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How to treat ailing and failing implants

How to treat ailing and failing implants. Roland M. Meffert Implant dentistry, spring, 1992. Ailing implant Failing implant Failed implant. Definition of ailing implant. Exhibits bone loss with pocketing; the situation seems to be static at the 3- to 4-month maintenance checks.

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How to treat ailing and failing implants

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  1. How to treat ailing and failing implants Roland M. Meffert Implant dentistry, spring, 1992

  2. Ailing implant • Failing implant • Failed implant

  3. Definition of ailing implant • Exhibits bone loss with pocketing; the situation seems to be static at the 3- to 4-month maintenance checks. • A lamina dura indicating a state of chronicity may be present at the borders of the osseous defect. Meffert, 1992, Implant dentistry

  4. Definition of failing implant • May evidence bone loss, pocketing, bleeding upon probing, purulence • Bone loss patterns are progressing irrespective of therapy. Meffert, 1992, Implant dentistry

  5. Definition of failed implant • Has mobility, a dull sound when percussed, and radiographically a peri-implant radiolucency • The failed implant must be removed since it is nonfunctional and bone loss will continue. Meffert, 1992, Implant dentistry

  6. Chemical treatment and the removal of LPS • Antibiotic tetracycline did not have much effect in removing the LPS endotoxin from the hydroxyapatite (HA) when used in concentration of 50mg/ml (pH 2 to 3) and it significantly altered the inner and outermost calcium to phosphorus ratios of the HA coating. • Hydrogen peroxide did not remove LPS to any degree. Zablotsky et al., 1991, Unpublished data

  7. Chemical treatment and the removal of LPS • Chlorhexidine gluconate and stannous fluoride seemed to bind bind rather than remove the LPS to the coated surface. • Both chlorhexidine and HA are highly charged and there may be an interaction which would bind the LPS to the HA surface; the same may be true of stannous fluoride. Zablotsky et al., 1991, Unpublished data

  8. Chemical treatment and the removal of LPS • The treatment of choice to remove endotoxin from the HA-coated surface according to the study of Zablotsky et al. was citric acid (pH 1, 40% concentration) applied to the surface for 30 seconds to 1 minute. • A longer application time of 2 to 3 minutes significantly altered the thickness of the HA and seemed to weaken the HA substrate. Zablotsky et al., 1991, Unpublished data

  9. Chemical treatment and the removal of LPS • A modified plastic Cavitron tip(Denstply) also removed endotoxin to a great degree. • The air abrasive instrument would remove endotoxin but it might be contraindicated at the surgical site due to the possible introduction of emboli. Zablotsky et al., 1991, Unpublished data

  10. Meffert, 1992, Implant dentistry

  11. Detoxification of endotoxin-contaminated titanium and hydroxyapatite-coated surfaces utilizing various chemotherapeutic and mechanical modalities Mark H. Zablotsky DanaL. Diedrich Roland M. Meffert Implant dentistry, spring, 1992; 1 : 154-158

  12. Zablotsky, 1992, Implant Dentistry

  13. Zablotsky, 1992, Implant Dentistry

  14. Table 3. Mean Residual LPS Counts/min/mm2 (“Contaminated Grit-Blasted Titanium Alloy-Untreated “) Zablotsky, 1992, Implant Dentistry

  15. * Significantly greater amounts of LPS than untreated control (p<0.05) ** Significantly less of LPS than untreated control (p<0.05) *** Significantly less of LPS than burnished control (p<0.05) Zablotsky, 1992, Implant Dentistry

  16. * Significantly less amounts of LPS than burnished control (p<0.01) Zablotsky, 1992, Implant Dentistry

  17. The rationale for utilizing outer membrane from a member of the Enterobacteriaceae • The outer membranes contain LPS in its natural configuration (associated with phospholipids and membrane proteins in a membrane matrix). Extracted LPS is less desirable for studies such as this because the extraction procedure can chemically alter the LPS and generate aggregates in a variety of physical forms. Zablotsky, 1992, Implant Dentistry

  18. The rationale for utilizing outer membrane from a member of the Enterobacteriaceae • The LPS and outer membrane of E.coli are well characterized genetically and biochemically, making them well suited to experimental manipulation. Zablotsky, 1992, Implant Dentistry

  19. The rationale for utilizing outer membrane from a member of the Enterobacteriaceae • The toxic lipid A portion of LPS has the same general structure in almost all the Eubacterium. LPS is amphiphilic and its physical interactions with a surface such as titanium alloy will be similar. That is, E. coli LPS should bind to the titanium alloy implant/ abutment in the same manner and to the same degree as L:PS from Bacteroides, Treponema, and other genera. Zablotsky, 1992, Implant Dentistry

  20. LPS binding to titanium and Its charateristics • It can be concluded that LPS would have a reduced affinity for polished abutments when compared with grit-blasted titanium surface. • It is interesting to note that burnishing the contaminated grit-blasted titanium surface with a cotton pellet dipped in sterile saline for 1 minute was effective in reducing LPS levels significantly below untreated controls. Zablotsky, 1992, Implant Dentistry

  21. LPS-infected HA surface & Citric acid treatment • A short (30-60 seconds) application of citric acid removed LPS without significantly altering the residual coating. • This treatment was also successful in returning the contaminated HA coating to a biologically acceptable surface on which human gingival fibroblasts could proliferate. Zablotsky et al, 1991, Unpublished data

  22. LPS-infected HA surface & Citric acid treatment • Action mechanism of citric acid on the HA surface is thought to be a demineralized phenomenon of the most superficial layer of HA. • This obviously does not occur with the toxic titanium or titanium alloy surface. Athough a 1 minute application of citric acid was superior to saline burnishing for the same time interval, residual levels were not significantly less. Zablotsky et al, 1991, Unpublished data

  23. LPS-infected HA surface & Stannous fluoride • The application of stannous fluoride to contaminated titanium alloy appears to bind greater levels of LPS to the surface when compared with untreated controls. • The mechanism for this is unknown, but may be due to changes in charge interactions among stannous fluoride, LPS, and HA and/or to the binding of the glycerol carrier in the stannous fluoride solution. Zablotsky et al, 1991, Unpublished data

  24. Results • The air-powder abrasive unit removed significantly greater amounts of LPS than all other treatment modalities on titanium samples. (p<0.05) • A 60-second burnish with sterile water was able to remove significant amounts of LPS when compared with untreated controls. (p<0.05) Zablotsky, 1992, Implant Dentistry

  25. Results • Citric acid was superior in the removal of LPS from HA-coated surfaces when compared with the controls or chloramine T. (p<0.01) Zablotsky, 1992, Implant Dentistry

  26. Conclusion • Titanium alloy surfaces are at a lower risk to the binding of endotoxin than HA-coated surfaces. • If fixture modification is performed as part of a pocket elimination procedure, the use of chemotherapeutic agents or air-powder abrasives are probably not indicated. Zablotsky, 1992, Implant Dentistry

  27. Conclusion • If regenerative techniques such as osseous grafting and guided tissue regeneration, are contemplated, chemotherapeutic agents or air-powder abrasive techniques appear to have merit in the treatment of the toxic surface. Zablotsky, 1992, Implant Dentistry

  28. Guided bone regeneration in the treatment of periimplantitis Persson L.G. Ericsson I. Berglundh T. Lindhe J. Clinical Oral Implants Research, 1996: 7: 366-372

  29. -ligation Fixture installation abutment connection procedure extraction + ligation surgery biopsy -6 -3 0 1 2 -3 month -9 Experimental Procedure • Systemic antibiotics : 3 weeks • Flap and degranulation • 1% delmopinol HCl • (5-10 min per fixture) • ePTFE • New cover screws • Brånemark machined fixtures Persson et al., 1996, COIR

  30. Result & Conclusion • Even if the inflammatory process was eliminated as result of treatment, the amount of new bone formation that occurred following GBR was minute or absent. • Dense connective tissue capsule was interposed between the previously exposed part of the titanium fixture and the bone. Persson et al., 1996, COIR

  31. Result & Conclusion Dense connective tissue capsule between cleaned, contaminated surface and newly formed bone. Persson et al., 1996, COIR

  32. Conclusion • Even if the inflammatory process was eliminated as result of treatment the amount of new bone formation that occurred following GBR was minute or absent. • Despite the systemic antibiotic regimen, but in the absence of local debridement, the plaque associated infiltrate remained (or reoccurred), and at most implant sites, it extended to the bone tissue. Persson et al., COIR, 1996

  33. Conclusion • The assumption that the delmopinol treated fixture surface in the present material was not clean enough to allow “re-osseointegration” to occur. • Delmopinol HCl is suggested to be surface active and capable to reduce the free surface energy (Collaert 1992). This may have changed the surface properties of the titanium dioxide layer of the implants and retarded/presented “re-osseointegration” Persson et al., COIR, 1996

  34. Tissue response of Re-implanted cover screw • Retrieved cover screw from 5 patients. • Either rinsed in saline or exposed to ultrasonic cleaning and sterilization. • Subsequently implanted and retained for 6 weeks in the abdominal wall of the animals. Pristine sterile cover screws were used as controls. • Re-implanted cover screws, in comparison to the pristine cover screws, elicited a tissue response that included the formation of a thicker fibrous capsule and the presence of a larger number of macrophages in the vicinity of the implants. Sennerby et al., JOMI, 1989

  35. Resolution of peri-implantitis following treatment Persson L.G. Araújo M.G. Berglundh T. Gröndahl K. Lindhe J. Clinical Oral Implants Research, 1999: 10: 195-203

  36. Bone marker Radiograph treatment extraction Fixture abutment + ligation -ligation biopsy Procedure -11 -7 -2 0 1 2 3 4 5 6 7 8 9 10 11 months Breakdown period Preparatory period Healing period Experimental Procedure Persson et al., 1999, COIR

  37. Treatment Lt. Rt. • Systemic antibiotics : 3 weeks • Flap and degranulation • Cotton pellets soaked in saline • New cover screws • Brånemark machined fixtures • Systemic antibiotics : 3 weeks • Flap and degranulation • Abrasive pumice with rotating brush • New cover screws • Brånemark machined fixtures Persson et al., 1999, COIR

  38. Result & Conclusion Borderline between the “old” original bone and newly formed bone Persson et al., 1999, COIR

  39. Result & Conclusion • Substantial regrowth of bone within the defect. • Thin connective tissue capsule separating newly formed bone from the implant. • The amount of “re-osseointegration” that had taken place was small Persson et al., 1999, COIR

  40. Surface energy, Contamination and Tissue Response • Native titanium oxide layer provides the implant with a high surface energy(reduced contact angle)which seems to facilitate implant to tissue interaction and integration. • If the implant during handling becomes contaminated, a low energy surface (increased contact angle) will form which, following implant installation, may elicit a foreign body reaction. • Such a contaminated implant will be surrounded by a dense, connective tissue capsule which separates the “foreign body” from the adjacent host tissue. Bair & Meyer JOMI 1988

  41. Result • The lateral aspect of the coronal part of the fixture, I.e. the previously contaminated portion, was in all experimental sites covered by a dense connective tissue capsule that separated the newly formed bone from the implant. • This capsule which was between 50 and 200 m wide, was consistently devoid of inflammatory cells but contained large numbers of collagen fibers which runs a course parallel to the fixture surface. Persson et al., COIR, 1999

  42. Table 1. Results from morphometric measurementperformed in sites L2/L3 and R2/R3. Mean values and SD

  43. Table 1. Results from morphometric measurement of the peri-implant bone tissue performed in sites L2/L3 and R2/R3. BMU= bone multicellular units. Mean values and SD

  44. Conclusion • Submarginal ligature placement and plaque accumulation on the implant surface induced an inflammatory reaction in the periimplant mucosa that was associated with marginal bone loss and the establishment of a crater-like, circumferential bone defect. • Following antibiotic therapy there was a substantial regrowth of bone within the defect. Persson et al., COIR, 1999

  45. Conclusion • The inflammatory lesion was resolved and that new-bone formation had occurred in the previous defect • The amount of “re-osseointegration” that had taken place was small, a thin connective tissue capsule was found to separate the implant surface from the newly formed bone at all experimental implant sites. Persson et al., COIR, 1999

  46. Conclusion • The Oxytetracycline and Calcein blue markers were present in the coronal portions of the newly formed bone. This indicates that most of the bone formation occurred early during healing. • Both systemic antibiotics and local therapy with or without abrasive debridement of the implant surface predictably resolves a peri-implantitis but may not promote what has been called “reosseointegration” Persson et al., COIR, 1999

  47. Osseointegration following treatment of peri-implantitis and replacement of implant componentsAn experimental study in the dog Persson L.G. Ericsson I. Berglundh T. Lindhe J. J. Clin. Periodontol., 2001: 28: 258-263

  48. Bone marker Radiograph Procedure extraction fixture abutment + ligation -ligation treatment biopsy -12 -9 -5 0 1 3 15 19 months Experimental Procedure Persson et al., 2001, JCP

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