Implant 5 – Treatment Planning I

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Medical History: medical conditions + drugs that may affect implant and surgical outcome; Risk factors

  1. Misch and Resnik. Medical Evaluation of the Dental Implant Patient (CH 20). pp 406-420. Contemporary Implant Dentistry, Misch, C.E., 3rd Edition, 2008, Mosby Year Book.

  2. Rose L and Mealey B. Implant complications associated with systemic disorders and medications. (CH 2) pp 9-45.

  3. Sugerman, P., Barber, M.: Patient selection for endossous dental implants; Oral and systemic considerations. Int J Oral Maxillofac Implants. 2002 Mar-Apr; 17(2):191-201

  4. Ong, C et al: Systematic Review of Implant Outcomes in Treated Periodontitis Subjects. J Clin Periodontol 2008; 35:438

  5. RasperiniG, Siciliano VI, et al. Crestal bone changes at teeth and implants in periodontally healthy and periodontally compromised patients. A 10-year comparative case-series study. J Periodontol. 2013 Nov 11. [Epub ahead of print]

  6. KlokkevoldP, Han T: How do smoking, diabetes and periodontits affect outcomes of implant treatment? Int J Oral Maxillofac Implants. 2007; 22 (suppl)173-202

  7. Dowel, S et al: Implant success in people with type 2 diabetes mellitus with varying glycemic control. A pilot study. JADA: 138:2007:355-361

  8. StrietzelFP, Reichart PA, et al. Smoking interferes with the prognosis of dental implant treatment: a systematic review and meta-analysis. J Clin Periodontol. 2007 Jun;34(6):523-44. Review.

  9. BainCA Implant installation in the smoking patient. Periodontol 2000. 2003;33:185-93. Review.

  10. Fugazzotto, P et al: Implant Placement with or without Simultaneous Tooth Extraction in Patients Taking Oral Bisphosphonates: Postoperative Healing, Early Follow up and Incidence of Complications in Two Private Practices. J Periodontol 2007; 78:1664-1669

  11. Colella, Cannavale, Pentenero, Gandolfo: Oral implants in radiated patients: A systematic review. Int J Orla Maxillofac Implants 2007; 22(4):616-623

  12. Holahan, C et al: Effect of osteoporotic status on the survival of titanium dental implants. Int J Oral Maxillofac Implants. 2008:Sep-Oct; 23(5)905-10

  13. ClaudyMP, Miguens SA Jr, et al Time Interval after Radiotherapy and Dental Implant Failure: Systematic Review of Observational Studies and Meta-Analysis. Clin Implant Dent Relat Res. 2013 Jun 7. [Epub ahead of print]

  14. SharafB, Dodson TB. Does the use of prophylactic antibiotics decrease implant failure? Oral Maxillofac Surg Clin North Am. 2011 Nov;23(4):547-50

  15. AhmadN, Saad N. Effects of antibiotics on dental implants: a review. J Clin Med Res. 2012 Feb;4(1):1-6.

  16. EspositoM, Grusovin MG, Worthington HV. Interventions for replacing missing teeth: antibiotics at dental implant placement to prevent complications. Cochrane Database Syst Rev. 2013 Jul 31;7:CD004152.

  17. Ata-AliJ, Ata-Ali F, Ata-Ali F. Do antibiotics decrease implant failure and postoperative infections? A systematic review and meta-analysis. Int J Oral Maxillofac Surg. 2013 Jun 25. pii: S0901-5027(13)00258-0. doi: 10.1016/j.ijom.2013.05.019. [Epub ahead of print]

  18. Alissa R, Sakka S, Oliver R, et al. Influence of ibuprofen on bone healing around dental implants: a randomised double-blind placebo-controlled clinical study. Eur J Oral Implantol. 2009 Autumn;2(3):185-99.


Topic:Patient selection

Author:Sugerman, P., Barber, M

Title:Patient selection for endossous dental implants; Oral and systemic considerations.

Source:J Oral Maxillofac Implants. 2002 Mar-Apr; 17(2):191-201

Type:Discussion

Rating: Good

Keywords:patient selection, endossous dental implant, oral, systemic consideration

Purpose:The aims of this article were to define “reasonable health” for dental implant treatment and to provide a systematic approach to the selection of dental implant patients.

Discussion:

TITANIUM TOXICOLOGY The survival or success of endosseous dental implants may be influenced by a number of local and systemic conditions. Some of these conditions affect the process of osseointegration directly. The following are noted in particular.

  • PHYSICAL STATUS

    • The American Society for Anesthesiology (ASA) has defined a 6-point scale of physical status

  • AGE

    • Younger patients may show greater crestal bone resorption around dental implants.It is therefore recommended that implant placement be delayed until growth and development have ceased or are minimal

    • However, implant failure does not correlate with age or sex. Increasing age has no effect on osseointegration or the rate of crestal bone resorption around dental implants.

  • PATIENT EXPECTATION

    • Although dental implants can enhance esthetics, phonetics, and bite force, it is important to identify unrealistic expectationsthat patients may have about implants and implant- retained prostheses.

  • HYPOHIDROTIC ECTODERMAL DYSPLASIA is characterized by hypodontia, hypotrichosis, and hypohidrosis. Dental implants have been used successfully in patients with severe hypodontia associated with ectodermal dysplasia.In a recent prospective study, implant placement and prosthetic rehabilitation in young children with ectodermal dysplasia did not restrict transverse or sagittal growth. However, vertical alveolar growth resulted in the occasional submergence of endosseous implants, necessitating revision and the placement of longer abutments.

  • SMOKING:Many studies have shown that smoking interferes with osseointegrationand accelerates bone resorption around dental implants

  • OSTEOPOROSIS:osteoporosis appears not to influence implant survival.Moreover,endosseous dental implants may actually stimulate mandibular bone formation in a load-dependent manner.

  • DIABETES MELLITUS: endosseous dental implants are usually successful in patients with diabetes, although uncontrolled diabetes contraindicates dental implant placement. Consideration should be given to antibiotic prophylaxis for surgical procedures in diabetic patients.

  • SCLERODERMA:little is known about dental implants in patients with scleroderma.Endosseous dental implants may improve prosthesis function and comfort in scleroderma patients, although access for implant surgery and for oral hygiene may be compromised.

  • SJÖGREN SYNDROME: Implant-supported prostheses were shown to considerably increase prosthetic comfort and function in patients with Sjögren syndrome,preferable to soft tissue-supported prostheses.

  • MULTIPLE MYELOMA: Implant success has been reported in a patient with multiple myeloma.Unmanaged malignant disease in general must be considered a contraindication for the placement of endosseous dental implants.

  • PARKINSON’S DISEASE: Implant- supported prostheses should be considered in patients with Parkinson’s diseaseand other diseases affecting orofacial motor function.

  • BONE MARROW TRANSPLANTATION: Implant placement should be delayeduntil cytotoxic chemotherapy has ended and the mar- row graft has taken. Bone marrow transplant patients may develop oral graft-versus-host disease that is clinically similar to oral lichen planus

  • HIV: endosseous dental implants have been placed successfully in HIV-positive patients

  • SYSTEMIC DRUGS: Consultation with the patient’s physicianprior to dental implant placement is desirable for patients on anticoagulants or long-term systemic corticosteroids.

  • CHRONICALLY INFECTED IMPLANT SITES: Periodontitis and periapical lesions should be diagnosed and treated prior to dental implant placement.

  • ORAL LICHEN PLANUS Endosseous dental implants may be used in patients with nonerosive forms of OLP, although patients should be warned of possible lesion exacerbation related to surgery and possible implant failure if gingival lesions become erosive

  • HEAD AND NECK RADIOTHERAPY: Implant placement following head and neck radiotherapy is associated with a significant risk of osteoradionecrosis, especially with irradiation above 50 Gy. Recommended a 6- to 12-month recovery period after irradiation prior to dental implant placement

Presurgical hyperbaric oxygen may reduce the dental implant failure rate in irradiated jawbone from 60% to 5%

  • TARDIVE DYSKINESIAS Tardive dyskinesia may complicate dental implant therapy.Alternatives to endosseous dental implants should be considered for patients with neurologic disorders including orofacial dyskinesia, trigeminal neuralgia, or orofacial dysesthesia.

Topic: Implants in patients with periodontitis

Authors: Ong, C et al:

Tittle:Systematic Review of Implant Outcomes in Treated Periodontitis Subjects.

Source: J Clin Periodontol 2008; 35:438

Type: Systematic Review

Rating: Good

Keywords:periimplantitis, failure

Purpose:To determine implant outcomes in partially dentate patients who have been treated for periodontitis compared with periodontally healthy patients.

Methods:

All longitudinal studies (until March 2006) of endosseous dental implants of at least 6 months of loading were searched. Studies presented with one or more of the outcome measures (implant survival, success, bone-level change, peri-implantitis) were included. Screening, data abstraction and quality assessment were conducted independently and in duplicate.

Results:

From 4448 citations, 546 full-text papers were screened and nine studies were included. Overall, the non-periodontitis patients demonstrated better outcomes than treated periodontitis patients. However, the strength of evidence showed that the studies included were at a medium to high risk of bias, with lack of appropriate reporting and analysis of outcomes plus lack of accounting for confounders, especially smoking. Furthermore, the studies showed variability in the definitions of treated and non-periodontitis, outcome criteria and quality of supportive periodontal therapy. Meta-analysis could not be performed due to heterogeneity of the chief study characteristics.

Conclusion:

There is some evidence that patients treated for periodontitis may experience more implant loss and complications around implantsthan non-periodontitis patients. Evidence is stronger for implant survival than implant success; methodological issues limit the potential to draw robust conclusions.

Topic:crestal bone height change

Authors:Rasperini G, Siciliano VI

Title:Crestal bone changes at teeth and implants in periodontally healthy and periodontally compromised patients. A 10-year comparative case-series study.

Source:J Periodontol. 2013 Nov 11.

Type:Comparative case-series

Rating:Good

Keywords:alveolar bone loss, peri-implantitis, periodontitis, smoking

Purpose:To compare the 10 year radiographic crestal bone changes around teeth and implants in periodontally compromised and periodontally healthy patients.

Methods:120 patients (60 with prev hx of perio, 60 healthy) were followed for 10 years post loading for radiographic crestal bone height of dental implants and adjacent teeth. 10 patients were smokers. Digital films were calibrated. Radiographic crestal bone change was calculated by subtracting the creatl BL at baseline from the crestal BL at the 10 year follow up.

Results:After 10 years, implant survival was 80-95% and 100% for teeth. In all categories evaluated, natural teeth were significantly more stable radiographically compared to implants. Adjacent teeth did not seem to be influenced by the presence or absence of bone loss ≥3mm at adjacent implants.

Conclusion:Long-term results show that natural teeth have greater survival and less marginal bone loss compared to dental implants. This was still true when looking at teeth with reduced periodontal attachment (treated and maintained). The decision to extract teeth in favor of dental implants should be carefully considered in partially edentulous patients.

Topic:Risk factors for implants

Authors: Klokkevold P, Han T

Title:How do smoking, diabetes and periodontits affect outcomes of implant treatment?

Source:Int J Oral Maxillofac Implants. 2007; 22 (suppl)173-202

Type:Review

Rating: Good

Keywords:dental implants, dental implant survival, diabetes, periodontitis, smoking, tobacco

Purpose: To evaluate the available literature to assess whether smoking, diabetes, and periodontitis have an adverse effect on the outcomes of implants placed in patients with these conditions.

Method: The dental literature was searched using the MEDLINE, Cochrane Collaboration, and EMBASE databases. Using specific inclusion and exclusion criteria, 2 reviewers evaluated titles, abstracts, and full articles to identify articles relevant to this review. All searches were conducted for articles published through May 2005. Data from included articles for each of the risk factor groups, smoking, diabetes, and periodontitis, were abstracted and analyzed.

Results: A detailed search of the literature and evaluation of relevant articles identified 35 articles for inclusion in this systematic review. Nineteen articles were identified for smoking, 4 articles were identified for diabetes, and 13 articles were identified for periodontitis. One article met the criteria for both smoking and periodontitis. Implant survival and success rates were reported for smokers versus nonsmokers; diabetic patients versus nondiabetic patients; and patients with a history of treated periodontitis versus patients with no history of periodontitis. The findings revealed statistically significant differences in survival and success rates for smokers (better for nonsmokers), with greater differences observed when the data were analyzed according to bone quality (less for loose trabecular bone). No difference in implant survival rate was found between patients with and without diabetes. Likewise, no difference in implant survival rates was found between patients with a history of treated periodontitis compared to patients with no history of periodontitis.

Conclusion: The results of this systematic review of the literature demonstrated that smoking has an adverse effect on implant survival and success. The effect of smoking on implant survival appeared to be more pronounced in areas of loose trabecular bone. Type 2 diabetes may have an adverse effect on implant survival rates, but the limited number of studies included in this review do not permit a definitive conclusion. A history of treated periodontitis does not appear to adversely affect implant survival rates but it may have a negative influence on implant success rates, particularly over longer periods.

Topic:Diabetes

Author:Dowel, S et al

Title:Implant success in people with type 2 diabetes mellitus with varying glycemic control. A pilot study.

Source:JADA: 138:2007:355-361

Type:Cohort study

Rating:Good

Keywords:Diabetes, dental implants, implant success

Purpose:The authors conducted a prospective cohort study to explore the relationship between implant success and glycemic control in patients with type 2 diabetes mellitus.

Methods:The authors used a two-phased enrollment, stratified by glycated hemoglobin (HbA1c) levels, to evaluate 50 implants in 35 subjects. The authors assessed nonsubmerged, nonrestored implants after placement, during healing and at abutment placement (35 newton centimeters) for restoration after four months. Outcomes assessed included implant success or failure, clinical complications and adverse events.

Results:The HbA1c levels of the subjects ranged from 4.5 to 13.8 percent. All 50 implants were integrated clinically. The authors identified three minor complications in three patients having HbA1c levels ranging from 7.4 to 8.3 percent. None of these complications affected the clinical management of the cases, and the authors did not identify any adverse events.

Conclusion:There was no evidence of diminished clinical success or significant early healing complications associated with implant therapy based on the glycemic control levels of subjects with type 2 diabetes mellitus. These findings support the continued investigation of the effects of glycemic control on implant therapy toward the development of therapeutic guidelines that will optimize implant therapy in patients with diabetes.

Topic:smoking and implant

Authors:Strietzel FP, Reichart PA, et al.

Title: Smoking interferes with the prognosis of dental implant treatment: a systematic review and meta-analysis.

Source:J Clin Periodontol. 2007 Jun;34(6):523-44. Review.

Type: Retrospective Study

Rating: Good

Keywords:dental implants; meta-analysis;odds ratio; smoking; success rate; survival rate

P: To investigate if smoking interferes with the prognosis of implants with and without accompanying augmentation procedures compared with non-smokers.

M&M:A systematic electronic and handsearch (1989 and 2005; English and German language; search terms “dental or oral implants and smoking”; “dental or oral implants and tobacco”) was performed to identify publications providing numbers of failed implants, related to the numbers of smokers and non-smokers for meta-analysis. Publications providing statistically examined data of implant failures or biologic complications among smokers compared with non-smokers were included for systematic review.

R: Of 139 publications identified, 29 were considered for meta-analysis and 35 for systematic review. Meta-analysis revealed a significantly enhanced risk for implant failure among smokers [implant-related odds ratio (OR) 2.25, confidence interval (CI(95%)) 1.96-2.59; patient-related OR 2.64; CI(95%) 1.70-4.09] compared with non-smokers, and for smokers receiving implants with accompanying augmentation procedures (OR 3.61; CI(95%) 2.26-5.77, implant related). The systematic review indicated significantly enhanced risks of biologic complications among smokers. Five studies revealed no significant impact of smoking on prognosis of implants with particle-blasted, acid-etched or anodic oxidized surfaces.

C:Smoking is a significant risk factor for dental implant therapy and augmentation procedures accompanying implantations.

Topic:smoking and implant

Authors: Bain CA

Title:Implant installation in the smoking patient.

Source:Periodontol 2000. 2003;33:185-93.

Type:Review.

Rating: good

Keywords:implant, failure, smoking,

Purpose:to review the association between smoking and implant failure; potential mechanisms, and benefits of smoking cessation.

Discussion:

  • Effects of smoking on general health:smoking has been shown to affect health in many ways such as; cancers especially lung cancer, chronic lung disease, myocardial infarctions, strokes and ischemic heart disease. Research show that 50% of smokers die from a smoking related disease, and life expectancy of smokers is reduced by 7.5 years. Smoking also has been shown to have an adverse effect on bone density.

  • Effects of smoking on wound healing: smoking is a complicating factor in post-surgical wound healing. Smokers show less reduction in PD after SRP, poorer healing after mucogingival surgeries, less favorable healing following OFD, greater loss of bone height, reduction in post-ext socket fill and more painful ext socket. Smoking compromises healing of duodenal ulcers. Also, in a study about healing after orthopedic surgery, it was shown than there are more delayed union or non-unions in smokers.

  • Influence of smoking on the actions of polymorphonuclear leukocyte, macrophages, circulation and blood flow:Several studies have shown that smoking causes reduced phagocytosis, delayed margination and diapedesis as well as compromised aggregation and adhesion of leukocytes to the endothelium in venules and arteries. Peripheral endothelial dysfunction, vessel wall injury and capillary loss is common in smokers, also reactive hyperemia and sequestration of blood cells in the microcirculation. Coronary flow reserve is also decreases after smoking high-nicotine cigarettes.

  • Smoking and implant failure:

    • Smoking and particularly heavy smoking increases the failure rates for machined titanium implants, likely due to a compromise of the blood supply in bone during early healing

    • This increased failure rate clusters largely in the maxilla, with much smaller differences between smokers and non-smokers for implant in the mandible.

    • Smoking is associated with a particularly high failure rate for implants placed into grafted maxillary sinuses.Some operators may consider this to be too great a risk to take, if the patient is unable or unwilling to stop smoking.

  • What happens if the potential implant patient stops smoking:Smoking cessation has been demonstrated to improve success rates in machined implant patients. In fact, implant placement may well be an effective motivator in assisting a smoker with cessation.

  • Bone density, smoking and implant success: There appears to be a relationship between heavy smoking and reduced bone density. This is seen in various areas of medicine, as well as in implant surgery and might explain high failure rates in Type 4 bone

  • Do different materials and surfaces make a difference:There is early evidence that rough surface implants, prepared with a double acid etched technique, have a high success rate in smokers. With success rates around 10% better overall (98.7% vs. 88.7%) and 15% better in the maxilla (97.3% vs. 82.1%) than our original results with machined Branemark implants in smokers, these are at present considered to be the implant of choice in smokers who cannot or will not stop smoking for implant placement.

Topic:Oral Bisphosphonates

Author: Fugazzotto P

Title:Implant Placement with or without Simultaneous Tooth Extraction in Patients Taking Oral Bisphosphonates: Postoperative Healing, Early Follow up and Incidence of Complications in Two Private Practices

Source:J Periodontol 2007; 78:1664-1669

Type:Retrospective study

Rating: Good

Keywords:Bisphosphonates; dental implants; osteonecrosis

Purpose:The purpose of this article was to document the results of treatment of patients with a history of oral bisphosphonate therapy in two private periodontal practices.

Methods:61 female patients were treated in two private offices. All patients were receiving oral bisphosphonate therapy in the form of alendronate or risedronate, 35 or 70 mg/week. All these participants were treated with implant placement and restoration or tooth extraction, immediate placement, and restoration. These patients were then followed for 12 to 24 months after implant placement. The incidence of hard and soft tissue complications, including the development of osteonecrosis were noted.

Results:There were no reported cases of osteonecrosis immediately postoperatively during the follow-up period in any of the 61 patients. One patient demonstrated a small tissue dehiscence at the 1-week postoperative exam. No other complications occurred. All implants were functioning successfully by the Albrektsson criteria 12 to 24 months post-insertion.

Discussion: While the concern with BON is very much real with IV bisphosphonate. A history of oral bisphosphonate use for a mean period of 3.3 years was not found to be a contributing factor to the development of osteonecrosis following implant placement. Due to the size of the patient population, larger controlled studies and retrospective studies are needed.

Topic:Radiation

Authors: Colella, Cannavale, Pentenero, Gandolfo:

Title:Oral implants in radiated patients: A systematic review

Source:Int J Orla Maxillofac Implants 2007; 22(4):616-623

Type:Systematic review

Rating: Good

Keywords: Dental implants, oral cancer, radiation therapy

Purpose:To evaluate and compare the effects of pre- and post-implant radiation therapy. Incidence of implant failure was linked to multiple variables and assessed.

Methods:A thorough review of the relevant literature was performed. Studies were original studies based in humans from 1990- 2006. The man outcome considered was implant failure, defined as implant mobility, implant removal necessitated by progressive marginal bone loss or infection (biologic failure). Restorative status was not considered a determinate of success (sleeping implants were considered a positive outcome). Overall implant failure rate was compared for pre-implantation radiation therapy vs. post-implantation. Four variables were considered: implant location (maxilla vs. mandible), dose of radiation, delay from radiation to implant placement, and timing of implant failure.

Results:18 articles were considered eligible for inclusion in the review.Implant failure in post-implantation radiation therapy: 6 studies overall reported 124 implants with 4 failures (3.2%). Implant failure in pre-implantation radiation therapy: An overall failure rate of 5.4% was reported, which was not significantly different from post-implantation. 22/46 failures reported the cause of failure, with 9 due to lack of osseointegration, 12 due to marginal bone loss, and 1 due to biting trauma. Implant failure in the maxilla was 17.5% and 4.4% in the mandible, a difference that was significant. Vascularized free flaps were associated with the lowest rate of implant failure. Radiation dose: Radiation doses lower than 45 Gy were associated with the lowest rate of implant failure, with 5% being reported at higher doses. Delay of radiation treatment to implant placement: All implant failures occurred within 36 months after treatment. Timing of implant failure: No failures occurred within one month, 3.1% failed within the first month and 0.8% failed after 1 year.

Discussion:Based on this study, the timing of implant placement (pre- or post-therapy)is not linked to a significant difference in implant failure rate, however significantly better outcomes were noted in the mandible.

Topic:osteoporosis
Authors:Holahan, C et al
Title:Effect of osteoporotic status on the survival of titanium dental implants.

Source: Int J Oral Maxillofac Implants. 2008:Sep-Oct; 23(5)905-10

Type:

Rating: Good

Keywords: dental implants, implant survival, osteoporosis

Purpose:Primary Objective is to perform a retrospective chart review to determine the effect of osteoporotic status on survival of dental implants in postmenopausal women. Secondary Objectives included assessing the effects of smoking status, age, and arch location on implant survival as a function of osteoporotic status.

Method: a retrospective chart review was completed on all women who were 50 years of age or older at the time of dental implant placement at the Mayo Clinic between Oct 1, 1983 and Dec 31, 2004. The medical and dental charts were evaluated to collect the following:

  1. BMD T-score within 3 years of implant placement

  2. Osteoporotic diagnosis based on BMD T-score

  3. Arch location of the implants

  4. Smoking status at time of implant placement

  5. Any implant failures (implant removal due to any reason other than infection or manufacturing defects)

The review resulted in 192 patients (646 implants). Implant survival was estimated using the Kaplan-Meier method. Follow up duration was calculated from date of implant placement to date of failure or last follow up.

Results:

  • The Kaplan-Meier t- and 10-year survival rates for the 64 implants in 192 patients were 93.8% and 92.5% respectively. The mean follow up was 5.4 years (range 11 days to 20.4 years). Mean age of women studied was 63.4 years (range 50.3 to 84.9 years)

  • Osteoporotic diagnosis of patients based on BMD T-score was: 49% diagnosed as non-OP, 29.7% had osteopenia and 21.4% had osteoporosis. 37 implant failures were found: 10 implant failures in the osteoporosis group, 10 implant failures in the osteopenia group and the other 17 failures occurred in patients with non-OP diagnosis.

  • No significant association between arch location and implant failure was identified.

  • 12.5% of patients were smoking at the time of implant placement. Smoking had a significant effect on implant failure. Implants in smokers were 2.6 times more likely to fail (5- and 10- year implant survival rate for smokers was 87.3%). Non-smokers had 94.6% and 93.1% survival rates.

Conclusion:

  • Dental implant survival rates in this group of patients were encouraging with a 10-year survival rate of 92.5%.

  • Implants placed in smokers were 2.6 times more likely to fail than those placed in nonsmokers. The difference between those were most evident in the first year after implant placement.

  • A diagnosis of osteoporosis or osteopenia is not a contraindication to dental implant therapy.

Topic: Biological Principles

Authors:Claudy et al

Title:Time interval after radiotherapy and dental implant failure: systematic review of observational studies and meta-analysis

Source:Clinical implant dentistry 2013;1-10

Type:Systematic Review

Rating:Good

Keywords:dental implants, meta-analysis, osseointegration, osteoradionecrosis, radiotherapy

Purpose: To compare the risk of failure of dental implants placed within 6 and 12 months after the end of radiotherapy versus the risk of those implants placed after 12 months from the end of radiotherapy.

Materials and method

Four electronic databases were searched for articles published until February 2013 without language restriction: Lilacs, Medline, Scopus and the Cochrane Central Register of Controlled Trials. Two reviewers independently assessed the eligibility criteria and extracted data. Meta-analysis was performed.

Results:Overall 3,749 observational studies were identified. After the screening of titles and abstracts, 236 publications were selected, and finally 10 articles were included in the analysis. The Relative Risk of failure (1.34) was higher in individuals who had dental implants installed between 6 and 12 months after receiving radiotherapy.

Discussion:The main finding was that placement of dental implants between 6 and 12 months postradiotherapy was associated with 34% higher risk of failure. This is statistically significant and clinically relevant. Literature suggests that patients treated with radiation doses exceeding 50 Gray Units (Gy) are at increased risk of failure of osseointegration because of the loss of ability to repair and neovascularize the irradiated bone. Hyperbaric Oxygen therapy (HBO) reduces the risk of failure of the implant because it increases the number of capillaries and fibroblasts. However, this was not observed in this review which agrees with results of Esposito who found that HBO is not essential.

Conclusion:

Minimum waiting period of 6 months postradiotherapy prior to dental implant placement is unlikely to be the most suitable, and healing periods with duration over 1 year may be beneficial.

Topic:prophylactic antibiotics

Authors:Sharaf B, Dodson TB.

Title:Does the use of prophylactic antibiotics decrease implant failure?

Source:Oral Maxillofac Surg Clin North Am. 2011 Nov;23(4):547-50

Type:literature review

Rating:high quality evidence used

Keywords: antibiotic use, implant failure

Background:Despite the high success rate, implant failures do occur. Failure can attributable to implant-related, patient-related, and surgical technique-related factors. Bacterial colonization of the implant surface and surgical site infection have be implicated in early implant failure. Once an infection ensues at the implant site, its eradication is usually difficult, and may lead to removal of the implant. For this reason, various regimens have been suggested to minimize early infections after implant placement. However routine use of antibiotics is not without risk.

Purpose: to answer the question, “in patients receiving dental implants, does the administration of prophylactic antibiotics reduce early implant failure?”

Materials and Methods:The authors searched using the following Medical Subject Headings (MeSH): antimicrobial agents, antibiotics or prophylactic antibiotics, and dental implants. Inclusion criteria:1) randomized controlled clinical trials, (2) meta-analysis or systematic review. The primary predictor variable was antibiotic therapy, classified as a preoperative dose of antibiotics, preoperative and postoperative antibiotic treatment, and no antibiotics. The primary outcome variable was implant failure. The secondary outcome variable was post- operative infection. Each article was reviewed and data summarized for the following variables: sample size, antibiotic use, implant failure, and postoperative infections. The treatment effect was measured using absolute risk reduction (ARR), which is defined as the absolute difference in failure rates between the intervention and control groups. The number needed to treat (NNT), calculated as the reciprocal of ARR, is defined as the number of implants that must be placed with antibiotic use to prevent 1 implant failure. Five articles were selected for review.Four studies were randomized controlled trials.

 

Results:a meta-analysis of the 4 RCTs included 1007 patients receiving a total of 2020 implants showed more implant failures in the groups not receiving antibiotics, with a statistically significant difference. The number of patients that needed to be treated with antibiotics to prevent 1 patient from having implant failure was 33.

Bottom Line: in the authors opinion, based on their review – significant reduction in implant failure was observed when patients received 2g Amoxicillin 1 hr preoperatively or 1 g amoxicillin 1 hr preoperatively followed by 500mg 4 times daily for 2 days postoperatively.

Critique:There are some drawbacks to the RCTs reviewed. The follow-up time varied from 3 months in 1 trialand 4 months in 2 trials to 5 months in 1 trial.Decreasing the follow-up period may decrease the number of failed implants and may overestimate the effect of antibiotics on the primary outcome variable: implant failure. Another drawback is the use of bone substitutes and other bone-regenerative procedures at the time of implant placement, which may affect implant healing and failure rates. The use of bone-regenerative procedures was reported in 2 studies.In addition, the effect of timing of implant placement (delayed or immediately after extraction) may potentially increase implant failure rates. Esposito and colleaguesdemonstrated in a logistic regression analysis that patients in the RCT who received immediate post-extraction implants had a 9% failure rate versus 2% in the delayed group, regardless of antibiotic use (P<.001).

Topic:Antibiotics

Author: Ahmad N, Saad N.

Title:Effects of antibiotics on dental implants: a review.

Source:J Clin Med Res. 2012 Feb;4(1):1-6.

Type:Systematic review

Rating: Good

Keywords:antibiotic, success rate, dental implants.

Purpose:to review the current literature and information on dental implants and prophylaxis. Our objectives are to ask whether or not antibiotics are beneficial to implants, and in what instances pre- and/or postoperative antibiotic regimes should be prescribed.

Material and methods: The systematic literature review was completed using the electronic databases, Pubmed, Medpilot and Medline. Retrospective or prospective controlled studies which met the inclusion criterion, were English studies conducted between 1955 to January 2009. Administrations of various prophylactic antibiotics regimens were accepted. An unsuccessful dental implant was characterized by any implant which failed within the first 3 months, and studies with follow ups within the first 5 months were included. Studies with loading were not included and only studies using low risk patients were included.

Results:Out of 853 studies, only 6 studies were included in this systematic review that met the criteria. 11406 implants used in this literature review, cases with no antibiotics had a 92 % success rate, cases with pre-op antibiotic alone had a 96% success rate, cases with post-op antibiotic alone had a 97% success

Conclusion:The cost-benefit ratio of any therapy, including all potential adverse effects, must be determined. The negative effects associated with use of antibiotic therapy must be assessed in comparison to the costs and morbidity related to treating infective endocarditis or infected prosthetic materials.

Critics:many studies were excluded because they did not include comparisons between no antibiotics, pre-op, post-op antibiotic use.

Topic: Antibiotics

Authors: Esposito M, Grusovin MG, Worthington HV

Tittle:Interventions for replacing missing teeth: antibiotics at dental implant placement to prevent complications.

Source: Cochrane Database Syst Rev. 2013 Jul 31;7:CD004152.

Type: Systematic Review

Rating: Good

Keywords:antibiotics, failure, survival

Purpose:To assess the beneficial or harmful effects of systemic prophylactic antibiotics at dental implant placement versus no antibiotic or placebo administration and, if antibiotics are beneficial, to determine which type, dosage and duration is the most effective.

Methods:

Cochrane Oral Health Group’s Trials Register (to 17 June 2013), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2013, Issue 5), MEDLINE via OVID (1946 to 17 June 2013) and EMBASE via OVID (1980 to 17 June 2013). Selection criteria: RCTs with a follow-up of at least three months, that compared the administration of various prophylactic antibiotic regimens versus no antibiotics to people undergoing dental implant placement. Outcome measures included prosthesis failures, implant failures, postoperative infections and adverse events.

Results:

Six RCTs with 1162 participants were included:

  • 3 trials compared 2 g of preoperative amoxicillin versus placebo (927 participants)

  • 1 compared 3 g of preoperative amoxicillin versus placebo (55 participants),

  • 1 compared 1 g of preoperative amoxicillin plus 500 mg four times a day for two days versus no antibiotics (80 participants), and

  • 1 compared four groups: (1) 2 g of preoperative amoxicillin; (2) 2 g of preoperative amoxicillin plus 1 g twice a day for seven days; (3) 1 g of postoperative amoxicillin twice a day for seven days, and (4) no antibiotics (100 participants).

  • The overall evidence was considered to be of moderate quality.

  • The meta- analyses of the six trials showed a statistically significant higher number of participants experiencing implant failures in the group not receiving antibiotics. The number needed to treat for one additional beneficial outcome (NNTB) to prevent one person having an implant failure is 25, based on an implant failure rate of 6% in participants not receiving antibiotics. There was borderline statistical significance for prosthesis failures, with no statistically significant differences for infections, or adverse events. No conclusive information can be derived from the only trial that compared three different durations of antibiotic prophylaxis since no event (implant/prosthesis failures, infections or adverse events) occurred in any of the 25 participants included in each study group.

Conclusion:

Scientific evidence suggests that antibiotics are beneficial for reducing failure of dental implants. Specifically 2 g or 3 g of amoxicillin given orally, as a single administration, one hour preoperatively significantly reduces failure of dental implants. It might be sensible to suggest the use of a single dose of 2 g prophylactic amoxicillin prior to dental implant placement. It is still unknown whether postoperative antibiotics are beneficial, and which antibiotic is the most effective.

Topic:antibiotics and implant failures/infections

Authors:Ata-Ali J, Ata-Ali F, Ata-Ali F.

Title:Do antibiotics decrease implant failure and postoperative infections? A systematic review and meta-analysis.

Source:Int J Oral Maxillofac Surg. 2013 Jun 25.

Type:Systematic review and meta-analysis

Rating:Good

Keywords:dental implants, infection, disease, antibiotic, meta-analysis, implant surgery

Purpose:To systematically review and perform a meta-analysis to determine does the use of antibiotics reduce the frequency of implant failure and postoperative infection.

Methods:A manual and PubMed electronic search was conducted for RCTs that met the inclusion criteria with a control group that did not receive antibiotics. Four RCTs were included in the final review.

Results:Four RCTs included had a total of 2063 implants in a total of 1002 patients. Antibiotic use significantly lowered implant failure rate with an OR 0.331. One needs to treat 48 patients in order to prevent one patient from having an implant failure. In contrast, antibiotic use did not significantly reduce the incidence of post op infection. The meta-analysis found that there is evidence in favor of systemic antibiotic use in patients receiving dental implants.

Conclusion:

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22. Pathogenesis / Disease Activity: Pathogenesis and Inflammation

 HOME PERIO TOPICS 

Provide an overview of the pathogenesis of periodontitis. Describe the sequence of events in order of occurrence.

  1. Listgarten M. A. Nature of periodontal disease: Pathogenic mechanisms. J Periodontal Res. 1987; 22: 172-78

  2. Schroeder H: Discussion: Pathogenesis of periodontitis. J. Clin. Periodontol. 13:426-430, 1986. (Review)

  3. PAGE R & K. KORNMAN: The pathogenesis of human periodontitis: an introduction. Periodontology 2004 Vol. 14, 1997, 9-11

  4. KORNMAN K,R. PAGE & M. TONETTI: The host response to the microbial challenge in periodontitis: assembling the players. Periodontology 2000, Vol. 14, 1997, 33-53

  5. Kinane DF: Causation and pathogenesis of periodontal disease. Periodontol 2000. 25:8-20,2001 (Review)

  6. DARVEAAUN R, NET ANNER& ROYC . PAGE: The ,microbial challenge in periodontitis. Periodontology 2000, Vol. 14, 1997, 12-32

  7. PAGE R, S. OFFENBACHER, SCHROEDER, G. SEYMOUR & K. KORNMAN: Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontology 2OW. Vol. 14, 1997, 216-248

Describe Page & Schroeder’s model in detail.

  1. Page RC, Schroeder HE: Pathogenesis of inflammatory periodontal disease. A summary of current work. Lab. Invest. 34:235-249, 1976 (Review)

Discuss Gingivitis

  1. Van Dyke TE, Offenbacher S, et al. What is gingivitis? Current understanding of prevention, treatment, measurement, pathogenesis and relation to periodontics. J Int Acad Perio 1:3-15; 1999. (Review).

  2. Page RC. Gingivitis. J. Clin. Periodontol. 13:345-355, 1986. (Review)

Does all gingivitis become periodontitis? Is gingivitis a prerequisite for periodontitis?

  1. Schroeder HE, Lindhe J : Conversion of stable established gingivitis in the dog into destructive periodontitis. Arch. Oral. Biol. 20:775-782, 1975.

  2. Soames JV, Entwisle DM, Davies RM : The progression of gingivitis to periodontitis in the beagle dog. A histologic and morphometric investigation. J. Periodontol. 47:435-439, 1976.

How do periodontal pockets form? Which tissues are destroyed first?

  1. Ritchey B, Orban B. The periodontal pocket. J. Periodontol. 23:199-213,1952.

  2. Takata T, Donath K : The mechanism of pocket formation – A light microscopic study of undecalcified human material. J. Periodontol. 59:215-221, 1988.

  3. Saglie, Carranza, Newman and Pattison: Scanning electron microscopy of the gingival wall of deep periodontal pockets in humans. J Periodontal Res. 1982; 17: 284-293

List enzymes implicated in periodontal destruction and their origin. Do these enzymes have any therapeutic or diagnostic significance?

  1. REYNOLDS J & MURRAYC . MEIKLE: Mechanisms of connective tissue matrix destruction in periodontitis. Periodontology 2000, Vol. 14, 1997,144-157

  2. Van der Zee E, Everts V, Beertsen W: Cytokines modulate routes of collagen breakdown. J Clin Periodontol. 24:297-305, 1997.

  3. Lee W, et al. Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: Role of active enzyme in human periodontitis. J Periodont Res 1995; 30:23-33

  4. SCHWARTZ, Z., J. GOULTSCHIN D. DEAN & B. BOYAN: Mechanisms of alveolar bone destruction in periodontitis. Periodontology 2000, Vol. 14, 1997, 158.1 72

  5. Mogi M, J. Otogoto, N. Ota and A. Togari: Differential Expression of RANKL and Osteoprotegerin in Gingival Crevicular Fluid of Patients with periodontitis. J DENT RES 2004 83: 166

  6. Nonnenmacher C, K. Helms, M. Bacher, R.M. Nüsing, C. Susin, R. Mutters, L. Flores-de-Jacoby and R. Mengel: Effect of Age on Gingival Crevicular Fluid Concentrations of MIF and PGE2. J DENT RES 2009 88: 639

  7. Johnson RB, Serio FG, Dai X: Vascular endothelial growth factors and progression of periodontal diseases. J Periodontol 70:848-852, 1999

How can the host response be modified as a part of periodontal therapy?

  1. Salvi GE, Lang NP. Host response modulation in the management of periodontal diseases. J Clin Peridontol 2005; 32 (Suppl. 6): 108–129.

  2. Bhatavadekar NB, Williams RC. Commentary: new directions in host modulation for the management of periodontal disease. J Clin Periodontol 2009; 36: 124–126


Provide an overview of the pathogenesis of periodontitis. Describe the sequence of events in order of occurrence.

Topic: Nature of periodontal disease

Authors: Listgarten M.

Title: A. Nature of periodontal disease: Pathogenic mechanisms.

Source: J Periodontal Res. 1987; 22: 172-78

Type: Discussion

Rating: Good                                                               ARTICLE

P: Discussion article on the nature of periodontal disease and pathogenic mechanisms.

D: The oral microbiota, one of the most complex in the body, comprises over 300 species. Of these, about 30 are routinely observed and account for the majority of the cultivable strains. Health of periodontal tissues is maintained in a relatively stable state through the establishment of host-parasite equilibrium compatible with minimal tissue destruction and ready replacement or repair of damaged structures. Alterations in this equilibrium may develop as a result of local or systemic changes that decrease host resistance or from qualitative/quantitative alterations of periodontal microbes which result in increased virulence. These upsets may account for “bursts of disease activity. Bacteria can contribute to periodontal disease by direct injury of the host tissues (toxins, enzymes, toxic metabolic end products) or they can also act indirectly by triggering host mediated responses that may result in self-injury.

Role of bacteria and host-mediated tissue injury is discussed in detail.

Bacteria

  • Non-specific theory of plaque induced periodontal disease (Loesche): Sheer mass of microorganisms (MOs) generate sufficient noxious stimuli to induce inflammatory response in host. Seen in gingivitis.

  • Certain forms of periodontal disease (AgP) caused by particular organisms which cause disease by various mechanisms

Direct toxicity: Variety of substances of bacterial origin which are capable of causing injury. They are usually of large molecular weight and may include some enzymes. Classically toxins have been divided in endotoxins and exotoxins.

  • Exotoxins: proteins released by live microorganisms into their immediate environment where they can cause direct tissue injury. Some exotoxins have a specific affinity for certain cell types. Neurotoxins for nerve tissue, leukotoxins for neutrophils or epitheliotoxins for epithelial cells.

Leukotoxin

  • produced by Aa , associated with outer membrane of A.a cell wall from which it may be shed as membranous vesicles

  • shown to have correlation with periodontal disease.

  • shown to readily lyse human PMNs (Brehni et al)

  • able to kill human monocytes and weaken local host defense (Taichman et al)

Endotoxins: Lipopolysacchirides (LPS) which are structural components of Gram (-) bacteria. Their release occurs primarily after lysis of the cells. Endotoxins can exert a wide diversity of biological events, yet they share a common molecular structure. The linear molecule which is oriented perpendicularly to the bacterial cell surface consists of 3 distinct regions.

  1. Lipid A region which forms part of the outer half of the outer membrane of the cell wall. It is responsible for direct toxicity.

  2. Thecentrally located core polysaccharide

  3. The polysaccharide side chains, where the 0-somatic antigensreside, extend peripherally beyond the outer membrane.

The carbohydrate components provide the lipid A with hydrophilic properties, which enhance its pathogenicity and may increase the resistance of the bacteria to phagocytosis.

Endotoxins:

  • Enhance bone resorbing quality of osteoclasts

  • They can also bind to surface of PMNs or macrophages which internalize the endotoxin. Subsequent internalization of the endotoxin causes the cells to release their lysosomal enzymes extracellularly, with resulting damage to the local tissues and the generation of peptides that are vasoactive and chemotactic for PMNs.

  • Activate complement through the indirect pathway, with the consequent generation of complement-derived mediators of inflammation.

  • Act as modulators of bacterial cell uptake by phagocytic cells, with the endotoxin able to promote or inhibit phagocytosis depending on concentration.

  • Interfere with new attachment to denuded root surfaces.

Enzymes: Bacteria may exert pathogenicity in part through tissue invasion. Assorted enzymes may facilitate bacterial tissue penetration by removing various structural barriers and destroying host proteins that play a key role in host defenses like IgG’s.

  • Proteases, specifically collagenase, hyaluronidase, and chondroitin sulfatase are of particular interest in periodontal disease. They can be found in spirochetes and black pigmented bacteroides.

  • Metabolic products: End products of bacterial metabolism e.g. ammonia, indole, hydrogen sulfide, fatty acids also contribute to initiation and disease progression. Local changes in pH due to metabolism may also affect survival of certain microorganisms.

Indirect toxicity:

Effect on host cells: Bacterial enzymes may play an important role in neutralizing some of the oxygen -dependent antibacterial host defenses. Alterations in tissue oxygen levels may also favor the establishment of anaerobic infections that are associated with periodontitis. Bacterial protease can contribute to indirect injury of the host by destroying the functional activity of humoral antibodies directed against bacterial antigens.

Effect on bacterial cells: Bacterial interactions may play an important role in controlling the ability of microorganisms to colonize the tissues.

Host-mediated tissue injury

  • Caused by inflammation by triggering variety of injurious stimuli including thermal, mechanical, chemical trauma

  • Complement activation (IgG and IgM react with assorted bacterial antigens to form insoluable complexes). The formation of insoluble antigen- antibody complexes can activate the complement cascade with the resulting release of a number of mediators of inflammation into the extracellular environment. These can contribute to the influx of PMNs, the generation of additional vasoactive molecules and the outpouring of hydrolytic enzymes of lysosomal origin into the extracellular environment.

  • The lipoteichoic acid and lipopolysaccharides of the gram-negative cell wall are able to activate the complement cascade through the alternative pathway. While activation of complement has an overall beneficial effect in proecting the host against bacterial attack, some tissue destruction is unavoidable. Tissue injury is due in part to the complement-mediated influx of phagocytic cells and the release of lysosomal enzymes, and the production, by lymphocytes and macrophages, of assorted lymphokines that are able to kill cells and resorb bone.

Topic: Pathogenesis

Authors: Schroeder H

Title:Discussion: Pathogenesis of periodontitis.

Source: J. Clin. Periodontol.13:426-430, 1986.

Type: Review

Rating: Good                                                              ARTICLE

Keywords: Pathogenesis, periodontitis

Purpose: Discussion on the pathogenesis of periodontitis

Discussion:

  • Periodontitis is a local infectious disease caused and chronically maintained by a mixed, predominantly anaerobic bacterial infection of the subgingival portions of the periodontium. There are several difficulties in attempting to classify periodontal disease.

  • Author suggests the use of gingival pocket depth as a diagnostic criterion because it is the precursor of periodontal pocket. A gingival pocket is a shallow pocket (1-2mm) and histopathologically is similar to the periodontal pocket. No doubt that the development of gingival pockets is due to bacterial plaque extending apically along root surface. Once a gingival pocket has formed, gingivitis is no longer reversible with simple reestablishment of OH. Any pocket lined with pocket epithelium presents a pathophysiologic situation of associated with high tissue permeabilityincreased tissue reactivityinfected w/ subgingival bacteriaunattainable to remove w/ OH.

  • Transition from a gingival to a periodontal pocket is also due to the host response. There is no spontaneous shift back from the established lesion to the early.

  • The width and shape of infrabony pocket is also important and should be assessed radiographically.

  • Bone resorption occurs when plaque approaches 0.5 to 2.5 mm to the bone.Large bowel – shaped defects associated with periodontal pockets but extending further than the plaque radius, are probably related to lateral invasion of the soft tissues with plaque.

  • BOP is useful only for the early stages of gingivitis since evaluating it is subjective with regard to severity.

BL:The diagnosis and the pathogenesis of a particular patient with periodontitis are usually unknown. Factors other than bacteria may influence the pathogenesis of periodontitis, like OH, food impaction, iatrogenic factors, all of which interfere with the host-parasite relationship

Topic:Pathogenesis

Authors:Page R, Kornman K

Title:The pathogenesis of human periodontitis: an introduction
Source: Periodontology 2000 Vol. 14, 1997, 9-11

Type:Review

Rating:Good                                                               ARTICLE

Keywords:pathogenesis

Review:The major developments since the 1976 article by Page & Schroeder have been the discovery of the pathways through which bacteria activate host cells and systems in a manner that tissue destruction ensues and elucidation of the pathways through which the extracellular matrix components of the gingival and periodontal ligament are destroyed and alveolar bone is resorbed. Based on the current understanding, evidence is now sufficient for the development and application of new preventive measures, diagnostics and treatments targeted at blocking or altering these pathways.

Conclusion:Periodontitis is not a single homogenous disease but rather consists of a family of closely related diseases each of which may vary somewhat in etiology, natural history and response to therapy. There is a common chain of events of pathogenesis that is influenced by other factors including genetic and other risk factors may differ from one form of disease to another. Antigens and various other virulence factors, and in some cases invading bacteria, comprise the microbial challenge, and the host responds with an immediate inflammatory andimmune response that can influence the challenge. The host response results in production of cytokines, eicosanoids, other inflammatory mediators such as the kinins, complement activation products and matrix metalloproteinases, which perpetuate the response and mediate connective tissue and bone destruction. All of these events are influenced by disease modifiers, both genetic and environmental or acquired. The clinical picture observed is a result of the sum of these events. The severity and rate of progression of disease feedback to influence the nature and magnitude of the microbial challenge by, for example, influencing the pH and availability of oxygen and various nutrients in the periodontal pocket.

Topic:Pathogenesis

Authors: Kornman KS, Page RC, Tonetti MS.

Title:The host response to the microbial challenge in periodontitis: assembling the players.

Source:Periodontol 2000. 1997 Jun;14:33-53.

Type:Review

Rating: Good                                                              ARTICLE

Keywords:pathogenesis, host response

Purpose:To describe the histologic, cellular and molecular changes that occur during the transition from health to disease initiation and progression.

Discussion:Periodontitis is an infectious disease process. Bacteria and their products interact with the junctional epithelium and penetrate into the underlying connective tissue. Inflammation is caused and leukocytes (especially neutrophils) exit the post-capillary venules and end up in the sulcus. Collagen and other components of extracellular matrix are destroyed. Supra-g plaque extends apically and into the gingival sulcus, cells of JE are stimulated to proliferate and a gingival pocket is formed. At an early stage there is an enlarging leukocyte infiltrate and subsequently the lesion becomes dominated by B-cells that produce antibodies. As the disease worsens, periodontal pockets deepen, the components of the extracellular matrix of the gingiva and PDL are destroyed and alveolar bone is resorbed.

Scene 1. Acute bacterial challenge phase: the epithelial and vascular elements respond to the bacterial challenge.

Epithelial membranes, flushing by saliva and GCF protect the tissues from initial bacterial invasion. High turnover rate of epithelium is associated with rapid replacement of damaged cells.

When bacteria start to accumulate the release metabolic products (including fatty acids and the lipopolysaccharides (LPS) of Gram- bacteria) that activate JE cells to release various inflammatory mediators such as IL-8, IL-1αPG-E2, MMPs, TNF. Neural components of the epithelium influence the local vascular response. The bacterial products and epithelial response activate mast cells to release histamine and activate vascular endothelial cells to release IL-8 within the vessels to assist in localizing neutrophils.

Scene 2. Acute inflammatory response phase: the tissues respond to the early signals.

The wide extracellular spaces oh the JE allow neutrophil migration. The vascular leakage and activation of serum proteins such as complement, begin to amplify the local inflammatory response and produce further endothelial cell activation. Leukocytes and monocytes are recruited. Neutrophils exit the inflamed vessels and form a wall between plaque and gingival tissues. They are capable of killing bacteria by phagocytosis and prevent extension apical and lateral extension of plaque. PMNs are the majority of cells in the sulcus and mononuclear cells the majority of tissue infiltrate. IL-8 appears to be critically involved in PMN recruitment.

Macrophages produce mediators of the immune and inflammatory responses including IL-1β, IL-1 receptor antagonist, IL-6, IL-10, IL-12, TNF, IFN, MMPs, PG-E2 and chemotactic substances such as monocyte chemoattractant protein (MCP) and macrophage inflammatory protein (MIP).

Scene 3. Immune response phase: activation of mononuclear cells shapes the local and systemic immune response.

The changes in this phase are associated with periodontal pocket. Soon after inflammation starts the exudate from the vessels becomes predominated by mononuclear cells. T-cells, B-cells and plasma cells become evident in the tissues. T-cells produce IL-2, 3, 4, 5, 6, 10 and 13, TNF-IFN, TGFand chemotactic substances. Plasma cells become prominent in the tissues and produce immunoglobulins such as IgG, IL-6 and TNF-Fibroblasts are also activated and produce MMPs and tissue inhibitor of matrix metalloproteinases (TIMPs). Macrophages become effector cells and depending on the nature of the challenge secrete a restricted set of cytokines and express surface receptors that influence the antigen specific immune response that directly targets the pathogen. Their products alter the local environment in several ways. They produce chemokines that recruit additional monocytes and lymphocytes, they favor collagen degradation (through the production of specific factors such as PGE2 and MMPs) and they activate CD4+ T-lymphocytes and to differentiate to cytokine producing T cells that help B cell differentiation and antibody production.

IL-1 is a major mediator in periodontitis. IL-1β comes mainly from activated macrophages and fibroblasts. IL-1α comes mainly from keratinocytes of the junctional or pocket epithelium. Production is induced by LPS, other bacterial components and by IL-1 which is autostimulatory. IL-1 upregulates complement Fc receptors on neutrophils and monocytic cells, and adhesion molecules on fibroblasts and leukocytes. It enhances production of MMPs and PGs by macrophages, fibroblasts and neutrophils. Finally, it upregulates major histocompatibility complex expression by B and T cells and facilitates their activation, expansion, and Ig production.

Scene 4. Regulation and resolution phase: determinants of protective components in the sulcus and collagen balance in the tissues.

This phase represents the initial loss of attachment. T-cells and macrophages are producing selective subsets of prostanoids and cytokines that favor net loss of collagen and bone and less effective antibody production. The inflammatory mediator load increases and includes contributions by the fibroblasts of interleukins (16, 8), PGE2, TNFa, collagen, MMPs and TIMPs. Plasma cells are prominent.

Topic:Review of Pathogenesis of Periodontal Disease          burst hypothesis             Article

Authors: Kinane D. et al

Title:Causation and pathogenesis of periodontal disease

Source:Periodontology 2000. 25:8-20,2001

Type:Review

Rating: Good                                                              ARTICLE

Keywords:Review, pathogenesis, periodontitis, gingivitis, microbiology

Purpose:To review the causation and pathogenesis of periodontal disease.

Discussion:

  • Gingivitis must precede periodontitis, however, not all gingivitis progresses to periodontitis. Periodontitis has subject and site predilection, is a continuous process that undergoes exacerbation periods (“burst hypothesis”).

  • Prevalence of periodontitis in the USA is 35% in adults (13% moderate to severe, 22% mild).

  • Even in clinically healthy gingiva neutrophils are found in the junctional epithelium, PMN’s are attracted to the area by bacterial products and epithelial cells proteins, but if they become overloaded, “degranulation” and tissue damage occurs from toxic enzymes.

  • Most individuals show signs of gingivitis 10-20 days after plaque accumulation

  • In gingivitis, capillary beds open, there is a transudate and influx of inflammatory cells (macrophages and neutrophils as phagocytic cells; lymphocytes as immune response-related cells).

  • Progression from gingivitis to periodontitis requires time, why some patients develop the periodontitis more readily than other is multifactorial including risk factors of particular bacterial species, age, socioeconomics and race, smoking, systemic disease, and genetics. Destructive processes are initiated by bacteria but propagated by host cells.

  • Microorganisms of normal flora are present in gingivitis while exogenous or usual anaerobic seem to be implicated in periodontitis.

                             The Classification of Kinane and Lindhe

Clinical condition

Histopathological condition

 Pristine gingiva

 Histological perfection (no inflammatory infiltrate)

 Normal healthy gingiva

 Initial lesion of Page and Schroeder (histologically has features of inflammatory infiltrate)

 Early gingivitis

 Early lesion of Page and Schroeder (lymphoid cells immediately below JE, loss of collagen)

 Established gingivitis

 Established lesion with no bone loss or apical epithelial migration

 Plasma cell density between 10-30% of leukocyte infiltrate

 Periodontitis

 Established lesion with bone loss and apical epithelial migration from the CEJ

 Plasma cell density > 50% (plasma cells predominance reflects bone loss)

Topic:Pathogenesis

Authors: DarveauRP et al

Title:The microbial challenge in periodontitis

Source:Periodontology 2000. 1997 Jun;14:12-32.

Type:Review

Rating: Good                                                              ARTICLE

Keywords:dental plaque, biofilm, P. gingivalis, calculus, plaque, innate host response

P: The article reviews the composition of dental plaque, the ability of the bacteria to develop strategies that help them survive in the oral environment and the host defense system that constantly monitors the bacterial colonization status and prevents bacterial invasion into the tissues.

D:

Biofilm: matrix-enclosed bacterial populations adherent to each other and/or to surfaces or interfaces.

Dental plaque formation: Microbial coating of a freshly cleaned tooth surface occurs rapidly. Two initial colonizers are Strep. GordoniiandA. naeslundii. Rapid colonization is favored by the ability of co-aggregation (two genetically distinct bacteria recognize and bind to each other; co-aggregation is based on the specific interaction of a proteinaceous adhesion produced by one bacterium and a respective carbohydrate or protein receptor found on the surface of another bacterium). Some bacteria can bind to each other without co-aggregation. Fusobacteriumspecies co-aggregate with all other oral bacteria, and thus play a major role to biofilm formation.

Dynamics of the dental plaque growth and host inhibition:

·     Dental plaque growth is favored by inter-species cooperation, GCF and biofilm formation (aqueous channels).

·     Host inhibition of supragingival plaque is mainly for the mechanical and anti-microbial properties of saliva. Subgingival plaque is inhibited by limited space and host innate defense system, which components are brought with the GCF.

·     Plaque doubling times are more rapid in early development and slower in more mature films.

·     Saliva:IgA, lactoferrin, lysozyme, peroxidase, antimicrobial proteins (histatins: antifungal and antibacterial activity)

·     GCF:contains nutrients for bacteria. However, also contains lysozyme, vascular permeability enhancers (bradykinin, thrombin, fibrinogen), antibodies, lymphocytes

Role of the dental plaque biofilm in periodontal disease:

·     Non-specific bacterial sheddingprobably represents the major mechanism by which the host is informed of the amount and type of bacterial colonization occurring on the biofilm.

·     Bacteria can have direct or indirect effects (indirect: bacteria activate one cell type which in turn activate another) on host cells.

·     Host cell response is grouped in myeloid (cytokine secretion) and non-myeloid (various inflammatory mediators).

·     The dental plaque biofilm microbial composition can influence innate host inflammatory surveillance. LPS is one of the most probable mechanisms by which the host can sense different biofilm bacteria. Biofilm composition may result in a destructive response.

·     The expression of bacterial virulence requires participation from the dental plaque biofilm. Host cell contact by pathogenic bacteria was shown to activate regions of the bacterial chromosome termed pathogenicity islands.

Potential role of P. gingivalis in periodontitis can be suppression of the innate host inflammatory response to bacteria.

LPS from this bacteria does not activate E-selectin, which would allow for vascular permeability of the endothelial cells for the PMNs to migrate and attack the bacteria.Pg has also shown to impair other bacteria from stimulation E-selectin expression. E-selectin can be activated indirectly by TNF-α and IL-β, however, PgLPS is a poor activator of these cytokines. This is in stark contrast to observations in clinical periodontitis of a large cellular inflammatory infiltrate and increased production of a variety of molecular mediators of inflammation.

·     A gradient of IL-8 expression exists in normal tissue to guide leukocytes to the site of bacterial colonization (in presence of P.g, epithelial cells lose their ability to secrete IL-8, rendering the host unable to locate the source of microbial colonization).

·     P.g is considered an opportunistic pathogen (may be a pathogen provided by the right combination of dental plaque).

·     Aa and Pg invade host cells, providing not only a source of potential re-infection after mechanical debridement, but also a more difficult situation for the host to recognize the bacterial challenge.

Biofilms and therapy:

·     Biofilms are notoriously resistant to surfactants and antibiotics as well as opsonization and complement –mediated phagocytosis and killing.

·     The release of membrane vesicles and cell wall fragments serve to protect bacteria in the biofilm by acting as decoys that bind innate host defense components.

·     The resistance of subgingival biofilms to normal host defenses has important consequences for the patient and for periodontal therapy. Physical removal is essential.

Microbial composition associated with different clinical states of periodontal health:

·     Gingival health: Mostly gram-positive, streptococci and actinomyces, with about 15% gram-negative rod species. Bacterial load is relatively low in gingival health. An individual is more likely to manifest gram-negative bacteria and perio pathogens in healthy sites with increasing age and periodontal disease history.

·     Gingivitis: Increased microbial load and a corresponding increase of gram-negative bacteria.

·     Periodontitis: Increased total microbial load. Elevated proportions of P.g. T.f. and A.a. Elevated counts of the red and orange complex bacteria. Those species will determine the host response.

Clonal analysis has provided new insights into transmission and pathogenesis:

·     Molecular epidemiological tools have identified more intraspecies variation than previously thought (restriction endonucleases analysis, restriction fragment length polymorphism, ribotyping).

·     Transmission of periodontal bacteria occurs more likely through intimate contact, mostly within the family but not within general population communities (school, work environment)

·     Clonal type analysis is being used to determine the presence of different clonal types. Various clonal types of the same bacteria can be found within the same host. Very limited number of clonal types have been identified due to the magnitude of samples necessary to prove clonality.

·     The virulence of numerous clonal types is not clear.

Topic:pathogenesis of perio disease

Authors: Page R, Offenbacher S,

Title:Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions

Source:Periodontol 2000. 1997 Jun;14:216-48

Type:review

Rating: good                                                              ARTICLE

Keywords:periodontal pathogenesis, immune system, periodontitis

Purpose:To present the basic concepts and facts about pathogenesis of human periodontitis based on literature.

Discussion:

  • Periodontitis is a family of diseases that differ in etiology but have a common underlying chain of events. The severity and rate of progression of disease feedback to influence the nature and magnitude of the microbial challenge. Many modifying influences may affect the onset and progression of disease or the response to various kinds of therapy. These influences may last for life, or vary in magnitude of effect at different times.

  • Bacteria are essential but insufficient to cause disease, host factors are equally important. A.a. produces different clinical disease patterns in different people. This appear to be determined by combinations of factors like genetics and smoking.

  • P. gingivalis, A.a. and B. Forsythus cause most cases of periodontitis except for acute necrotizing periodontitis (ANP).

  • Subgingival microbial plaque behaves as biofilm. The behavior of the bacteria (mainly gram -) in it is different. They resist the host defense and also antibiotics. Physical disruption and removal are effective ways of dealing with biofilms.

  • Periodontitis enhances the risk for various systemic diseases, including atherosclerosis, coronary heart disease, stroke and infants with low birth weight.

  • Studies have shown that periodontopathic bacteria can be transmitted among individuals living in close contact.

  • P. gingivalis is special in that its lipopolysaccharide does not activate the expression of E-selectin in vascular endothelial cells (which then triggers binding of leukocytes) therefore blocking the local neutrophil response to itself and other microorganisms in the plaque.

  • The disease process is characterized by destructive periods followed by periods where this process subsides. There is experimented evidence that the responses in periodontal disease behave as if they occurred in a close system and many different balances can occur inside it through the biofilm/host interaction.

  • As the microbial challenge increases clinical signs of inflammation in the gingival margin begin. The junctional epithelium plays a key role, initiating vascular endothelial responses and neutrophils migrate to the sulcus. Macrophages, lymphocytes and plasma cells are the majority of cells in the tissues. If the bacteria are not eliminated inflammation worsens and connective tissue and bone are destroyed. In this procedure host cells, for example fibroblasts or epithelial cells, can be activated to produce prostaglandin E2and matrix metalloproteinases resulting in destruction of the components of the extracellular matrix. These cause apical extension of the epithelium and pocket formation. Rete pegs of junctional epithelium to the connective tissue are also formatted.

  • The stages of periodontitis according to its pathogenesis are initial, early, established and advanced lesions.

  • Several studies agree to the conclusion that bone absorption is observed in a 2.5mm range around bacteria, but Schroeder pointed out lesions much greater than 2.5mm around single teeth.

  • Thesusceptibility to periodontal disease differs between patients as some of them may only develop gingivitis whereas others with the same pathogens and comparable amounts of plaque may proceed to periodontitis, depending on several factors as the host’s response.

  • Cytokines belong to a large protein family that comprises the major regulators of the immunoinflammatory response in periodontitis. Interleukins and chemokines are subfamilies of the cytokines, while interferon – and TGF-also belong to the cytokines.

  • Both Th1 and Th2 clones of T helper cells can be met in periodontal lesions. The first one produces mostly interferon-γ and the second IL-6, IL-7 and IL-8. Whether any of these clones is associated with a specific clinical status is not yet clear.

  • Prostaglandins and leukotrienes are major initiators of inflammation and PGE2is the major mediator of pathological alveolar bone destruction. The progress of the disease is not on dimensional or unidirectional. It is constantly being adjusted as a result of multiple and changing microbial challenges and multiple local and systemic host defenses. Clinically periods of quiescence are followed by bursts of destructive disease activity. The mechanisms that force the transition from one condition to the other are not completely known. Bone absorption is a result of uncoupling the tightly coupled process of bone resorption and bone formation, and more significant after 25-30 years of age.

  • Periodontitis is a multifactorial disease. Bacteria are essential but insufficient to cause it. Several hereditary, host and other risk factors (such as diabetes mellitus, smoking, stress, HIV infection, socioeconomic factors, oral hygiene) coexist and modify the severity and type of the disease. Except for diabetes it is associated with major systemic diseases, such as cardiovascular disease and pre-term low birth weight delivery. Genetics has been shown to influence early onset periodontitis and adult forms. This influence is mediated through polymorphisms in the genes responsible for producing factors important in the pathogenesis of periodontitis (IL-1, IgG2m TNF-).

Describe Page & Schroeder’s model in detail.

Topic:Pathogenesis

Author:Page R., Schroeder H.

Title:Pathogenesis of Inflammatory Periodontal Disease: A Summary of Current Work

Source:Lab. Invest. 34:235-249, 1976

Type:Review

Rating: Good                                                              ARTICLE

Keywords:Gingivitis, Periodontitis, Chronic inflammation, Microbial plaque

Purpose: to discuss and review the current ant historic literature about the pathogenesis of periodontal disease

Discussion:Bacterial substances in plaque comprise the primary etiologic agent in gingivitis and periodontitis; however, many significant features of the disease cannot be accounted by this factor alone. There is a new belief that intrinsic host-related factors play an important role in the destructive process.

Historic Perspective

In the 18th and 19th centuries clinical observation was the predominant method used to understand the pathogenesis of the inflammatory periodontal lesion. In the late 19th century, there was a period of structural and morphologic analysis that began to examine the microscopic structures. During the past decade, the increased power of the electron microscope has provided additional insight into many of the cellular aspects and ultrastructural alterations.

Early concepts of pathogenesis

Gothieb (1946) presented the concept of “cementopathia”. He hypothesized that interference with continuous cementum deposits result in a lack of attachment of the collagen fibers of the gingiva and PDL. Goldman postulated an initial degenerative change in these fiber followed by epithelial cell proliferation and migration. Aisenberg (1948) showed that epithelial cells migrate apically between presumably normal connective tissue bundles. Cohen (1958), expressed the idea that the periodontal lesion may begin as a failure of the oral epithelium to replace the reduced enamel epithelium in the interproximal areas. James and Counsell (1927), and Fish (1935), introduced the zone of injury: Inflammatory cells accumulate in the JE and CT at the base of the sulcus. The zone of injury is located just coronal to the apical termination of the junctional epithelium.

Current view: the Page and Schroeder model.

Initial lesion (2-4 Days):

Lesion is localized to the gingival sulcus. The JE and most coronal portion of the CT are involved.

  1. Classic vasculitis of vessels subjacent to the JE

  2. Exudation of fluid from the gingival sulcus

  3. Increased migration of leukocytes (PMNs mainly) into the JE and gingival sulcus

  4. Presence of serum proteins, especially fibrin, extravascularly

  5. Alteration of the most coronal portion of the JE

  6. Portion of perivascular collagen disappears, and the resultant space is occupied by fluid, serum proteins (especially fibrin) and inflammatory cells.

Early Lesion (4-7 days):

  1. Presence and accentuation of the features described for the initial lesion (no clear cut dividing line).

  2. Accumulation of lymphoid cells immediately subjacent to junctional epithelium at the site of acute inflammation

  3. Cytopathic alterations in resident fibroblasts possibly associated with interactions with lymphoid cells.

  4. Further loss of collagen fiber network supporting the marginal gingiva. (Collagen loss may reach 60-70% within the reaction site)

  5. Beginning proliferation of the basal cells of the junctional epithelium

Established Lesion (2-3 weeks):

  1. Persistence of the manifestations of acute inflammation

  2. Predominance of plasma cells but without appreciable bone loss

  3. Presence of immunoglobulins extravascularly in the CT and JE

  4. Continuing loss of CT substance noted in the early lesion

  5. Proliferation, apical migration, and lateral extension of the junctional epithelium. Early pocket formation may or may not be present.

Advanced Lesion:

  1. Persistence of features described for the established lesion

  2. Extension of the lesion into alveolar bone and PDL with significant bone loss

  3. Continued loss of collagen subjacent to the pocket epithelium with fibrosis at more distant sites

  4. Altered plasma cells in the absence of altered fibroblasts

  5. Read More ›

Implants- Biological Principles: Osseointegration and bone interface

HOME Implant Home 

  • Giannobile, et al. Bone as a Tissue (CH 4). Clinical Periodontology and Implant Dentistry, Lindhe, J.; Lang, K. 5th Edition, 2008, Blackwell Munksgaard (Volume 1).

  • Lindhe, Berglundh, Lang. Osseointegration (CH 5). Clinical Periodontology and Implant Dentistry, Lindhe, J.; Lang, K. 5th Edition, 2008, Blackwell Munksgaard (Volume 1).

  1. Boioli L et al: A meta-analytic, quatitative assessment of osseointegration establishment and evolotuin of submerged and non-submerged endosseous titanium oral implants. Clin Oral Implants Res. 12: 579-88, 2001 (Duplicate from Implant I)

  2. Albrektsson T et al: The long term efficacy of currently used dental implants: A review and proposed criteria of success. Int J Oral Max Implants 1:11-26, 1986 (Duplicate from implant I)

  3. Albrektsson, T et al: Biological aspects of implant dentistry: Osseointegration. Periodontology 2000 4:58-73, 1994

  4. Trisi, P., Rebaudi A: Progressive bone adaptaion of titanium implants during and after orthodontic load in humans. Int J Periodontics Restorative Dent. 2002 Feb; 22(1):31-43

  5. Abrahamsson I, Berglundh, T, et al. Early bone formation adjacent to rough and turned endosseous implant surfaces. An experimental study in the dog Clinical Oral Implants Research, 15 (2004), pp. 381–392

  6. Berglundh T, Abrahamsson I, et al. Bone healing at implants with a fluoride-modified surface: an experimental study in dogs. Clinical Oral Implants Research, 18 (2007), pp. 147–152

  7. Mathieu V, Vayron R, et al. Biomechanical determinants of the stability of dental implants: Influence of the bone-implant interface properties. J Biomech. 2014 Jan 3;47(1):3-13. doi: 10.1016/j.jbiomech.2013.09.021. Epub 2013 Oct 10.

  8. Greenstein G, Cavallaro J, Tarnow D. Assessing bone’s adaptive capacity around dental implants: a literature review. J Am Dent Assoc. 2013 Apr;144(4):362-8.

  9. Mangano C, Piattelli A, et al. Evaluation of peri-implant bone response in implants retrieved for fracture after more than 20 years of loading. A case series. J Oral Implantol. 2013 Aug 21. [Epub ahead of print]

  10. Barewal R et al: Resonance Frequence Measurment on Implant Stability in Vivo on Implants with a Sandblasted and Acid – Etched Surface. Int J Oral Maxillofac Implants 2003; 18:641-651

  11. Alsaadi, G et al: A Biomechanical assessment of the relation between the oral implant stability at insertion and subjective bone quality assessment . J Clin Periodontol 2007; 34:359-366


Topic: Platform-Switched laser-microchannel implants          assessment of osseointegration

Authors:Boioli L et al

Title: A meta-analytic, quantitative assessment of osseointegration establishment and evolution of submerged and non-submerged endosseous titanium oral implants

Source: Clin Oral Implants Res. 12: 579-88, 2001
Type: Meta-analysis

Rating: Good

Keywords: dental implants, submerged, non-submerged, life table analysis, survival rates, review

Background: Two implant placement methods are used in oral implantology: submerged (S, two-stage surgical procedure) and non-submerged (NS, one-stage surgery). However, a quantitative assessment of their influence on implant osseointegration, summarising the whole present experience, is not directly possible, owing to the lack of normalisation of the published results

Purpose: to help improve the quantitative assessment of this influence by defining normalisation criteria, which would allow the pooling of the results of the studies meeting them and, hence, the statistical treatment of the overall longitudinal results.

Methods:

  • A survey of the literature was performed on studies report on implants placed either with a submerged (S) or a non-sub- merged (NS) procedure. Only root-analogue, threaded implants, exclusively made of titanium, were considered.

  • Among the studies meeting all criteria, 65 concerned S implants and 18 NS implants. One study concerned both S and NS implants.

  • Survival life tables are established (up to 15 and 10 years respectively for S and NS implants placed in normal situations) for extended samples (13049 S and 5515 NS implants).

  • Early (before loading) failure rates and 95% confidence level ranges of cumulative implant survival rates (CSR) have been evaluated.

Results:

  • Both categories match current survival requirements, but with a quite different behavior over time.

  • NS implants, while osseointegrating better initially, are subject to causes of osseointegration loss, which persist over a longer period of time.

  • Implant design characteristics (including the type of surface) seem to be more relevant than the placement procedure for the implant’s behavior.

Conclusion:

  • S and NS implants give acceptable results in terms of survival, and for both categories (but especially for S implants) the placement stage remains a discernible individual cause of failure

  • S implants have been studied more than NS implants, and present less dispersed results; NS implants are particularly affected by a reduced sample after 5–6 years of observation: the findings for this period still require confirmation;

  • NS implants seem to show a better osseointegration establishment, but, unlike S implants, an osseointegration loss process lasting for a longer period of time; subject to further confirmation, the type of placement procedure seems to be of lesser importance for the behavior of the implants, compared with implant design characteristics, including those related to their surface.

Topic: Implant Success

Authors: Albrektsson T, Zarb, Worthington, Eriksson

Tittle: The long term efficacy of currently used dental implants: A review and proposed criteria of success.

Source: Int J Oral Max Implants

Type: Discussion article

Rating: Fair

Keywords: success, osseointegration

Purpose: This paper is an attempt to evaluate currently used dental implant systems and to propose criteria of success.

Discussion:

Observations:

Osseointegration: is a histological definition, and only partially a clinical and radiographic one. An implant can only be judged as osseointegrated in the context of a continuum of observation, since undermining interfacial changes may be gradual, and not evident at the radiographic resolution level at least in the short term. 




Topic:microscopic evaluation ofosseointegration

Authors:Albrektsson T, Johansson C, Sennerby L

Title:Biological aspects of implant dentistry: Osseointegration.

Source:Periodontology 2000 4:58-73, 1994

Type:Discussion/Review

Rating:Good

Keywords:osseointegration

Purpose: To analyze current knowledge on osseointegration.

Discussion:

Radiographic evaluation:

Due to the surrounding bone tissue, an implant may seem to be in direct bone contact even though there is obvious soft tissue coat in reality. The maximal resolution level of radiography, under ideal conditions, is 0.1 mm, which is 10 times the size of a soft tissue cell.

Light microscopic investigations of bone-to-implant interface:

The use of modern cutting and grinding techniques has clearly demonstrated that direct bone-to-implant contact at the light microscopic resolution level is possible with many different metallic and ceramic materials. In loaded clinical cases there are indications that what is referred to as osseointegration depends on material used as one of several factors being important for implant take.

Ultrastructural investigation of experimental implants:

Ultrastructural analysis of the implant-bone interface is technically very difficult, since ultrathin sections are needed for transmission electron microscopy. Most ultrastructural investigations have been performed in animals using metal-coated polycarbonate implants, which permits sectioning, or metal plugs from which the tissue has been separated before sectioning.

Comments on published ultrastructural investigations:

The in vivo interface scenario seems to be completely different from that observed in vitro. In vitro the only cells in direct contact with the implant surface were red blood cells and macrophages, during the early healing phase, and later, multinuclear giant cells. The inner most interface was the last area to be mineralized, and this process seemed to be acellular. The amorphous layer, and in some instance the electron-dense layer, cold be distinguished before extracellular matrix became mineralized.

The commercially pure titanium bone interface in relation to other interfaces:

The interface descriptions found in the literature point to a variability of the interface morphology both for bone-bonding (hydroxyapatite or bioglass) and non-bone-bonding materials (titanium), which is why this type of classification cold be criticized.

The ultrastructure of the bone-titanium interface:

There is one type of amorphous layer in the bone-to-metal interface, even if the width and the content (mineral, collagen, and proteoglycans) has been debated.

Evaluation of retrieved oral implants removed despite a remaining anchorage:

In general, a nonmineralized amorphous layer 200-400 nm wide was bordering the mineralized bone with an electron-dense lamina limitans-like line (50 nm thick). Areas with nonmineralized tissue containing collagen and sometimes osteocytes or vessels were present along the interface.

Conclusion: The only acceptable mode of defining osseointegration is based on clinical examination finding stable implants: a process in which clinically asymptomatic rigid fixation of alloplastic materials is achieved and maintained in bone during functional loading.

Topic: Anatomy       bone adaptaion

Authors: Trisi, P., Rebaudi A

Title:Progressive bone adaptaion of titanium implants during and after orthodontic load in humans.

Source: Int J Periodontics Restorative Dent. 2002 Feb; 22(1):31-43

Type: Histology

Rating: Good

Keywords: orthodontics, implants

Purpose: To evaluate implant stability and peri-implant bone reaction by histologic and clinical evaluation after therapeutic orthodontic loads.

Methods: 41 adult patients received titanium implants (Exacta) as an orthodontic anchorage device; 12 patients received a retromolar or palatal implant to obtain tooth movement. Seven implants were removed at the end of the orthodontic therapy, after 2, 4, 6, and 12 months of orthodontic load, and processed for histologic examination.

Results: It was possible to distalize maxillary and mandibular molars and a group of teeth (molars and premolars), and to obtain tipping, uprighting, intrusion, extrusion, and transfer of anchorage in other parts of the mouth. The results showed that orthodontic therapy is facilitated and quickened using implants. All implants remained stable in the bone up to 12 months of loading, and all were osseointegrated. Microfractures, microcracks, and microcalli were observed around implants that had been placed in both low- and high-density bone. The remodeling rate was still elevated after 18 months.

Conclusion: Loading implants after 2 months of healing was shown to be safe and is considered the standard for orthodontic implants.

Topic: Osseointegration

Title: Early bone formation adjacent to rough and turned endosseous implant surfaces. An experimental study in the dog

Author: Abrahamsson I, Berglundh, T, et al.

Source: Clinical Oral Implants Research, 15 (2004), pp. 381–392

Type: Histologic study, animal model

Rating: Good

Keywords: SLA, osseointegration, implant surface

Objective: To validate a proposed model (as proposed by Berglundh et al. 2003) and to evaluate the rate and degree of osseointegration at turned (T) and sand blasted and acid etched (SLA) implant surfaces during early phases of healing.

Methods: Twenty Labrador dogs received totally 160 experimental devices (solid screw implant with either a SLA or a T surface configuration) as to evaluate healing between 2h and 12 weeks. Histometric and morphometric analyses were performed.

Results: The sections provided an overview of the various phases of tissue formation, while the decalcified, thin sections enabled a more detailed study of events involved in bone tissue modeling and remodeling for both SLA and T surfaces. The initially empty wound chamber became occupied with a coagulum and a granulation tissue that was replaced by a provisional matrix. The process of bone formation started already during the first week. The newly formed bone present at the lateral border of the cut bony bed appeared to be continuous with the parent bone, but on the SLA surface woven bone was also found at a distance from the parent bone. Parallel-fibered and/or lamellar bone as well as bone marrow replaced this primary bone after 4 weeks. In the SLA chambers, more bone-to-device contact, more initial woven bone and earlier lamellar bone formation was found than in the T chambers.

Conclusions:Osseointegration represents a dynamic process both during its establishment and its maintenance. While healing showed similar characteristics with resorptive and appositional events for both SLA and T surfaces, the rate and degree of osseointegration were superior for the SLA compared with the T chambers.

Topic:  Osseointegration

Authors: Berglundh T, Abrahamsson I, et al.

Title: Bone healing at implants with a fluoride-modified surface: an experimental study in dogs.

Source: Clinical Oral Implants Research, 18 (2007), pp. 147–152

Type:Animal study

Rating:Good

Keywords:dental implants, histology, osseointegration, titanium

Purpose: Study early stages of osseointegration to implants with a fluoride-modified surface.

Methods: Six mongrel dogs, about 1-year old, were used. All mandibular premolars and the first mandibular molars were extracted. Three months later, mucoperiosteal flaps were elevated in one side of the mandible and six sites were identified for implant placement. The control implants (MicroThread) had a TiOblast surface, while the test implants (OsseoSpeed) had a fluoride-modified TiOblast surface. Both types of implants had a similar geometry, a diameter of 3.5 mm and were 8 mm long. Following installation, cover screws were placed and the flaps were adjusted and sutured to cover all implants. Four weeks after the first implant surgery, the installation procedure was repeated in the opposite side of the mandible. Two weeks later, biopsies were obtained and prepared for histological analysis. The void that occurred between the cut bone wall of the recipient site and the macro-threads of the implant immediately following implant installation was used to study early bone formation.

Results:The amount of new bone that formed in the voids within the first 2 weeks of healing was larger at fluoride-modified implants (test) than at TiOblast (control) implants. It was further observed that the amount of bone-to-implant contact that had been established after 2 weeks in the macro-threaded portion of the implant was significantly larger at the test implants than at the controls.

Conclusions:It is suggested that the fluoride-modified implant surface promotes osseointegration in the early phase of healing following implant installation.

Topic: biomechanical determinants of implant stability

Authors: Mathieu V, Vayron R, et al.

Title:Biomechanical determinants of the stability of dental implants: Influence of the bone-implant interface properties.

Source: J Biomech. 2014 Jan 3;47(1):3-13. doi: 10.1016/j.jbiomech.2013.09.021.

Type: review

Rating: good

Keywords: Biomechanical properties; Bone; Implant; Osseointegration; Stability

Background: Dental implants are widely used however, risks of failure are still experienced and remain difficult to anticipate. The stability of biomaterials inserted in bone tissue depends on multiscale phenomena of biomechanical (bone-implant interlocking) and of biological (mechanotransduction) natures.

Purpose: to provide an overview of the biomechanical behavior of the bone-dental implant interface as a function of its environment by considering in silico (via computer simulation), ex vivo and in vivo studies including animal models as well as clinical studies.

Discussion:

Description of the bone-implant interface: the interface has a complex nature due to (i) its roughness, (ii) the fact that bone is in partial contact with the implant, (iii) adhesion phenomena between bone and the implant and (iv) the time-evolving nature of the interface properties.

  • Geometrical description; bone-implant distance and micromotions: When primary stability is not sufficient, micro-movements may appear preventing good healing conditions and leading to the formation of fibrous tissue and to surgical failure. Some studies show that micromotion should not exceed 150 µm, however the precise threshold is not yet known.

  • Mechanical description: stresses and the interface; When functional loading exerted via the implant exceeds “a certain stress”, the implant is regarded as being “overloaded”, leading to possible complications such as peri-implant bone resorption. However, stresses below that are beneficial for the implant outcome and stimulate bone remodeling phenomena. The determination of the value of that threshold remains unclear.

  • Dynamic description: bone remodeling and osseointegration; implant osseointegration was discovered by Branemark. Diagram bellow shows the multi-scale and multi-time nature of the different phenomena occurring during osseointegration; Factors related to implant properties (dashed lines), to the surgeon (dotted line) and the ones relating to bone properties (solid lines).

Implant stability: a space-time multiscale issue

  • Measurement of the multiscale bone properties around the interface:

    • Histology: the gold standard measurement.

    • Small angle X-ray scattering (SXAS): is used to assess thickness, orientation, and shape/arrangement of the mineral crystals in bone tissue. Gives information about bone mineralization but no information about mechanical properties

    • Nanoindentation: investigates biomechanical properties in the microscopic scale. Has shown that Young’s modulus and hardness values are lower in the vicinity of the implant than in mature bone.

    • Scanning Acoustic Microscopy (SAM): qualitative assessment of the biomechanical microstructural properties of bone-implant interface

    • Micro Brillouin scattering: uses the photo acoustic interaction between a laser beam and a sample to measure bone speed of sound

  • Homogenization approaches of bone tissue around the interface: homogenization techniques have been developed to climb the hierarchy of scales in newly formed bone tissue, from the nanoscale up to the macroscopic level.

  • Multiscale biomechanical modeling of the bone-implant interface: Various approaches have been developed to model the mechanical behavior of the bone–implant interface such as; Finite element methods (FEM), Frictional coulomb law, non-linear anisotropic FEM, …

Implant stability assessment

  • X-ray and MRI based techniques: Limited resolution of clinical X-ray based techniques due to metal artifacts related to the presence of the implant metallic components. MRI has also been proposed but is also of limited interest due to magnetic fields disturbance. Maximum resolution level of radiography is 0.1mm which is ten times the size of a soft tissue cell. X-ray or MRI based techniques are not commonly used in order to assess the biomechanical properties of bone to implant interface

  • Invasive biomechanical methods: Tensional test, Push out/Pull out test, Removal torque analysis

  • Non-invasive biomechanical methods:

    • Empirical approaches; Hitting the implant with an instrument and listen to the noise made by the system. Insertion torque during the surgical procedure.

    • Impact based approaches: PerioTest device (Schulte et al. 1980) was originally used for evaluation of tooth mobility. Measurement leads to PerioTest value (PTV), -8 to 50. PTV correlates to mobility and level of marginal bone.

    • Resonance frequency analysis: Measurement of the first resonance frequency of the bone–implant system. Uses an L-shaped transducer or a “Smartpeg”, which is a piece screwed in the implant abutment. Measurement gives an index called Implant Stability Quotient (ISQ 0-100), system is commercialized under the name Osstell. A correlation was shown between initial ISQ value and; (i) cutting torque, (ii) bone measurements assessed empirically by the surgeon during implant placement, (iii) Cortical bone thickness, (iv) Anatomical region of implantation. Limitations:

      • Only captures the first resonance frequency, which is of limited value from a structural mechanics point of view (“oversimplification”)

      • Sensitivity of ISQ value to the implant stability depends on the implant type

      • Relationship between ISQ values and BIC remains unclear

      • Fixation and orientation of the transducer (or smartpeg) influence significantly the ISQ values

      • ISQ values are related to the bone properties at the scale of the organ, but properties at the scale of 50-200μm are critical for osseointegration

    • Quantitative ultrasounds methods: Used to assess bone mineral status, enamel thickness. Several studies show the potentiality of QUS to investigate bone quality around implants, further work is necessary.

Topic:Bone           adaptive capacity

Author:Greenstein G, Cavallaro J, Tarnow D.

Title: Assessing bone’s adaptive capacity around dental implants: a literature review.

Source:J Am Dent Assoc. 2013 Apr;144(4):362-8

Type:Review

Reviewer: Phillip Crum

Rating: Good

Keywords:Bone; dental implants; osseointegration; resorption

Purpose:To review concepts pertaining to bond adaptation that may account for high survival rates of prostheses that are subjected to increased stresses.

Discussion:

Bone Mechanotransduction

  • Mechanotransduction=the mechanism that permits bone to detect stimuli.

  • It is thought that bone cells sense and respond to their mechanical environment by changing their biological and biochemical actions.

  • It is strain, not stress, that precipitates alteration of the bone response

  • 3 Possible stimuli for Osteocytes

    • 1-Direct mechanical stimulation

    • 2-Fluid flow induced by shear stress

    • 3-Bone Microdamage

  • The prevailing concept suggests that under dynamic loading, bone matrix deformation produces an interstitial fluid flow. This flow creates shear stress that stimulates osteocytes. Osteocytes act as mechanosensors and convey signals to adjacent cells (osteoblasts) through the intercellular communication network.

Rules For Bone Adaptation to Mechanical Stimuli

  • According to Turner, the following 3 rules characterize the response of bone to stress

    • Bone adaptation is determined by dynamic, rather than static, loading, and it is the alteration of stress, not its consistency, that produces bone modifications

    • A short episode of mechanical loading is required to begin the adaptive response

    • Bone cells accommodate to customary mechanical loading, making them less responsive to routine loading signals.

  • From these, it can be deduced that abnormal stress and strains drive structural change.

Stresses and Strains on Bone

  • Magnitude of occlusal load, cycle number, direction and frequency all can affect the quantity of stress.

  • The relationship between stress and strain establishes the modulus of elasticity (stiffness) of a material.

  • According to Frost, a certain amount of stress is required to maintain bone homeostasis.

    • Microstrains from 0 to 50atrophy

    • 50 to 1500normal bone modeling

    • 1500 to 3000overload

    • >3000possible destruction

Bone Microdamage

  • Fatigue: bone has lost strength and stiffness due to repetitive loads.

  • Microcracks: a discontinuity in the calcium-rich matrix and reflects fissures and breaks in the hydroxyapatite.

Bone’s Proliferative response to stress around dental implants

  • If the load is above a certain threshold, bone loss or loss of osseointegration can occur.

  • If functional load is below a destructive threshold, it can be stimulatory and induce apposition of bone and increased osseous density.

  • There is much evidence that supports the concept that bone can respond to stress and modify itself to withstand increased mechanical forces.

Remodeling

  • Jee estimated that about 20 percent of the cortical and cancellous bone surfaces (endosteal and periosteal) are remodeling at any point in time.

  • The replacement rate of cortical bone is 7.7% per year

  • The replacement rate of cancellous bone is 17.7% per year

  • Garetto showed that within 1mm of implants, there was a layer of bone that remodeled rapidly. The turnover rate was three to nine times faster per year within the 1mm of the implants.

  • Bones such as the mandible that experience loading from varying directions exhibit more platelike trabecular architecture. An advantage of this structure is its ability to manage forces from different directions.

  • High load areas usually manifest dense platelike architecture, whereas low load areas usually demonstrate low-density rodlike structures.

Conclusion: There are 2 possible explanations for the success of prosthetic constructs. First, is that bone is stronger than expected and can tolerate increased stress. Second is that as long as the stress/strain level does not increased beyond a threshold that causes bone destruction, bone has the ability to remodel and model and increase its osseous density.

Topic: Fracture

Authors: Mangano C, Piattelli A, Mortellaro C, Mangano F, Perroti V, Iezzi G

Title: Evaluation of peri-implant bone response in implants retrieved for fracture after more than 20 years of loading. A case series

Source:J Oral Implantol. 2013 Aug 21

Type: Case series

Rating: Good

Keywords: Bone remodeling, human histology, implant surfaces, retrieved dental implants

Purpose: To present a histological case series of the peri-implant bone responses in implants retrieved for fracture after more than 20 years loading period.

Methods: 5 implants retrieved for bodily fracture in 5 patients were found to be analyzed. The surface of these implants was obtained by sandblasting, followed by acid-etching for 30 minutes. The implants were then washed with hydrogen peroxide and dried with high heat. None of the implants were immediately loaded. In 3 cases, implants supported partial fixed bridges, while in 2 cases there was a mandibular ovendenture supported by 2 implants. Four implants were located in the mandible, and 1 in the maxilla. All implants were retrieved with a 5-mm trephine bur. Histological analysis and histomorphometry of the percentages of bone-implant contact were carried out.

Results: Compact, mature bone in close contact with the implant surface was observed in all specimens, with no gaps or connective tissue at the interface. Primarily newly formed bone was observed in proximity of the implant surface. In the most coronal portion of one implant, connective tissue adhering to the implant surface was detected. Bone-to-implant contact percentage ranged from 37.2-76%.

Conclusion: Implant effectiveness is largely dependent on biological stability and integration between bone and implant. Endosseous implants may function over a wide range of degrees of osseointegration.

Topic:sandblasted and acid-etched implant surfaces
Authors:Barewal R et al.
Title: Resonance frequency measurement of implant stability in vivo on implants with a sandblasted and acid-etched surface.

Source: J Oral Maxillofac Implants 2003; 18:641-651

Type: Clinical Study

Rating: Good

Keywords: bone, clinical trials, dental implants, early healing, endosseous dental implantation,

implant stability, resonance frequency analysis

Purpose: to understand pattern of stability changes and early healing around single-stage roughened-surface implants during the first 2 ½ months in different bone types.

Methods: Twenty patients had 1 to 4 implants placed in the posterior maxilla or mandible. Bone type was classified into 1 of 4 groups according to the Lekholm and Zarb index (1985). RFA was used for direct measurement of implant stability on the day of implant placement and consecutively once per week for 6 weeks and at weeks 8 and 10.

Results:

Conclusion: The lowest values for interfacial stiffness between the bone and the implant were found at 3 weeks, particularly in type 4 bone. Healing responses of Types 2 and 3 bone were more similar to Type 1 than to Type 4 bone. The RF values at 6 weeks did not differ from those at 10 weeks in all bone types; this supports the idea of a 6-week healing period for ITI implants in Types 1, 2, and 3 bone. The lack of significant change in stability from 5 to 10 weeks for Types 1, 2, and 3 bone supports further testing of an even shorter healing protocol. With regards to Type 4 bone, the current 12- week healing period could be evaluated and potentially shortened.

Topic: implant stability per bone type

Authors: Alsaadi G, Quirynen M, Michiels K, Jacobs R, Steenberghe D

Title:A biomechanical assessment of the relation between the oral implant stability at insertion and subjective bone quality.

Source: Journal of Clinical Periodontology 2007; 34: 359-366.

Type: Clinical

Reviewer: Cynthia Goldin

Rating: Good

Keywords:biomechanics; bone quality; dental implants; insertion torque; oral implants; osseointegration; periotest; RFA

Purpose:To evaluate the validity of subjective bone quality assessment.

Methods:A total of 298 patients treated with implants. Bone quality assessment performed immediately after implant placement and using the Lekholm & Zarb index. Tactile sensation was assessed for cortical bone and trabecular bone during high speed drilling. A scale from 1 (very thick cortex/dense trabecular bone) – 3 / 4 (thin/ poorly mineralized trabecular bone). The bone quality was assessed during implant insertion by an electronic torque force measurement device, which measures the torque force while tapping or inserting the implant at slow speed. The rigidity of implant-bone continuum was assessed by resonance frequency analysis taken at implant insertion and before abutment insertion, through a peg attached to the fixture, and an ISQ value is presented. This runs from 1-100, the higher the ISQ the more stable the implant. Periotest also measured the rigidity. After connecting a temporary abutment 4 mm in length, this device measures the damping capacity of the implant bone continuum. A rod is placed perpendicular to the abutment at a distance of 2 mm and it is accelerated electromagnetically. When rod hits the implant, it is decelerated. The faster the deceleration, the greater implant stability. Values range from -8 (very stable) to +50 (extremely mobile).

Results:Subjective assessment was related to PTV, ISQ and placement torque in the crestal, the second and the apical third.

ISQ and PTV were also compared with the bone quality assessed according to the Lekholm & Zarb index. A significant relationship was detected.

– Grade 1: 5.3, 73.3

– Grade 3 or 4: 1.6, 55

ISQ and PTV recorded at implant insertion were also compared with the bone quality assessed according to the surgeon’s tactile sensation. A significant relationship was detected between ISQ, PTV and cortical bone grades and between ISQ and trabecular bone grades

For surgeon’s tactile sensation, a good correlation was noted for the presence of a thick cortex: – 4.6, 70.3 or a thin one: – 0.3, 65.9. For dense trabecular bone, the values were – 2.8, 69.4 while for poor trabecular bone, the values were – 1.7, 66.4

Conclusion:

Subjective assessment of bone quality is related to PTV, ISQ and placement torque measurements at implant insertion.

DesignedBy StevenJ. Spindler, DDS LLC

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Implants – Review of dental implants. Synopsis

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Longitudinal studies: survival and success of implants

  • Lang and Salvi. Implants in Restorative Dentistry (CH 52). Clinical Periodontology and Implant Dentistry, Lindhe, J.; Lang, K. 5th Edition, 2008, Blackwell Munksgaard (Volume 2).

  • Misch. Rational for Dental Implants. (CH 1). pp 3-25. Contemporary Implant Dentistry, Misch, C.E., 3rd Edition, 2008, Mosby Year Book.

  • Cochran, D: Implants Therapy I. Proceeding of the 1996 World Workshop in Periodontics 1:707-795, 1996

  • Fritz, M: Implants Therapy II. Proceedings of the 1996 World Workshop in Periodontics 1: 796-815,1996

  1. Boioli L et al: A meta-analytic, quatitative assessment of osseointegration establishment and evolution of submerged and non-submerged endosseous titanium oral implants. Clin Oral Implants Res. 12: 579-88, 2001

  2. Albrektsson T et al: The long term efficacy of currently used dental implants: A review and proposed criteria of success. Int J Oral Max Implants 1:11-26, 1986

  3. Misch CE, Perel ML, Wang HL, et al. Implant success, survival, and failure: the International Congress of Oral Implantologists (ICOI) Pisa Consensus Conference. Implant Dent. 2008 Mar;17(1):5-15.

  4. Klokkevold P et al: Current status of dental implants: A periodontal perspective. Int J Oral Maxillofac Implants 15: 56-65, 2000

  5. Salinas TJ, Eckert SE. In patients requiring single-tooth replacement, what are the outcomes of implant- as compared to tooth-supported restorations? Int J Oral Maxillofac Implants. 2008 Jan-Feb;23(1):56.

  6. Simonis P, Dufour T, Tenenbaum H. Long-term implant survival and success: a 10-16-year follow-up of non-submerged dental implants. Clin Oral Implants Res. 2010 Jul;21(7):772-7.

  7. Ueda T, Kremer U, Katsoulis J, Mericske-Stern R. Long-term results of mandibular implants supporting an overdenture: implant survival, failures, and crestal bone level changes. Int J Oral Maxillofac Implants. 2011 Mar-Apr;26(2):365-72.


Topic: Platform-Switched laser-microchannel implants      submerged and non-submerged implants

Authors: Boioli L et al

Title: A meta-analytic, quatitative assessment of osseointegration establishment and evolution of submerged and non-submerged endosseous titanium oral implants

Source: Clin Oral Implants Res. 12: 579-88, 2001
Type: Meta-analysis

Rating: Good

Keywords:dental implants, submerged, non-submerged, life table analysis, survival rates, review

Background: Two implant placement methods are used in oral implantology: submerged (S, two-stage surgical procedure) and non-submerged (NS, one-stage surgery). However, a quantitative assessment of their influence on implant osseointegration, summarising the whole present experience, is not directly possible, owing to the lack of normalisation of the published results

Purpose: to help improve the quantitative assessment of this influence by defining normalisation criteria, which would allow the pooling of the results of the studies meeting them and, hence, the statistical treatment of the overall longitudinal results.

Materal and methods:

  • A survey of the literature was performed on studies report on implants placed either with a submerged (S) or a non-sub- merged (NS) procedure. Only root-analogue, threaded implants, exclusively made of titanium, were considered.

  • Among the studies meeting all criteria, 65 concerned S implants and 18 NS implants. One study concerned both S and NS implants.

  • Survival life tables are established (up to 15 and 10 years respectively for S and NS implants placed in normal situations) for extended samples (13049 S and 5515 NS implants).

  • Early (before loading) failure rates and 95% confidence level ranges of cumulative implant survival rates (CSR) have been evaluated.

Results:

  • Both categories match current survival requirements, but with a quite different behavior over time.

  • NS implants, while osseointegrating better initially, are subject to causes of osseointegration loss, which persist over a longer period of time.

  • Implant design characteristics (including the type of surface) seem to be more relevant than the placement procedure for the implant’s behavior.

Conclusion:

  • S and NS implants give acceptable results in terms of survival, and for both categories (but especially for S implants) the placement stage remains a discernible individual cause of failure

  • S implants have been studied more than NS implants, and present less dispersed results; NS implants are particularly affected by a reduced sample after 5–6 years of observation: the findings for this period still require confirmation;

  • NS implants seem to show a better osseointegration establishment, but, unlike S implants, an osseointegration loss process lasting for a longer period of time; subject to further confirmation, the type of placement procedure seems to be of lesser importance for the behavior of the implants, compared with implant design characteristics, including those related to their surface.

Topic:Implant Success

Authors:Albrektsson T, Zarb, Worthington, Eriksson

Tittle: The long term efficacy of currently used dental implants: A review and proposed criteria of success.

Source: Int J Oral Max Implants

Type: Discussion article

Rating: Fair

Keywords: success, osseointegration

Purpose: This paper is an attempt to evaluate currently used dental implant systems and to propose criteria of success.

Discussion:

Observations:  Osseointegration: is a histological definition, and only partially a clinical and radiographic one. An implant can only be judged as osseointegrated in the context of a continuum of observation, since undermining interfacial changes may be gradual, and not evident at the radiographic resolution level at least in the short term. 


Topic:Implant success, survival, and failure

Authors:Misch CE, Perel ML, Wang HL

Title:Implant success, survival, and failure: the International Congress of Oral Implantologists (ICOI) Pisa Consensus Conference.

Source:Implant Dent. 2008 Mar;17(1):5-15.

Type:Consensus discussion

Rating:Good

Keywords:implant clinical success, implant clinical survival, implant clinical failure

Purpose: To propose 4 clinical categories that contain conditions of implant success, survival, and failure.

Discussion:

Survival conditions:

Satisfactory survival: an implant with less than ideal conditions, yet does not require clinical management

Compromised survival: implants with less than ideal conditions, which require clinical treatment to reduce the risk of implant failure

Implant failure: implants that require removal or have already been lost

Implant success: should include a time period of at least 12 months loading. Early implant success is 1-3 years, intermediate 3-7 years, long term success more than 7 years

Clinical indices:

Pain: Once implant has achieved primary healing, absence of pain under vertical or horizontal forces is a primary subjective criterion. Pain should not be associated with the implant after healing. Usually, pain form the implant body does not occur unless the implant is mobile and surrounded by inflamed tissue or has rigid fixation but impinges on the a nerve. Pain during function can place the implant in the failure category. Sensitivity during function may place the implant in the survival category and may warrant clinical treatment.

Mobility: Lack of clinical movement does not mean the true absence of mobility. Lack of mobility usually means that at least a portion of the implant is in direct contact with bone, although the percentage of bone contact cannot be specified. A clinically mobile implant indicates the presence of connective tissue between the implant and bone (failure).

Radiographic crestal bone loss: The marginal bone around implant crestal region is usually a significant indicator or implant health. The Pisa Consensus suggests that the clinical assessment for each implant monitors marginal bone loss in increments of 1.0 mm. The bone loss measurement should be related to the original marginal bone level at implant insertion, rather than to a previous measurement.

Probing depths: Probing depths may be of little diagnostic value unless accompanied by signs and/or symptoms. It is of benefit to probe and establish a baseline measurement after the initial soft tissue healing around the permucosal aspect of the implant. Increases in this baseline measurement over time most often represents marginal bone loss.

Peri-implant disease: Exudate or an abscess around an implant indicates exacerbation of the peri-implant disease and possible accelerated bone loss. An exudate persisting more than 1-2 weeks usually warrants surgical revision of the peri-implant area to eliminate causative elements.

The ICOI Pisa Implant Quality of Health Scale

Conclusion:

Implant success is as difficult to describe as the success criteria for a tooth. Implant failure is easier to describe than implant success or survival and may consist of a variety of factors. Any pain, vertical mobility, and uncontrolled progressive bone loss warrant implant removal.

Topic: Periodontal considerations around dental implants

Authors: Klokkevold P et al

Title: Current status of dental implants: A periodontal perspective

Source: Int J Oral Maxillofac Implants 15: 56-65, 2000

Type: Review

Rating: Good

Keywords: dental implants

Purpose: To provide an overview of the current status of implants as related to the practice of periodontics.

Discussion:

RESTORING FORM, FUNCTION AND ESTHETICS:

The prosthetic position was not thought to be critical to the success of implants, and therefore it was not a major consideration. However due to the esthetic demands of patients, implant therapy has become increasingly focused on prosthetically driven implant position. Several new evidence-based guidelines emerged from prosthetically driven implant positioning, including the need to reconstruct hard and soft tissues that had been lost, so a bone augmentation or bone regenerative procedure had to be considered.

PERI-IMPLANT PATHOLOGY AND IMPLANT FAILURE

Peri-implant pathology, or more specifically periimplant bone loss, has been attributed to several different factors, including poor surgical management, failure to achieve osseointegration, premature loading, biomechanical overload, peri-implant infection, and impaired host response.

PERI-IMPLANT TISSUE ANATOMY FROM THE PERIODONTAL PERSPECTIVE

Osseointegrated dental implants do not have any connective tissue fiber attachments. Osseointegrated dental implants by definition do not have any soft tissues intervening between the implant surface and the bone. There are no collagen fibers attached to the implant surface. There is a connective tissue network of fibers around the implant coronal to the level of supporting bone. The supra-bony connective tissue surrounding the implant is made up of circumferential fibers that run parallel to the implant surface.

BIOLOGIC DIMENSION OF SOFT TISSUES AROUND IMPLANTS

Regardless of the type of implant used and the soft tissue dimensions at the time of placement, the authors found that a 2-mm-long junctional epithelium and a 1-mm zone of connective tissue were consistently established.

PERI-IMPLANTITIS

Peri-implantitis is defined as an inflammatory process affecting the tissues around an osseointegrated implant in function that results in loss of supporting bone, while peri-implant mucositis is an inflammatory process distinguished from periimplantitis by the lack of bone loss.

TREATMENT OF PERI-IMPLANTITIS

The most important aspect of treatment for peri-implantitis is to stop the progression of bone loss by controlling bacterial infection. As with periodontal therapy, the goal of surgical therapy is complete debridement of the defect, decontamination of the implant surface, and possibly removal of any porous implant surface coatings. Once the inflammatory disease process is controlled, it is possible to attempt regenerative procedures. In addition to bacterial infection, biomechanical overload has been shown to contribute to periimplant bone loss. Bone loss associated with biomechanical overload is most frequently found to be localized around the coronal aspect of the bone-implant interface.

Radiographs should be taken periodically to evaluate potential loss of bone. It has been well established that the amount of bone loss around Brånemark-type implants is approximately 1 to 1.5 mm in the first year after loading and 0.1 mm annually thereafter.

At regular intervals (every 3 to 6 months), implant abutment/restoration surfaces should be debrided of plaque and calculus accumulations.

Conclusion:The combination of in-depth biologic knowledge together with extensive surgical training has given the periodontist the skills to provide the highest quality care to patients around the world.

Topic:Implants vs Fixed Partial Dentures

Title: In patients requiring single-tooth replacement, what are the outcomes of implant- as compared to tooth-supported restorations?

Author: Salinas TJ, Eckert SE.

Source: Int J Oral Maxillofac Implants. 2008 Jan-Feb;23(1):56.

Type: Systematic review

Rating: Good

Keywords: comparative study, prosthodontics, implants compared to FPD, FPD, restorative planning

Purpose:The study provides a systematic review of the literature to determine the long-term survival characteristics of single implant-supported crowns and fixed partial dentures.

Materials and Methods:

A search of the MEDLINE, EMBASE, and Cochrane Collaboration databases was conducted to identify articles that compared survival and success of fixed partial dentures and single implant-supported crowns. In addition to comparative cohort studies, articles that pertained specifically to single implant-supported crowns or fixed partial dentures were included in this review. Inclusion criteria for implant and fixed partial denture articles included a minimum 2-year study, primary publication in the English language, a minimum of 12 implants, implants designed to osseointegrate, and inclusion of data regarding implant and prosthetic performance. Data were analyzed using cumulative proportions of survival and success for both prosthetic types and for individual implants. Wilson score method was used to establish 95% confidence intervals for each population. The chi-square test for homogeneity was performed.

Results: The literature search failed to identify any articles that directly compared survival or success of single implant-supported restorations with fixed partial dentures. Following the search criteria, and independent analysis by reviewers, 51 articles were identified in the implant literature (agreement, 95.42%; kappa coefficient, 0.8976), and 41 were identified in the fixed partial denture literature (agreement, 90.97%; kappa coefficient, 0.7524). Pooled success of single-implant restorations at 60 months was 95.1% (CI: 92.2%-98.0%), while fixed partial dentures of all designs exhibited an 84.0% success rate (CI: 79.1%-88.9%).

Conclusions: Tthis systematic review of the scientific literature failed to demonstrate any direct comparative studies assessing clinical performance of single implant-supported crowns and tooth-supported fixed partial dentures. The analysis suggested differences at 60 months between survival of implant-supported single crowns and natural tooth-supported fixed prostheses when resin-bonded and conventionally retained fixed prostheses were grouped. This difference disappeared when implant-supported single crowns were compared with conventionally retained fixed partial dentures at 60 months. For other time periods, direct comparative data were unavailable.

Topic: Implant survival and success rate

Authors: Simonis P, Dufour T, Tenenbaum H.

Title: Long-term implant survival and success: a 10-16-year follow-up of non-submerged dental implants.

Source: Clin Oral Implants Res. 2010 Jul;21(7):772-7.

Type: Retrospective study

Rating: Fair

Keywords: implant survival, implant success, cumulative survival rate

Purpose: To evaluate the long-term results of dental implants using implant survival and implant success as outcome variables.

Methods: Of the 76 patients who received 162 implants of the Straumann Dental Implant System during the years 1990-1997, 55 patients with 131 implants were recalled 10-16 years after implant placement for a complete clinical and radiographic examination, followed by a questionnaire that examined the degree of satisfaction. The incidence of biological and technical complications has been carefully analyzed for each implant. Success was defined as being free of all these complications over the entire observation period. Associated factors related to peri-implant lesions were analyzed for each implant.

Results: The long-term implant cumulative survival rate up to 16 years was 82.94%. The prevalence of biological complications was 16.94% and the prevalence of technical complications was 31.09%. The cumulative complication rate after an observation period of 10-16 years was 48.03%, which meant that substantial amounts of chair time were necessary following implant placement. The majority of implant losses and biological complications were concentrated in a relatively small number of patients.

Conclusion: Despite a relatively high long-term survival rate, biological and technical complications were frequent. Patients with a history of periodontitis may have lower implant survival rates than patients without a history of periodontitis and were more prone to biological complications such as peri-implant mucositis and peri-implantitis.

Topic: implant-supported overdentures

Authors: Ueda T, Kremer U, Katsoulis J, Mericske-Stern R

Title:Long-term results of mandibular implants supporting an overdenture: implant survival, failures, and crestal bone level changes

Source: Int J Oral Maxillofac Implants. 2011 Mar-Apr;26(2):365-72.

Type: clinical

Rating: good

Keywords: crestal bone loss, dental implants, implant surgical, long-term follow-up study, manifestation of failures,

Purpose:To summarize the long-term clinical observations of edentulous patients treated with mandibular implant-supported overdentures.

Methods: 147 edentulous patients, fairly healthy, admitted to treatment with mandibular implant overdentures in university of Bern, Switzerland. The treatment plan was to connect the dentures to only two implants by means of single ball anchors or bars; in patients with severely reduced ridge (≤ 8mm) or narrow and curved anterior mandible, three implants would be placed. Strauman implants in all pts. One-part implants with 7,9,11,13 or 15 mm, and two-part implants 6,8,10,12, or 14 mm, all 3.3 or 4.1 mm diameter. Non-submerged, single-stage placement, unloaded healing time 3 months then prosths fabricated. Regular maintenance care was provided at least one time per year. The cumulative implant survival rate was calculated. Implant failures were described according to clinical signs at the time of removal and related to the patient’s specific history. Crestal bone measurements were performed using computer software based on panoramic radiographs.

Results:147 patients with 314 implants were evaluated for 10 to 24 years. Of these, 101 patients were still available. Success rate could not be calculated due to absence of regular radiographs to confirm a minimum annual bone loss. Thirteen implants failed during the observation period, resulting in a cumulative survival rate of 85.9% after 24 years. The reasons for removal of implants were peri-implantitis (two implants) and mobility (11 implants). Mean crestal bone loss was 0.54 ± 0.7 mm per implant site after an average observation time of 16.5 ± 3.9 years. The duration of loading had a statistically significant effect on bone loss. NSSD among different subgroups of implants.

Conclusion:The data exhibit a satisfactory survival rate of implants. An individual analysis of implants with late failures did not reveal a typical failure pattern, but loss of implants without signs of infection was more frequent than loss of implants with signs of peri-implantitis.

DesignedBy StevenJ. Spindler, DDS LLC

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