Chapter 42 Maintenance of Dental Implants: Implant Quality of Health Scale
Implant dentistry has evolved into a well-understood clinical science with expansive documented research to validate what, years ago, many believed to be experimental. There has been an incredible amount of focus on the biology and biomechanics of implant dentistry, and results have helped to develop and refine techniques based on proven data rather than unsubstantiated trial-and-error procedures. The evolution of research and understanding of biological concepts in implant dentistry has caused many areas of conflict and controversy. Theories and techniques have developed and changed, and the types of materials used in implant dentistry have changed dramatically.
The tremendous growth in this field created new ideas and terminology that are either undefined or being redefined based on new knowledge.1 What one study proves in certain cases, another may completely disprove. It can become confusing for a clinician to know the correct protocols, procedures, tools, and techniques to use. As materials and techniques are researched and developed, previous theories may undergo criticism and controversy. It does not necessarily negate the findings of the past; however, we must modify techniques and tools to keep current with the changes in technology and research. One area of expansion of knowledge and conflict of views relates to the maintenance of dental implants. Early research explored techniques and instruments that were current for the methods and materials of that time. Although many of those implants still exist and are functional in patients, research and advances in technology have given us newer materials and advances in implant design and structure that do not necessarily possess the same challenges from a maintenance perspective.
A thorough review of mucoepithelial attachment is essential before commencing any maintenance procedures. Controversies and parameters for probing and radiograph exposure essential to clinicians are also discussed here. Thorough reviews of the tooth versus implant differences, as well as identification of the bacterial similarities and differences, also are discussed. The literature review explores the success or failure of implants and discusses in length the parameters that need to be adhered to when evaluating implants and the peri-implant tissue.
Once the clinician understands the parameters of implants and teeth, a specific plan can be created for the patient and the clinician can advise what is expected during each phase of treatment and demonstrate various oral hygiene options to suit the patient’s needs during each stage of therapy. Patients must be thoroughly educated and retrained before deciding to commence implant therapy.2 The ability of the patient to understand financial, time, and maintenance obligations is crucial and must be made clear to the patient initially and during subsequent appointments. In addition to educating patients, clinicians will need to assess compliance with a home care routine3 and must possess the clinical competencies to perform maintenance procedures. As the number of dental implants placed in patients continues to increase, there is a need to understand the importance of maintenance as it relates to long-term implant success.4 The role of the dental hygienist in implant maintenance and care is increasing and becoming more defined5 (Box 42-1).
Implants and their prosthetic devices are different from natural teeth and may require different procedures and instruments for both professional and patient care.6 Instruments must be effective at removing biofilms and accretions, and procedures performed by patients and/or clinicians should avoid damage to all portions of the implant, abutment, restoration, and tissues.7 Establishment and maintenance of a soft tissue seal around the transmucosal portion of the implant can enhance the success of an implant. This barrier is fundamentally a result of wound healing. The maintenance of healthy peri-implant tissues may contribute to implant success factors. Tissues and an implant sulcus free of inflammation and infection, as well as an absence of virulent bacteria, can enhance a patient’s general and oral health.
The differences between tooth and implant biologies make dental implants more susceptible to inflammation and bone loss in the presence of bacterial plaque accumulation.8 Biofilms are the primary causative factor of periodontal disease processes. Sticky masses of bacteria with a polysaccharide matrix, water, and bacteria accumulate on hard and soft surfaces in the oral cavity and can be disturbed and removed with mechanical or chemical obliteration. If undisturbed, mature plaque will form. Current chemotherapeutics cannot penetrate thick biofilm, and rough surfaces have been found to hold more biofilm9 than smooth surfaces. Bacteria will migrate from teeth to implants and from implant to implant.10 Similar to teeth, clinical findings of failing implants include inflammation, pockets, and progressive bone loss.11 Another similarity lies in the bacteria responsible for periodontitis and peri-implantitis.
When evaluating the peri-implant microbiota, Lee et al.12 compared microbial changes between patients with a history of periodontal or peri-implant infections and implants that have been in function for a length of time. This study found a history of periodontitis had a greater impact on the peri-implant microbiota than implant-loading time. The major influence on the peri-implant microbiota was, however, the microbiota on remaining teeth. Porphyromonas gingivalis and Bacteroides forsythus, red complex periodontal pathogens, colonized several implants, although all implants were successfully osteointegrated. Thus it is important to educate patients about their responsibility to decrease plaque effectively, especially if they have a history of periodontal disease.
Plaque biofilm development and maturation have similarities for natural teeth and dental implants. The gingival sulcus in periodontal health and the perimucosal attachment of a successful dental implant are essentially similar.13 In a study by Mombelli and Mericske-Stern of the plaque from 18 edentulous patients with successful dental implants, facultative anaerobic cocci (52.8%) and facultative anaerobic rods (17.4%) were reported. However, the pathogens P. gingivalis and spirochetes were absent, and minimal (7.3%) gram-negative rods were present.13
Generally, pellicle—a naturally occurring glycoprotein in the saliva—first adheres to the intraoral structure, whether it be a tooth or an implant. Gram-positive cocci bacteria are the first “early colonizers,” beginning with single cocci and progressing to streptococci forms (Box 42-2).
Without appropriate oral hygiene measures (e.g., brushing, flossing, interdental cleaning), additional bacteria colonies including gram-negative rod-shaped bacteria synergistically grow with the established gram-positive bacteria. The gram-negative bacteria are frequently facultative or strict anaerobic bacteria and are considered “late colonizers.” Many, if not the majority, of these gram-negative bacteria are black pigmented and are classified under a number of genera (e.g., Bacteroides, Prevotella, Porphyromonas, Fusobacterium).
Plaque biofilm reported to be associated with failing dental implants also consists largely of gram-negative rods.14 Clinically, failing dental implants are characterized by soft tissue inflammation, increased probing depths, increased mobility, and peri-implant radiolucency. Specific pathogens in implant pockets greater than 6 mm include Actinobacillus actinomycetemcomitans, Prevotella intermedia, and P. gingivalis, in more than one third of the sites, as confirmed by DNA analysis.15
More specific studies on plaque biofilm around dental implants suggest similarities16 between periodontal diseases and failing implants, but differences have also been reported.17,18 Mombelli18 did not detect spirochetes in plaque samples from well-maintained and clinically healthy implants. Rams et al. noted higher proportions of staphylococci (15.1%)19 than usually found in gingivitis (0.06%) and periodontitis (1.2%) sites.19 This finding suggests that staphylococci may be more significant in developing peri-implantitis lesions than previously recognized.
Changes involve both the hard and soft tissues surrounding an implant. The implant may exhibit all the signs of peri-implant mucositis, as well as exudate, increase of pocket depth, and bone loss. If left untreated, significant bone loss, infection, and mobility could result, leading to the failure of an initially integrated implant.
Comparisons of plaque biofilms have been reported in a limited study of Brånemark and ITI (Straumann Institute) implants and are remarkably similar in controlled studies. Mombelli et al.20 compared 10 patients with Brånemark implants and 10 patients with ITI implants and sampled the deepest pockets around the implants. After 3 and 6 months, several periodontal pathogens were cultured and isolated, including P. gingivalis, P. intermedia, Fusobacterium nucleatum, and various spirochetes. None of the implants was colonized by A. actinomycetemcomitans. Longer investigations by Leonhardt et al.21 extended these microflora reports on dental implants in 19 patients. At 3 years, the osteointegrated implants were colonized predominantly by P. gingivalis, P. intermedia, and A. actinomycetemcomitans.
Natural dentitions with dental implants appear to increase the risk for implant infections, compared with completely edentulous patients. This suggests that natural teeth may serve as a reservoir for periodontal pathogens that may extend their growth to contiguous implants in the same oral cavity.22 Quirynen and Listgarten23 reported that proportions of coccoid forms (65.8%), motile rods (2.3%), and spirochetes (2.1%) in implant pocket areas were similar to the microorganisms in natural teeth (55.6%, 4.9%, and 3.6%, respectively).
Fully edentulous patients exhibited more coccoid forms (71.3%), fewer motile rods (0.4%), and no spirochetes. Quirynen and Listgarten23 concluded that microflora in partially edentulous implant patients were potentially more pathogenic than fully edentulous patients. Implants with longevity of more than 3 or 4 years appear to have greater numbers of bacteria than implants in place for 1 or 2 years.24
Peri-implant mucositis is an inflammatory change of the soft tissue surrounding an implant. Peri-implant mucositis around an implant is similar to gingivitis around a tooth. There is no loss of attachment apparatus for teeth with gingivitis nor loss of bone for implants with peri-implant mucositis. The primary etiology is plaque biofilm. Like gingivitis, peri-implant mucositis is reversible once the etiologic agent, plaque biofilm, is removed. If allowed to progress, peri-implantitis may result, which includes loss of osteointegration, similar to loss of attachment and bone with periodontitis.
Removal of supragingival plaque with use of toothbrushes can significantly reduce the amount and composition of the subgingival microbiota. This reduction should translate to decreased risk of periodontal disease initiation or recurrence. Furthermore, the decreased prevalence of periodontal pathogens in supragingival plaque lowers potential reservoirs of these species.25
The absence of adequate keratinized mucosa in endosseous dental implants, especially in posterior implants, was associated with higher plaque accumulation and gingival inflammation, but not with more annual bone loss, regardless of their surface configurations.26 The implant type, with the presence or absence of keratinized tissue, may be a challenge for oral hygiene procedures for many patients. The clinician should stress the importance of adequately performing plaque control and select products and procedures well suited to the needs and ability of the patient.
Patients rely on clinicians to suggest or recommend products for oral hygiene procedures. As with most patients, the “tell-show-do” method of home care instruction is important. Documentation in the patient record regarding recommendations and instructions, as well as the patient’s compliance and effectiveness, will be important to evaluate long-term success for each patient.27,28 When choosing and recommending implements for oral hygiene, the clinician should take into consideration the location, length, and angulations of abutments, superstructure design, anatomical limitations, patient habits, motivation, and manual dexterity of each patient.29
Contributing factors that may influence product selection are plaque and calculus accumulation, as well as the general health of the patient (including diseases and medications). To avoid patients becoming discouraged and poorly motivated, it is wise to keep oral hygiene instructions simple.30,31 Partially edentulous patients exhibit higher pathogenic bacterial counts than edentulous patients, which may cause seeding of pathogenic bacteria from one site to another.32
The final prosthesis should allow for access by the patient and clinician to keep the areas plaque free.33 The clinician should instruct the patient in the use of toothbrushes (manual or automatic); floss (with threading devices, if necessary); tufted brushes; interdental brushes (with coated wires); toothpicks; and oral irrigators. Patient instructions may include the use of antimicrobials, such as cetylpyridium chloride (Crest Pro-Health, Proctor and Gamble, Cincinnati, Ohio) or chlorhexidine gluconate (Peridex, OMNII-3M, West Palm Beach, Fla.; Perioguard, Colgate, New York, N.Y.) due to substantivity and ability to inactivate oral bacteria.34 Chlorhexidine gluconate can be used as a rinse or applied specifically to the site with brushes or cotton swabs.
If oral irrigation is used, the patient should be instructed to use the lowest setting and direct the irrigation flow through the contacts to avoid excessive pressure to the implant tissue cuff. Incorrect use could alter tissue adaptation and induce bacteremia around the implant.35 Additionally, clinicians should recommend that the patient be gentle, yet thorough, postsurgically to avoid complications of healing from aggressive hygiene procedures.
Maintaining a smooth surface of titanium without pits and scratches can prevent plaque accumulation.36 Instrument selection should depend on tip designs that are not bulky (to avoid unnecessary tissue manipulation), and the design should facilitate manipulation by the clinician. A clinician may also evaluate the prosthesis design, location of deposits, and tenacity of calculus to help select appropriate instruments.
Metallic ultrasonic and sonic scalers have been reported to gouge titanium.37 A plastic or rubber sleeve over an ultrasonic scaler appears not to alter titanium.38 Conventional ultrasonic scalers with a nonmetal tip also are suitable for implant maintenance.39 Air polishers are effective and safe for maintenance procedures around implants.40,41
Stainless steel–tipped instruments have been found to be detrimental to a smooth titanium surface.42 This is important to consider when sharpening implant hygiene instruments to ensure a sharpening stone free of steel scrapings. A variety of nonmetallic, plastic, graphite, nylon, or Teflon-coated instruments are available and have been proven to be safe to use on titanium implant surfaces.37–49 Improved gingival and soft tissue architecture result from scaling with these instruments. A titanium curette and a rubber cup with flour of pumice are suitable for cleaning implant surfaces.43,44
After the removal of calculus, polishing with a rubber cap and toothpaste, fine prophy paste, commercial implant polishing pastes, and tin oxide have been shown to be safe for titanium surfaces.45,46 A rubber point or soft untufted rotary brush can also be used.47
The primary purpose of instruments used is to thoroughly remove plaque and calculus. Ramaglia et al. demonstrated that a plastic curette and air-powder-water spray did not alter the implant surface, but these instruments may leave deposits. These deposits should be removed by irrigation to avoid any adverse tissue healing.50
As dental implants become more widely used as replacements for missing teeth, clinicians will certainly see increases in clinical problems in complex cases.14 Frequent recall visits after implant placement and restorations are necessary for evaluation and establishment of good oral hygiene after treatment. Healthy tissue should have no inflammation with a primary etiology of plaque and calculus formation. The recall visit also is a time to detect potential problems to encourage early intervention should a problem arise. An appropriate periodontal probe should be used for pocket measurements.
Unlike the attachment to the porosities of teeth, the adherence and tenacity of calculus around implants are usually less binding. This can decrease the chance of traumatizing the tissue and perimucosal seal during procedures to remove deposits. With adequate oral hygiene, subgingival calculus should be minimal, if present at all. Because titanium usually does not have calculus embedded into it, adequate oral hygiene should prevent the accumulation of heavy accretions. If crestal bone loss has occurred, the type of implant surface or coating exposed may encourage plaque or calculus adherence.
Healthy implant tissues may have a tight seal and can create challenges while scaling. Because the perimucosal seal is more fragile than a normal tooth sulcus, it is important to use short, exploratory working strokes with light pressure. Depending on the location of the calculus, a horizontal, vertical, or oblique stroke may need to be used while avoiding tissue trauma.51 When an instrument must be used subgingivally to remove calculus or excess cement, insertion and instrumentation should be gentle and light strokes should be in a semicircular pattern. Attention to placing the blade carefully under the deposit and drying calculus or cement with compressed air may make detection and removal easier and more comfortable for the patient.
Poor tissue tone (i.e. flaccid, friable tissue) around an implant abutment can harbor food, plaque, and calculus and increase the occurrence of inflammation and infection. If maintenance and hygiene procedures cannot adequately improve tissue tone, surgical correction may be necessary to reduce chronic inflammation and infection.
Hygiene procedures performed by the clinician and patient can be limited by prosthetic designs that have bulky restorations and inadequate embrasures, preventing ready access to the implant–gingival margin interface area.52 Because loss of osseous support is a factor in implant failure, problems that may arise from a prosthesis may prove difficult to maintain in the treatment planning phase.53 Periodic occlusion monitoring may detect discrepancies to indicate occlusal changes needed.54
Chlorhexidine gluconate has been shown to reduce plaque in the oral cavity and around dental implants.55 Long-term use of antimicrobials such as chlorhexidine gluconate, cetylpyridium chloride, or phenolic compounds may be used along with brushes and floss to minimize staining.20 It is significant to note that the alcohol in newer generations of chlorhexidines serves to preserve and stabilize the solution.56 Studies have shown a decrease of antimicrobial benefits in preparations that are alcohol free.56 If the clinician uses subgingival irrigation, the cannula should be inserted carefully in the peri-implant tissue to avoid gouging the surface. Care should be taken to avoid inserting the cannula to the base of the implant sulcus to prevent fluid distention into surrounding tissues.57 Chlorhexidine gluconate has proved to be a useful irrigant.58 It is also wise to use a neutral sodium fluoride in a patient with dental implants because certain acidic fluorides can alter titanium.59,60
A study on nonsurgical mechanical treatment on sites with peri-implantitis lesions with microencapsulated minocycline (Arestin, Orapharma, Johnson and Johnson, Warminster, Pa.) and 0.12% chlorhexidine gel found r/>