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Cement-retained implant restorations have become popular because they are relatively simple to place, fit passively, are esthetically superior to screw-retained restorations, and have no screws to come loose.
In addition, cement-retained restorations make it easier for the clinician to contral occlusion and are more economical than screw-retained prostheses.
But these advantages come with a caveat: the possibility that excess cement left on the implant or in the surrounding soft tissues may cause peri-implant disease resulting in inflamed tissue and possible crestal bone loss.
In this current issue of The PerioDontaLetter, we explore the relationship between excess dental cement and peri-implant disease.
We also discuss a recent study that points to an association of periodontal disease and Alzheimer’s disease.As always, we invite your comments and suggestions.
How to Prevent Implant Failure Due to Incorrect Implant Cementation Technique
Early retention of dental implant restorantions was predominantly by
screw-retention to the dental implant fixtures.
With the advent of single tooth dental implants and esthetically driven multiple unit restorations, cement retention to the abutment became the preferred method of securing the restoration.
Many early dental implant fixtures have undergone considerable design changes since their initial introduction into the dental field. Many of these changes have focused on the collar design to protect and preserve crestal bone.
The smooth or machined collars of implants have now been designed with roughened, random surfaces which increase surface area and provide and enhanced bone response to the implant.
Figure 1. Six months after placement of the implant restoration, tooth #10 exhibited clinical signs of inflammation — swelling, bleeding and gingival discoloration. (See Figures 2 and 3)
Other dental implant manufacturers have suggested non-matching implant-abutment designs (plataform switching) to reduce crestal bone loss.
A roughened surface crestal design is also in popular use to enhance cellular response through contact guidance of bone and soft tissue progenitor cells.
Incorrect management of the restorative cementation step can result in soft tissue irritation and crestal bone loss and can negate these biologically-driven design changes, the purpose of which is maintaining bone and therefore soft tissue retention.
Excess cement within the implant sulcus can result in gingival bleeding and has been associated with clinical and radiographic signs of peri-implant disease.
Iatrogenic Cement Peri-implantitis
Excess cement in the implant sulcus has been called iatrogenic cement peri-implantitis.
The most likely origin of the problem is that the cement retains microbes similar to those responsible for inflammatory periodontal diseases, and the rough surface of the cement provides a nidus for the microorganisms which can lead to peri-implant disease.
While these diseases can be restricted to soft tissue (mucositis), they can also progress to the supporting bone (peri-implantitis) causing crestal bone loss.
Wilson recently published results of a clinical study on excess cement utilizing the perioscope for direct visualization. He found an 81 percent positive correlation of excess cement retention and continued gingival bleeding or suppuration. Following the removal of excess cement, 74 percent had no signs of peri-implant disease.
Similar results were obtained in a recent histological study by Cobb and Callan who demonstrated that residual subgingival cement establishes an inflammatory condition which was correlated to loss of bone around dental implants.
They further observed this phenomenon even in the presence of acceptable restorations and without clinically observable inflammation.
These findings appear to be consistent, irrespective of cement used to secure the restoration. Initial signs of inflammation and peri-implant disease were found as early as four months and as late as nine years after fixed implant restorations were cemented.
Figure 2. Flap reflection revealed excess cement as the primary etiology creating the inflammation process and bone resorption.
Figure 3. The cement was removed with hand instruments.
Figure 4. Subgingival cement caused significant buccal loss necessitating removal of this implant.
Figure 5.Upon removal of the implant, the extent of remaining subgingival cement can be more readily observed.
The favorable tissue response associated with the removal of subgingival cement is analogous to the improvement in gingival inflmmation when calculus is removed from natural tooth roots.
Numerous cementation techniques have been discussed anecdotally, but there is a dearth of published information on favorable methods of cementing of implant-supported restorations.
Some suggested approaches include:
- Place a minimal rim of cement in the gingival aspect of the crown margin.
- Seat the crown on an abutment replica or die and remove it prior to cementation leaving the excess cement on the die.
- Utilize “custom abutments” which limit the gingival extend of the crown to no more than 1 1/2mm which faciliates cement removal.
- Limiting the taper of the abutment and including flutes may also provide some protection from excess subgingival cement.
Screw-retained restorations may be indicated when:
- The subgingival extent of crown margins exceeds 1 1/2mm.
- Implant restorations with short abutments provide minimal retention.
Dental Cement Removal
It is axiomatic when cementing an implant-supported crown that the clinician exercise considerable caution regarding the complete removal of excess cement.
This may be facilitated by using radiopaque cement.
If peri-implant desease is present on must suspect that residual cement may be the predisposing cause. In such cases, immediated steps to identify and remove the cement should be undertaken.
This process may require surgical access to be effective.
It seems that excess cement found in the presence of peri-implant disease should be removed by whatever methods are necessary. Surgical interventions is justified when this cannot be accomplished non-surgically.
Figure 6. Radiographic evidence of subgingival cement allowed the clinician to debride the area and preserve the implant.
The occurrence of infection, inflamation, and bone loss associated with dental implants, represents clear evidence that the long-term prognosis for the implant is in question.
Such findings suggest the possibility of residual subgingival cement and signal the need for aggressive treatment in an attempt to reverse the process and prevent futher complications for the patient’s oral and systemic health.
The Connection Between Periodontal Disease and Alzheimer’s Disease
Periodontitis is a lifelong, highly prevelant, chronic inflammatory disease associated with stroke, cardiovascular disease, systemic inflammation and endothelial dysfunction.
A new study by Noble et al published in the Journal of Neurology, Neurosurgery and Psychiarty sugests there may also be a relation-ship between periodontal disease and dementia.
Dementia is a major public health problem likely related to a complex interaction between genetics, smoking and diseases associated with systemic inflammation, including diabetes and stroke. These risk factors have a similar systemic inflammatory profile to periodontis which sugests that they may also provide a common pathway of atherogenesis related to systemic inflammation.
In a study of 2,355 people aged 60 years and older, Noble et al reported an association between a common periodontal pathogen, Porphyromonas gingivalis, and cognitive impairment. The researches found individuals with high levels of P. gingivalis had 200 percent increased incidence of impaired verbal memory and subtraction test performance. This association adds to a growing body of evidence for a relationship between poor oral healt and dementia.
Oral health problems including periodontal disease, caries, edentilism and inadequate preventive care are more prevalent with increasing age resulting in increased exposure to periodontal pathogens.
One possible reason is a decreased ability to perform plaque control due to arthritis and other physical impairments. Exposure to periodontal pathogens is ubiquitous in older adults who often suffer from arthritis and thus have more difficulty keeping their mounths healthy.
Furthermore, cognitive function is thought to be associated with nutrition. Loss of teeth in older adults may be associated with poor nutrition. Consequently, there may be a relationship between loss of teeth and atherosclerotic changes.
Could Good Oral Health Help Prevent Dementia?
In a editorial commentary. Dr. Robert Stewart at the Institute of Psychiatry Kings College London, notes the oral health of people with cognitive impairment should, at the very least, receive more clinical attention.
He adds: “If there are good reasons to suspect a link between oral health and cognition, why has this received so little attention to date? The obvious but rather prosaic reason is the historic separation between medicine and dentistry. Clinical specialists have long been a hindrance to effective research (an example being the lack of attention paid to the vascular etiology of dementia) and it is about time that we accepted that disorders do not necessarily follow the way we structure our professions.”