrounded by a less dense vascularized connective tissue. Thus the epithelial components around implants appear to be consistent with the epithelial components around teeth.
  75. 75. Carmagnda et al 1999 examined bone tissue alterations that occurred around implants at which the marginal level of bone support at fixture installation was different at buccal and lingual surfaces. Findings demonstrated that osseointegration occurred at implants placed in a chronic defect with large discrepancies and function, marked modeling and remodeling of bone tissue took place. Buccal surface bone regrowth and osseointegration occurred while at lingual wall substantial resorption of marginal bone and an enhanced number of bone multicellular units.
  76. 76. REFERENCES Glickman Irvin : Clinical periodontology 3rd ed. Lindhe jan : Clinical periodontology and implant diseases 3rd ed 1997. Schlunger saul et al : Periodontal diseases 2nd 1990 Abrahamsson I et al : Peri-implant tissues at submerged and non-submerged titanium implants J. clin periodontal 1999, 26:600-607 Haas Robert et al : The relationship of smoking on peri- implant tissue – A retrospective study JPD 1996, 76, 6: 592-6.
  77. 77. James Robert A: Periodontal considerations in implant dentistry JPD Aug 1973, vol 30, no. 2, 202-209. Jovanovic Sacha A: The management of peri-implant breakdown around functioning osseointegrated dental implants J. periodontology 1993; 64: 1176-1183. Truhlar Richard – Peri-implantitis cause and treatment. Journal of OMFS clinics of North America May 1998, Vol 10, No.2, 299- 306. Weber Hans Peter and Cochran David K: The soft tissue response to osseointegrated dental implants JPD 1998, 79, 79- 89.
  78. 78.