A.

Plaque and Calculus in the Disease Process

Plaque and calculus are two different types of deposits that are found on tooth surfaces.

Both plaque and calculus are implicated in the development of the inflammatory diseases of the gingiva and periodontium, namely gingivitis and periodontitis. For many years it was believed that plaque and calculus were both causative factors in inflammatory gingival and periodontal diseases. Today, we know that plaque is the etiologic or causative agent in gingivitis and periodontitis and that calculus is a contributing factor in that it favors plaque accumulation and hinders its removal.

Although they have different characteristics, a relationship exists between them. Plaque is a soft, sticky accumulation that occurs on dental and various other intraoral surfaces. It is the host to a complex micro-system of micro-organisms whose pathogenicity and virulence cause inflammatory diseases of the gingival & periodontal tissues. Plaque can be removed from tooth surfaces by direct brushing. It is possible to have a mouth with plaque but no calculus. Calculus is formed by the deposition of mineral salts in plaque. It is hard and firmly adherent to the tooth surfaces on which it forms and it cannot be removed by brushing. Calculus acts as a focal point for plaque accumulation, a nidus of bacteria and hinders complete removal of plaque. It is almost impossible to have a mouth with calculus but no plaque. We remove plaque and calculus by instrumentation and home care to allow natural immunity to resolve the inflammation and restore health.

The cause and effect relationship between supragingival plaque and gingivitis was demonstrated by Loe and his colleagues in 1965. When plaque was allowed to accumulate, gingivitis developed within 21 days. When plaque control was initiated, the gingivitis was reversed (by means of efficient plaque control, i.e., brushing and flossing) to clinical gingival health.

In a later study done in 1986, Loe and his co-workers found that as regards to periodontitis, not all people develop the disease to the same extent or even at all. Also, although the inflammatory process could be halted and clinical health restored, the damage caused by periodontitis was not reversible.

It is important to realize that genetic predisposition plays a role in the way people's tissues respond to plaque and calculus and that susceptibility to periodontitis varies. Top of Page B. Plaque Formation

Plaque formation can be divided into various stages.

Pellicle Formation:

The first stage is the formation of an organic dental pellicle, also known as the acquired or salivary pellicle. It is an amorphous, tenacious, membranous film, about 1-2 microns thick, that forms on teeth and other solid intra-oral surfaces (restorations; calculus; orthodontic appliances, dentures,etc.) It is easily removed by brushing but begins reforming in minutes and completely reforms very quickly. Bacteria are not required for pellicle formation, but they adhere to and colonize it shortly after the pellicle is formed.

Pellicle formation has a four stage deposition: Stage 1. bathed with salivary fluids

The surfaces are

Stage 2. Salivary Glycoproteins (positively and negatively charged) adsorb to the surfaces. This probably occurs due to ionic interaction. Stage 3. Stage 4. enzymes The glycoproteins lose their solubility The glycoproteins become altered by the action of the bacterial

Bacterial Colonization:

Bacteria borne in the saliva are continually being brought into contact with the organic dental pellicle. Some bacteria are retained in surface irregularities such as pits, fissures or open restorative margins. Others actively adhere to the pellicle by interacting with it. This interaction is determined by specific surface characteristics found on bacterial cell surfaces. Oral bacteria vary significantly in their ability to interact with the pellicle due to variations in their cell surface coatings. A group of protein molecules called adhesions located on the bacterial cell surfaces recognize and link to the pellicle glycoproteins promoting attachment of specific bacteria with the initial colonization of the pellicle, plaque is formed.

Growth and Maturation of Plaque:

Plaque, once disturbed, takes approximately twenty four hours to reform. This initially formed plaque is known as immature plaque. Immature plaque is generally lighter in color, less adherent and less potentially pathogenic. As plaque matures it increases in mass and thickness. Its microbiologic composition also changes. Mature plaque is potentially more pathogenic.

Plaque Retention Factors

These are conditions that favor plaque accumulation and hinder plaque removal by the patient and the dental professional. Examples of these are: Orthodontic Appliances Partial Dentures Malocclusions Faulty Restorations Calculus Deep Pockets Mouth Breathing Tobacco Use

Certain Medications

It is important that the patient be adequately educated in the cause and progression of periodontal diseases. Patients need to understand the importance of brushing and flossing and the need to remove plaque and calculus to maintain the health of their teeth and gums. Disclosing agents can be a very useful tool in showing patients where the plaque is and how it can be effectively removed. The educational aspect is as important as the technical skills and this must be communicated to the patient. Top of Page C. Calculus Formation

Relationship with Plaque: Calculus is formed by the deposition of calcium and phosphate salts in bacterial plaque. These salts are present in salivary and crevicular fluids. Plaque mineralization begins within 24-72 hours and takes an average of 12 days to mature. Calculus contributes to the disease by providing foci for plaque accumulation. It is not the causative or etiologic factor, plaque is. Calculus is porous and can act as a reservoir or nidus of bacteria and endotoxin related to the disease process. Calculus formation has been observed in germ-free laboratory animals but is far more abundant in similar germ-infected laboratory animals. The role of the bacteria in relation to calculus formation is not completely understood.

Classification and Location:

Calculus is classified by location into supra-gingival and sub-gingival calculus. Often, both types occur together. Calculus deposits are also referred to as light, moderate, or heavy (see fig. 1). Supra-gingival calculus is adherent to the teeth and is found on the lingual surfaces of the mandibular incisors in relation to the opening of Wharton's ducts and on the buccal surfaces of maxillary molars in relation to the opening of Stensen's ducts. Figure 1.

Subgingival calculus forms on root surfaces below the gingival margin and can extend deep into periodontal pockets. A more irregular subgingival cemental surface allows deposits to form into the cemental irregularities. This makes the attachment of the subgingiva calculus more tenacious and difficult to remove. It also tends to be darker or black in color. All calculus can however absorb extrinsic stains (coffee; tea; tobacco;etc) and appear dark brown or black.

Subgingival calculus can often be seen on radiographs on the mesial and distal aspect of teeth (see fig. 2) but explorer detection is needed to evaluate the amount of calculus present. Figure 2

Rate of Calculus Formation:

It is known that certain people form calculus faster than others. The following factors increase the rate of calculus formation.

Elevated salivary pH. Elevated salivary calcium concentration. Elevated bacterial protein and lipid concentration. Elevated concentration of protein and urea in submandibular salivary gland secretions. Low individual inhibitory factors. Higher total salivary lipid levels.

A number of anti-calculus agents have been tested. Some have shown modest positive results and have therefore been incorporated into some dentifrices. These commercially available "tartar control toothpastes" may be of some value in periodontal patients who are heavy calculus formers. Top of Page D. Treatment Approaches

Terminology and Definitions Scaling: The instrumentation of the crown and root surfaces of the teeth to remove plaque, calculus, and stains from these surfaces. Root Planing: A treatment procedure designed to remove cementum or surface dentin that is rough, impregnated with calculus or contaminated with toxins or microorganisms. Periodontal Debridement: This includes the removal of plaque, and calculus both above and below the gingiva. Prophy / Prophylaxis: A preventive procedure to remove local irritants to the gingiva, including debridements of calculus and removal of plaque. Scaling and root planing can be done utilizing a non-surgical (closed) approach or a surgical (open) approach. A non surgical approach is when access to the root surfaces is via the sulci or periodontal pockets. A surgical approach is when full thickness tissue flaps are reflected to expose the root surfaces and gain direct access to them. The efficacy of subgingival plaque and calculus removal utilizing a non surgical approach is limited. Pockets up to 5mm may be adequately debrided using a

closed approach, but deeper pockets often will require an open or sugical approach.

Ideal Sequence for Treatment for Periodontal Prophylaxis: Oral hygiene instruction for personal plaque control Evaluate and monitor Scaling to remove plaque and calculus Evaluate and monitor Additional scaling and other treatment options (antibiotic therapy, surgical therapy etc.) Top of Page E. Evaluation Mechanisms

The evaluation of the results of instrumentation of the various tooth surfaces is as important as the instrumentation itself.

The first evaluation is a short term one and is performed at the end of each session of instrumentation. It is performed with a sharp explorer to check the root surfaces are smooth and free from plaque and calculus deposits.

The second evaluation is a longer term evaluation, performed 4-6 weeks after instrumentation. At this evaluation, the clinician looks for maintenance of oral hygiene and a reduction in the level of inflammation in the tissues.

The tissues should be firm, light pink, well adherent to the tooth surface with a sharp, scalloped gingival margin.

The next choice in the sequence of therapies is dependent on the tissue response to the preceding therapy. The practice of evaluating and monitoring these responses is as important as the therapy itself.

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Acknowledgement

The author wishes to acknowledge the contribution of Dr. David Isaacs, whose valuable work made this paper possible.