David B. Rosen, D.M.D.- Practice Limited to Periodontics & Dental Implants

Doctor, Will Implants Work in My Mouth?

    It has been a meteoric rise, one of those medical wonders that captures the imagination of the press, resulting in lots of publicity.  It follows on the heels of hip replacements and new knees.  It's dental implants.  You just screw them in and, presto, new teeth.  The public has come to expect these results from medicine and dentistry.  And for the majority of our patients this philosophy comes close to being a reality.  However, the public is also under the misgiving that dental implants must be easier because they are smaller and bear less weight than knees or hips.  So with a 90+% success rate is there anything to worry about?  A part of the answer to this question has to be, we don't know.  And a part of the answer has to be, in some cases.  And a part of the answer has to be, not so far.

    Do you remember the modern beginnings of implant dentistry?  In the early days we placed sapphire and vitreous carbon and less than pure titanium.  There were smooth pins, blades and baskets.  We thought the connective tissue membrane around the implants were pseudo periodontal ligaments, a normal phenomenon for artificial roots.  Success was measured as the absence of mobility, no pain or visible infection.  Then Branemark, an orthopedic surgeon, came along and revolutionized our concepts of success.  Isn't it amazing how far we have come since the mid-1970's?  Seventeen to twenty year success rate studies hover above 90%.  The placement of implants when adequate bone exists in the implant site has become highly predictable.  Assessment of available bone is better and better with bone sounding, tomograms and CT scans.  Implant materials and surface technologies have increased the likelihood of osseointegration.  These advances have greatly contributed to implant longevity.  As with other medical advances overcoming technical inadequacy increased the focus on patient variations as causes of failure.  This newsletter reviews implant risk factors as we currently understand them.

    Implant failure is multifactorial.  Success is, first of all, an issue of wound healing.  Without the appropriate response in the sequence of wound healing events, osseointegration will not occur.  Any local or systemic factor that alters the healing process can reduce success.  Secondly, success is functional sufficiency.  The implant must function where it is placed without failure of the prosthesis or the implant-tissue interface.  Lastly, success is dependent upon the patient's ability to tolerate the care involved in placement and restoration.  Patients multiple risk factors need stamina to face complex care as treatment may mean multiple procedures.  Many cases are time consumptive and expensive as we overcome significant loss of structural integrity in the treatment area.

    These three areas of risk areas are intraoral risk factors, systemic conditions, and psychological risk factors.  Each is listed here with individual items that have been identified as associated with the risk factor.  The discussion which follows addresses the factors with an impact on survival rate of implants in current studies.  Each patient must be assessed as an individual.  The presence of multiple risk factors should engender higher level discussion of the risks involved in successful implant treatment.

    From a review of the retrospective studies on successful implants, an increased risk is associated with placement of implants in the maxillary posterior segment, with implant width and additive variable.  Scurria studied 99 consecutive, in whom 384 implants were placed.  At 3.6 years, a total of 34 implants had failed, 8.9%.  When prosthesis type was excluded from the modeling process, the data indicated posterior location of the implant and implant width under 4.0mm to be associated with implant failure.  Naert at al looked at 1956 Branemark implants in 660 patients over 16  years and found that 91.4% of the implants were surviving, almost identical to the survival rate of Scurria.  The failures were with shorter implant lengths, bone grafted sites, larger numbers of implants per patient and implants restored with acrylic veneers.  Single versus multiple abutments made no difference in survival rate.  Chuang and Dodson reviewed 677 patients where 2349 implants had been placed for five years.  Their survival rate was 90.91%.  Five factors were identified as significant in implant failure.  The local factors associated with failure were implant length, immediate implants, staging of implants and the well sized of the implant placement. 

    Teisi examined the capacity for osseointegration between smooth and rough surfaced implants.  Implants were examined histologically following removal for the presence of bony contact between the implant and the bone surface.  Smooth surfaced implants had only 6% osseous contact while rough surfaced implants developed 76% osseous contact.  Misch emphasized the need for threading to support posterior implant designs.  A broad consensus of researchers have listed the quality of bone as a significant risk factor.  Type four bone, the least trabeculated, appears correlated to osseointegration failures.  This factor is generally countered with 2 stage surgery and progressive loading.  Bragger studied implant use as fixed partial dentures, both implant supported and implant-tooth supported.  Significant variables in problems were bruxism and distal extensions of the prosthesis.  In 9.6% of the implants, pocket depth greater than 5mm was noted.  This did not differ from the incidence of problems on the natural teeth in the study, perhaps indicating an incidence of peri-implantitis similar to natural teeth.  This has not been supported by earlier studies.

    Warrer and Buser used monkeys to determine if more attachment loss would be experienced around implants with no keratinized mucosa should inflammation occur.  They induced plaque accumulation around implants in monkeys with and without keratinized mucosa around the implant necks.  The :implants without keratinized tissue had significantly more recession and slightly more attachment loss.  Warrer and Buser concluded that the absence of keratinized mucosa increases the susceptibility of the peri-implant region to plaque induced tissue destruction.  Papaioannou examined partially edentulous patients with severe periodontitis and implants.  In six patients, bacterial samples were taken from both deep and shallow sites around teeth and implants.  In shallow sites there were significant bacterial colonization differences between implant sites and natural tooth pockets.  However, as the sites became deeper on both natural teeth and implants the bacterial profiles became similar.  Papaioannou felt his observations confirmed the hypothesis that pockets around teeth act as bacterial reservoirs to seed implant sites.  This highlighted the importance of periodontal health being established prior to implant placement.

    As these local risk factors appear, it is important to recognize the presence of multiple factors.  Several risk factors stacked together increase the relevance of patient motivation since failure may occur during the implant process and developing the appropriate site biology may require significant interventions.

    As regards systemic risk factors, most investigators did not find age to be a relevant factor by itself.  Although wound healing is slower in older patients, the repair potential of otherwise healthy adults is adequate.  Elsubelhi and Zarb have reported on systemic factors in implant placement based on a 20 year investigation of 464 patients.  They found that, although estrogen depletion reduces bone mass in the edentulous but not the dentate mandible, no increase in implant failure was noted in women over versus under age 50.  However, August et al reported a higher implant failure rate in estrogen deficient post menopausal women in the maxillary arch.  Becker and colleagues found that the density of bone in the radius and ulna, a common index for osteoporosis, was unrelated to implant failure.  Rogers was unable to correlate gene upregulation of Interleukin-1B with implant failure.

    The systemic effects of diabetes on implant survival are controversial.  Evaluating diabetics with implants over a 1-17 year span, Accursi found no difference in survival rates between diabetics and non-diabetics.  He did, however, find initial bone loss in implants was larger in diabetics but the difference disappeared in subsequent years.  However, Morris did find that Type 2 diabetics had more implant failure.  He also noted that treatment with antibiotics and Chlorhexidine following surgery increased the success rate.  This might suggest that impaired immediate repair of the implant site predisposes to later development of implant bone loss in diabetics.

    Although there is little direct data to support them as risk factors, long-term steroid use, rheumatoid disease and reduced salivary flow resulting in reduced infection resistance are listed by many implant clinicians as compromising implant success.

    Psychological factors in implant risk center around the addictions.  As in periodontal disease, smoking is associated with a higher implant failure rate.  Habsha calculated the risk for late implant failure as 1.69-1.91 times as high for smokers than non-smokers.  Recently, a survival study has reported a similar longevity for smokers and non-smokers with a machined surface implant, placed in a two stage approach.  The study extends currently only over 5 years so definitive conclusions about the long term ability of surface design to overcome the effects of smoking on wound repair is as yet unconfirmed.  Patients who suffer from alcohol abuse are also poor candidates for implants as their ability to comply with therapy recommendations and repair capacities are impaired.  A third psychological issue is patient tolerance for multiple treatment procedures.  In addition, patients need appropriate expectations for the results of care.  Patients who presume unconditional success are less able to handle the disappointment of implants that do not integrate and subsequent surgical interventions.  Stress has been shown to increase the severity of several diseases through lowered resistance.  Patient consultation should include an estimate of the risks and the patient's resolve to overcome them.

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Copyright © 2003 David B. Rosen, D.M.D.
Last modified: March 06, 2004