Introduction to Understanding the Basics of Teeth vs. Dental Implants: Similarities and Differences

, 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
 

1.1 Definitions

Throughout the next sections of this book, the reader will encounter a host of terms. For purposes of clarity, this is a list of some important definitions taken from the American Academy of Periodontology (AAP) Glossary of Periodontal Terms [1]:

  • Peri-implant mucositis: 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.

  • Peri-implantitis: An inflammatory process around a dental implant which includes both soft tissue inflammation and loss of supporting bone.

  • Biotype: The thickness or dimension of the soft and hard tissue surrounding natural teeth or dental implants.

  • Osseointegration: A direct contact, on the light microscopic level, between living bone tissue and a dental implant.

  • Fibro-osseous integration: The interposition of healthy dense collagenous tissue between a dental implant and bone. Also known as fibro-osteal integration.

  • Implant, oral: Endosseous root-form implant – an implant placed into the alveolar process and/or basal bone that derives its support from a vertical length of bone and supports a prosthesis or other devices. Most commonly made of titanium, it can be cylindrical, tapered, etc.

  • Implant fixture: A synonym for a dental implant, especially an endosseous implant.

  • Implant abutment: That part of an implant system that connects the dental implant with a prosthesis or other devices.

  • Overdenture: Complete or partial removable denture supported by soft tissue and retained roots or implants to provide support, retention, and stability and reduce ridge resorption.

  • Recession: The migration of the marginal soft tissue to a point apical to the cementoenamel junction of a tooth or the platform of a dental implant.

  • Biologic width: The dimension of soft tissue composed of a connective tissue and epithelial attachment extending from the crest of bone to the most apical extent of the pocket or sulcus.

  • Occlusal trauma: Injury resulting in tissue changes within the attachment apparatus due to physiologic or parafunctional forces which may exceed its adaptive capacity.

  • Piezoelectric surgery: A surgery performed using an instrument which generates micro-vibrating motion via the application of electromagnetic forces on a polycrystal; the micro-vibration of the metallic tip results in ostectomy and osteoplasty of the bone in contact with the tip.

  • Peri-implant mucositis is a disease confined to the mucosa and is reversible.

  • Peri-implantitis includes both soft tissue inflammation and loss of supporting bone and is irreversible.

1.2 Epidemiology

The prevalence of peri-implant diseases has been reported to range from 5 to 63.4% according to different reports [2]. This variability is due to various studies reporting different findings depending on the study design, the definitions (threshold of bone loss) adopted for peri-implant diseases, population size, and other factors.

A better understanding of peri-implant diseases and a consensus on the diagnostic criteria will eventually help in reducing some of this variability in the prevalence of peri-implant mucositis and peri-implantitis.

1.3 Classification of Peri-Implant Diseases

A classification system for peri-implant diseases is highly desirable. This will assist healthcare professionals in determining accurate prevalence estimates, providing clear diagnoses, and assigning prognoses. It will also improve the communication between health professionals and researchers, as well as the evaluation of treatment outcomes. However, to date, there is no consensus on a certain classification system as far as the authors know. This is consistent with the lack of clarity on established diagnostic criteria, as well as management protocols of peri-implant diseases.

In this section, two proposed classification systems will be provided as examples:

  • The first was proposed by Froum and Rosen in [3]. This classification for peri-implantitis is based on the severity of the disease. A combination of bleeding on probing and/or suppuration, probing depth, and extent of radiographic bone loss around the dental implant is used to classify the severity of peri-implantitis into early, moderate, and advanced categories (Table 1.1, Figs. 1.1, 1.2 and 1.3).

  • The second classification system was proposed by Ata-Ali et al. in [4]. In their article Ata-Ali et al. proposed a classification for peri-implant mucositis and peri-implantitis based on the severity of the disease, using a combination of peri-implant clinical and radiological parameters to classify severity into several stages (stage 0A and 0B = peri-implant mucositis and stage 1 to 4 = peri-implantitis) (Tables 1.2 and 1.3).

Table 1.1

Classification of peri-implantitis as proposed by Froum and Rosen [3]

Staging

Definition

Early

PD ≥ 4 mm (bleeding and/or suppuration on probinga)

Bone loss <25% of the implant lengthb

Moderate

PD ≥ 6 mm (bleeding and/or suppuration on probinga)

Bone loss 25% to 50% of the implant lengthb

Advanced

PD ≥ 8 mm (bleeding and/or suppuration on probinga)

Bone loss >50% of the implant lengthb

aNoted on two or more aspects of the implant

bMeasured on radiographs from time of definitive prosthesis loading to current radiograph. If not available, the earliest available radiograph following loading should be used

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Fig. 1.1

Early peri-implantitis as proposed by Froum and Rosen [3]. (a) (left) Clinical photograph of early peri-implantitis at an implant at the maxillary left lateral incisor position. Note the inflamed tissue and exudate. (Froum and Rosen [3]). (b) (right) Radiograph of maxillary left lateral incisor with bone loss <25% of the implant length, depicting early peri-implantitis (Froum and Rosen [3])

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Fig. 1.2

Moderate peri-implantitis as proposed by Froum and Rosen [3]. (a) (left) Clinical view of an implant in the mandibular left first molar site. Note the exudate (Froum and Rosen [3]). (b) (right) Radiograph depicting moderate peri-implantitis, with bone loss of 25–50% of the implant length on the mesial and distal aspects of the implant (Froum and Rosen [3])

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Fig. 1.3

Advanced peri-implantitis as proposed by Froum and Rosen [3]. (a) (left) Clinical probing distal to the implant at the maxillary left canine site measured 8 mm (Froum and Rosen [3]). (b) (middle) Bleeding on probing was noted 15 seconds following removal of the probe (Froum and Rosen [3]). (c) (right) Radiograph depicting moderate peri-implantitis with bone loss <50% of the implant length (Froum and Rosen [3])

Table 1.2

Classification of peri-implant mucositis as proposed by Ata-Ali [4]

Staging

Definition

Stage 0A

PPD ≤ 4 mm and BoP and/or SUP, with no signs of loss of supporting bone following initial bone remodeling during healing

Stage 0B

PPD > 4 mm and BoP and/or SUP, with no signs of loss of supporting bone following initial bone remodeling during healing

PPD probing pocket depth, BoP bleeding on probing, SUP suppuration

Table 1.3

Classification of peri-implantitis as proposed by Ata-Ali [4]

Staging

Definition

Stage I

BoP and/or SUP and bone loss ≤3 mm beyond biological bone remodeling

Stage II

BoP and/or SUP and bone loss >3 mm and <5 mm beyond biological bone remodeling

Stage III

BoP and/or SUP and bone loss ≥5 mm beyond biological bone remodeling

Stage IV

BoP and/or SUP and bone loss ≥50% of the implant lengtha beyond biological bone remodeling

BoP bleeding on probing, SUP suppuration

aDepending on implant length, if peri-implantitis can be classified as simultaneously corresponding to more than one stage, the most advanced stage should be chosen

Currently, there is no consensus on a classification system for peri-implant diseases.

1.4 Peri-Implant Mucositis vs. Peri-Implantitis

1.4.1 Peri-Implant Mucositis

  • It has been proven that the disease process around dental implants is similar to that which occurs around teeth. Peri-implant mucositis around dental implants is seen as the equivalent of gingivitis around natural teeth. Peri-implant mucositis may or may not progress to peri-implantitis as gingivitis may or may not progress to periodontitis [5, 6].

  • Plaque accumulation on the titanium surface and the formation of a biofilm seem to be essential for the initiation and progression of peri-implant diseases in a way similar to that found around natural teeth [7–9].

  • Peri-implant diseases are linked to similar gram-negative bacteria associated with severe chronic periodontitis [5, 6, 10, 11].

  • When effectively treated, peri-implant mucositis can be reversed back to health [5, 6].

  • The relatively weak epithelial seal around dental implants is similar in function to that around natural teeth [12].

  • The structural difference between teeth and dental implants does not seem to influence the host response to the bacterial insult [13, 14].

The removal of the biofilm from the dental implant surface is the primary objective when treating peri-implant mucositis and will lead to the reversal of disease to a state of health the majority of the time if adequately performed.

1.4.2 Peri-Implantitis

  • Peri-implantitis is seen as the equivalent of periodontitis around natural teeth and similarly occurs when the overwhelming bacterial insult leads to a destructive host immune response.

  • Studies have shown that peri-implantitis and periodontitis lesions from human biopsies have many features in common [13, 15].

  • Bacterial species associated with periodontitis and peri-implantitis are similar. Moreover, Staphylococcus aureus may also be an important pathogen in the initiation of peri-implantitis [13, 16, 17].

  • The connective tissue adjacent to the pocket epithelium is infiltrated by inflammatory cells, with B-lymphocytes and plasma cells being the most dominant cell types. Similar markers are upregulated between peri-implantitis and periodontitis, including proinflammatory cytokines such as interleukin (IL)-1, IL-6, IL-8, IL-12, and tumor necrosis factor (TNF)-alpha [18, 19].

  • Despite those many similarities between teeth and dental implants, the severity and rate of disease progression may differ significantly in peri-implantitis when compared to periodontitis. Experiments that allowed undisturbed dental plaque formation on dental implants and teeth in humans and in dogs demonstrated a more advanced inflammatory cell infiltrate in the peri-implant mucosa. Features of experimentally created peri-implantitis and periodontitis have also been compared. The results suggested that clinical and radiographic signs of tissue destruction were more pronounced in peri-implantitis cases. Furthermore, the size of the inflammatory cell infiltrate in the connective tissue was larger, approaching the crestal bone around implants [13, 20–23]. This could be attributed to the differences in the orientation and insertion of collagen fibers around teeth compared to those around dental implants [22].

  • All implants appear to be susceptible to peri-implantitis [24, 25].

Despite the similarities in both the bacterial etiology and the immune host response components between periodontitis and peri-implantitis, peri-implantitis progresses at a faster rate with more pronounced bone loss. This could be attributed to the differences in orientation and insertion of collagen fibers around teeth compared to those around dental implants.

Early diagnosis and intervention by the elimination of the bacterial biofilm and correction of other possible contributory factors is the most effective way in preventing peri-implant diseases.

1.5 Teeth vs. Dental Implants

There are many differences between dental implants and teeth at both the microscopic and the macroscopic level. Some of those differences are best summarized in Table 1.4 and Fig. 1.4.

Table 1.4

Teeth are different from dental implants on both the micro- and the macroscopic levels

 

Teeth

Dental Implants

Periodontal fibers

Insert into cementum on the root surfaces of natural teeth

13 groups

Extend parallel to the surface of the implant and/or abutment

2 groups

Connection

Periodontal ligaments

Osseointegration

Connective tissue

Lower percentage of collagen fibers

Higher percentage of cells

More vascular

Higher percentage of collagen fibers

Lower percentage of fibroblasts. Looks very similar to a scar tissue

Less vascular

Blood supply to surrounding gingivae

Three different sources (the periodontal ligament space, the interdental bone, and the supraperiosteal region)

Two different sources (the supraperiosteal vessels and a few vessels from the bone)

Periodontal ligament space

Present

Absent

Resistance to mechanical and microbiological insults

More resistant

Less resistant

Biological width (BW)

JE: 0.97–1.14 mm

CT: 0.77–1.07 mm

BW: 2.04–2.91 mm

JE: 1.88 mm

CT: 1.05 mm

BW: 3.08 mm

Sulcus depth

≤ 3 mm when healthy

Could be >3 mm depending on multiple factors

Proprioception

Periodontal mechanoreceptors

Osseoperception

Tactile sensitivity

High

Low

Axial mobility

25–100 μm

3–5 μm

Fulcrum when lateral force applied

Apical third of the root

Crestal bone

Possible relief

Pressure absorption, distribution

Pressure concentration on the crestal bone

Adapted from different sources, mainly Tokmakidis et al. [85] and Ramoglu et al. [86].

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Fig. 1.4

Schematic illustration of hard and soft tissue around a tooth and an implant. (a) Hard and soft tissue anatomy around a natural tooth demonstrates bone support with a periodontal ligament, a connective tissue zone above the crest of bone with connective tissue fibers (Sharpey’s) inserting into dentin, a long junctional epithelial attachment, a gingival sulcus lined with sulcular epithelium, and oral gingival epithelium (outer surface of gingiva). (b) Hard and soft tissue anatomy around an implant demonstrates some similarities and some distinct differences. There is supporting bone in direct approximation to the implant surface without any intervening soft tissues (i.e., no periodontal ligament). A connective tissue zone is present above the level of bone with fibers running parallel to the implant surface and no inserting fibers. There is a long junctional epithelial attachment, a gingival or mucosal sulcus lined with sulcular epithelium, and oral gingival or mucosal epithelium (outer surface of soft tissue) (From Rose LF, Mealey BL: Periodontics: Medicine, surgery, and implants, St. Louis, 2004, Mosby)

Many articles and book chapters have reported on the similarities and differences that exist between tissues around teeth and those around dental implants. The reader is encouraged to consult the published literature on this topic including a recent review entitled “Peri-Implant and Periodontal Tissues: A Review of Differences and Similarities” [26]. Part of this section was adapted from this publication.

1.5.1 Soft Tissues around Implants and Teeth

  • The anatomy and histology of soft tissues surrounding dental implants and teeth is structurally similar. Those are made up of keratinized oral epithelium, non-keratinized sulcular epithelium, and the underlying connective tissue.

Similar to teeth, the junctional epithelium connects to the dental implant/abutment surface via hemidesmosomes and basal lamina [27]. The combined height of the junctional epithelium and connective tissue attachment is usually referred to as the “biologic width.” Early work by Gargiulo et al. [28] estimated this to be about 2.04 mm around teeth. However, a recent systematic review concluded that there is no universal dimension for biologic width around teeth with large intra- and interindividual variances (subject sample range, 0.2–6.73 mm) [87].

  • In a human histologic study, the length of the peri- implant seal was found to be about 4–4.5 mm [88]. When compared to the “biologic width” around teeth, the same attachment around dental implants was longer nearly by the factor of 1.5 mm [89].

  • This protective distance that exists between the alveolar crest of bone and the base of the gingival pocket should always be kept constant and respected in order to avoid bone loss around teeth. If for any reason, e.g., deeply placed restorative margin, this biologic distance is not maintained, then bone around the affected tooth will resorb in what seems like an adaptive mechanism, to mitigate the effects of those noxious stimuli. A similar principle applies to dental implants where changes in the soft tissue to bone relationship may be one of the reasons for the early crestal bone loss seen around dental implants [29].

  • Upon dental implant placement, the fast-moving epithelial cells will migrate apically until they reach the dental implant surface where they attach themselves rapidly through the basal lamina and the hemidesmosomes [30]. Another possible attachment modality hypothesized is an indirect epithelium-to-implant contact [31]. This is very similar to what happens around teeth following soft tissue flap reflection and healing.

  • Human studies have demonstrated that epithelium surrounding dental implants possess similar patterns of differentiation and function to gingival tissues [32]. However, what stops the epithelium from migrating further apically on the implant surface? The presence of granulation tissue adhering to the surface of the transmucosal components is considered the principal factor that prevents the apical migration of epithelium [33]. Berglundh speculated that this most likely occurs due to the interaction of the titanium surface with the soft tissue [34].

  • The following sequence of events occur once an dental implant is inserted into bone:

    • Formation and adhesion of the fibrin clot to the dental implant surface

    • Adsorption of the fibrin clot to the dental implant surface and adsorption of the extracellular matrix (ECM) proteins and connective tissue cells to the dental implant surface

    • Transformation of the clot into granulation tissue and migration of epithelial cells on top of the fibrin clot/granulation tissue [35]

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    Related posts:

    1. Mucositis
    2. Soft Tissue Deficiencies
    3. Tissue Complications/Peri-implantitis
    4. 16: Intramucosal Insert Surgery and Prosthodontics
    5. Experimental and Clinical Knowledge of Nanometer Scale Designing on Endosteal Implants
    6. The Posterior Maxilla

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Nov 21, 2018 | Posted by in Implantology | Comments Off on Introduction to Understanding the Basics of Teeth vs. Dental Implants: Similarities and Differences

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