Mucositis

, Reem Atout1, Nader Hamdan2 and Ioannis Tsourounakis3

(1)

University of Manitoba College of Dentistry, Winnipeg, Manitoba, Canada
(2)

Faculty of Dentistry, Dalhousie University, Halifax, Nova Scotia, Canada
(3)

Southwest Specialty Group, Winnipeg, Manitoba, Canada
 

3.1 Introduction

The definition of peri-implant mucositis has been revised over the years. It was originally described as “a reversible inflammatory change of the peri-implant soft tissue without bone loss” [1] and eventually was included in a collective term of “peri-implant diseases,” which were deemed to be infectious in nature [2]. According to the Glossary of Terms of the American Academy of Periodontology [3], peri-implant mucositis is “a disease in which the presence of inflammation is confined to the mucosa surrounding a dental implant with no signs of loss of supporting bone.”

3.2 Etiology

The primary etiology of peri-implant mucositis is microbial biofilm accumulation on the implant fixture [4, 5]. Shortly after placement, bacterial plaque colonizes dental implant surfaces [6, 7]. This biofilm is similar to the one identified around the natural dentition, and the inflammatory process seems to mimic that of gingivitis around natural teeth [8]. In an animal study Ericsson et al. [9] demonstrated that prolonged plaque accumulation on implant abutments resulted in inflammation of the peri-implant mucosa due to the establishment of an inflammatory cell infiltrate. This finding was supported by further human studies where it was demonstrated that the accumulation of plaque initiates peri-implant inflammation [8, 10, 11].

3.2.1 Risk Indicators

There are several risk indicators that may contribute to the development of peri-implant inflammation. To date there is some evidence to support the following as risk indicators for the development of peri-implant mucositis: poor oral hygiene, smoking, radiation therapy, and residual cement [12].

3.2.1.1 Poor Oral Hygiene

A clinical study performed by Pontoriero et al. [13] proved that there was a cause and effect relationship between the absence of oral hygiene and plaque accumulation and the development of peri-implant mucositis. Furthermore experimental peri-implant mucositis was reversed when oral hygiene measures were instituted [14]. A recent cross-sectional study supported the importance of good oral hygiene by multilevel analysis which determined that a high plaque score was a risk indicator for peri-implant mucositis [15].

3.2.1.2 Smoking and Radiation Therapy

Karbach et al. [16] examined 100 patients with a 1–19-year follow-up and showed that smoking was a significant risk indicator for the development of peri-implant mucositis. Similarly Roos Janseker et al. [17] and Rinke et al. [18] determined that smoking was a possible indicator for peri-implant mucositis.

In the same study that assessed smoking as a risk indicator for peri-implant mucositis, Karbach et al. [18] indicated that radiation therapy was also an “explanatory variable” for the presence of peri-implant inflammation.

3.2.1.3 Residual Cement and Poor Restoration Design

There is increasing evidence that the presence of residual cement in the subgingival tissues contributes to peri-implant tissue inflammation [19]. In a prospective study evaluating the influence of the restorative margin position and the amount of undetected cement, Linkevicius et al. concluded that the more apical the restorative margin, the greater the probability of undetected cement being present. The greatest amount of cement was detected when the restorative margin was placed 2–3 mm subgingivally. Furthermore if an undercut >2 mm is present on the implant restoration, the chance of residual cement increases significantly even if the restorative margin is shallow [20].

A current literature review investigated the role of cement as a risk indicator in peri-implant diseases. It concluded that there is an association with a tendency to higher disease prevalence with cemented, compared to screw-retained, implant restorations [21]. The authors advocated the collection of baseline data 2 weeks following the placement of the implant prosthesis with regular follow-up intervals for early detection of peri-implant mucositis and cement excess. A retrospective case analysis compared screw-retained restorations to cement-retained restorations in patients with and without a history of chronic periodontitis. This study demonstrated, that patients with a history of chronic periodontitis and residual cement tended to develop peri-implant diseases more rapidly (23.4 months compared to 40.8 months). Patients with a history of periodontal disease and screw-retained prostheses had a lower incidence of peri-implant disease. It was therefore recommended to consider screw-retained restorations in patients with a history of periodontal disease [22].

3.2.1.4 Potential Emerging Risk Indicators

There is weak evidence for diabetes, abutment surface characteristics, absence of keratinized tissue, genetics, gender, time function, alcohol consumption, and rheumatoid arthritis as risk indicators for peri-implant mucositis [12, 23]. However, these factors should always be considered when developing a treatment plan for future implant patients, or an individualized maintenance protocol for patient with existing implants.

3.3 Diagnosis

There is heterogeneity in the diagnostic criteria used in studies to define peri-implant mucositis [24]. In one study, peri-implant mucositis was defined as bleeding on probing around implants with no bone loss [25]. In another study, however, the case definition was identified as plaque, probing depth ≤ 5 mm, and evidence of inflammation by modified bleeding index [26]. More recently Felo et al. defined peri-implant mucositis [27] as bleeding on probing, modified gingival index >1.5, modified plaque index >1.5, and probing depth ≤ 3 mm.

Out of all the diagnostic parameters, bleeding upon probing has been consistently used in all studies as a tool for the diagnosis of peri-implant mucositis.

3.3.1 Bleeding on Probing

The clinical tool in the diagnosis of peri-implant mucositis is bleeding on gentle probing (<0.25 N) [28]. In an experimental animal study, healthy peri-implant sites showed an absence of bleeding on probing, while peri-implant mucositis sites showed an increase of bleeding on probing [29].

The presence of inflammatory signs such as edema, redness, and hyperplasia as well as bleeding upon probing is pathognomonic of peri-implant mucositis (see Figs. 3.1 and 3.2a–c).

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Fig. 3.1

Localized inflammation of the lingual mucosa of peri-implant tissues

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Fig. 3.2

(a) Visual signs of redness of marginal peri-implant tissues; (b) clinical probing depth less than 4 mm; (c) bleeding upon probing

3.3.2 Probing Depths/Radiographic Evaluation

Periodontal probing using a light force (0.2–0.3 N) has been deemed a reliable tool for diagnosing peri-implant diseases [30].

To confirm the diagnosis of peri-implant mucositis, stable probing depths, recorded from the time of prosthetic component connection, are of importance in conjunction with the establishment of baseline radiographs [31].

3.3.3 Prevalence

There are significant limitations in the present literature as to the prevalence of peri-implant diseases. Those relate more to issues of study design such as small sample sizes, randomization bias, cross-sectional nature, and short follow-up. Moreover, the variations applied to thresholds for bone loss also affect the disease classification and perceived prevalence. In a recent systematic review, the subject level prevalence of peri-implant mucositis was reported to range from 19 to 65% [32]. Further meta-analyses estimated the weighted mean prevalence of peri-implant mucositis to be 43% (CI: 32–54%) [33].

3.4 Management/Treatment Options

Removal of plaque from the abutment/implant surface is the main goal of treatment of peri-implant mucositis. This goal can be achieved with patient education, oral hygiene instruction, professional debridement, and ensuring that there is adequate access to the area in question.

There is currently evidence in the literature to support that peri-implant mucositis is reversible, similarly to gingivitis, when treated effectively with recommended therapeutic modalities [13, 14]. One study however did report that full resolution of experimentally induced peri-implant mucositis in humans was not fully reversed at 3 weeks when oral hygiene measures were reinstituted [14]. Another more recent study countered these results by observing that in an elderly population, reinstituted oral hygiene measures resulted in complete resolution of peri-implant mucositis [34]. It is important to note, however, that a return to baseline of inflammatory crevicular fluid biomarkers was noted in both studies (Figs. 3.3 and 3.4).

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Fig. 3.3

(ac) 3–5 mm clinical probing depths with bleeding on probing

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Fig. 3.4

(a) Baseline radiograph, (b) radiograph 1-year post-implant loading, (c) radiograph 6 years later exhibiting no evidence of bone loss beyond physiologic remodeling

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Fig. 3.5

(a) Closed embrasure space. (b) Radiographic evidence of poorly seated restorations and presence of cement. (c) Radiographic evidence of stable bone levels over a 5-year period. (d) Opening of embrasure space

Treatment of peri-implant mucositis is essential, as there appears to be evidence that the lack of periodic supportive peri-implant maintenance may result, for some patients, in the development of peri-implantitis. After 5 years of regular peri-implant maintenance, 18% of patients developed peri-implant disease as opposed to those with no maintenance where 43.9% developed peri-implantitis [35].

The primary goal of treatment of peri-implant mucositis is to prevent plaque accumulation. This is achieved by eliminating biofilms at the mucosal abutment interface and around implant-supported restorations. Challenges in achieving this goal for both the patient and the treating clinician are the design and surface texture of the implant abutment, the design of the prosthesis or superstructure, and the patient’s ability and compliance to perform adequate oral hygiene.

Upon initial diagnosis of peri-implant mucositis, the clinician will use a two-pronged approach for treatment (Table 3.1).

Table 3.1

Peri-implant mucositis management

Patient education

Systemic factors

Local factors

Peri-implant debridement

Maintenance

Smoking

Prosthesis design (poor access for oral hygiene)

Patient administered

Individualized protocol

Inability to perform oral hygiene

Cement

Professionally administered

The first approach aims at controlling or modifying local or systemic etiological factors such as smoking cessation counseling, prosthesis design modification, patient education, and oral hygiene instruction.

The second approach aims at maintaining peri-implant tissue health such as the establishment of a professional, patient-centered peri-implant debridement protocol, and a maintenance plan.

3.4.1 Patient Education

Prior to initiation of implant treatment, it is crucial to educate each patient on the importance of adequate plaque control and the need for appropriate maintenance of the implant prosthesis. This is of particular necessity in patients with a past history of chronic or aggressive periodontitis and associated tooth loss as a result of these diseases.

3.4.2 Systemic and Local Factors

3.4.2.1 Systemic Factors

Smoking

A discussion with the patient about the impact of smoking on peri-implant tissue health is very important. In a recent microbiological study, smoking seemed to affect the peri-implant microbiome, creating a high-risk bacterial community for peri-implant disease [36]. Smoking has now been identified in the literature as an independent risk indicator for peri-implant mucositis [37].

Systemic Factors Influencing the Ability to Perform Adequate Oral Hygiene
Inability to perform oral hygiene can be due to systemic factors, such as the development of conditions that affect the cognitive or physical abilities of an individual to perform adequate oral hygiene. Conditions such as Alzheimer’s, senile dementia, or Parkinson’s may place the onus of oral hygiene delivery on loved ones or healthcare staff. A thorough individualized assessment is paramount. Possible conversion of a fixed restoration to a removable prosthesis may be needed, in patient with full-arch implant supported restorations to assist in daily homecare maintenance.

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Fig. 3.6

(a) Over-contoured buccal restoration due to nonideal (palatal and coronal) implant placement. (b) Recontouring of restoration and placement of a soft tissue graft. (c) Suturing of soft tissue graft in place. (d) 5-year follow-up of healthy peri-implant tissues

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Fig. 3.7

Before and after prosthesis flange adjustment to facilitate oral hygiene measures. Disclosing paste on the intaglio aspect of the prosthesis assists in ensuring appropriate contours for the performance of adequate oral hygiene (Courtesy of Dr. J. Viquez)

3.4.2.2 Local Factors

Prosthesis Modification

An assessment will be made of the area to be treated, and an evaluation of the prosthesis will be performed, to ensure adequate access for plaque control. Adjusting restorations to allow for appropriate access to the peri-implant tissues as well as patient education is of paramount importance in the long-term maintenance of dental implants (Figs. 3.5 and 3.6).

Ridge lap restorations, closed embrasure spaces, and flanges on fixed implant-supported prostheses are all examples of prosthetic barriers to adequate oral hygiene. A study demonstrated that 48% of implants that presented with peri-implantitis had no accessibility/capability for proper oral hygiene. Furthermore, the authors stated that inadequate plaque control was found in around 74% of implants studied [38].

It is important to note, however, that it may not be advisable to simply adjust the prosthesis or superstructure but it may be necessary to fabricate a new prosthesis altogether after obtaining adequate tissue health (Figs. 3.7 and 3.8). Such may be the case of pink porcelain restorations with buccal flanges (Fig. 3.9).

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Nov 21, 2018 | Posted by in Implantology | Comments Off on Mucositis
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