Soft Dental Deposits

Dental plaque is an accumulation of microorganisms that form a well-structured and functional biofilm. It attaches to the surface of the teeth, restorations, and dental prostheses in the oral cavity and cannot be washed off with water. 

Materia alba is a nonorganized, boggy, soft, and porous deposit that comprises bacteria, leukocytes, epithelial cells, and food debris. It typically covers dental plaque and can be removed with water.

Etiology

Up to 80–90 % of dental plaque consists of water. Microorganisms make up the rest of the volume and represent most of the plaque’s solid matter. There, more than 500 different types of bacteria (including Mycoplasma species), as well as yeast, protozoa, and viruses exist. 

As mentioned above, plaque microorganisms survive as biofilms. During their lifetime, they are embedded into the extracellular matrix (ECM). This medium comprises about 30 % of the plaque’s weight and consists of both organic and inorganic components.

The organic component includes saliva glycoproteins, bacteria-derived polysaccharides (dextrans), albumins, and cell membrane lipids.

Calcium and phosphorus, as well as trace quantities of other minerals, such as sodium, potassium, and fluorine, account for the inorganic elements of dental plaque. These substances come from the saliva and gingival crevicular fluid, whereas fluorine is obtained from external sources only (such as fluoride toothpastes, gels, or oral rinses).

The mechanism of dental deposit formation follows a three-stage pattern:

1. First, a pellicle is formed. It provides the surface for bacterial attachment.

2. Then, the initial colonizers start to adhere to the surface and proliferate to form colonies.

3. The final stage is secondary microbial colonization when plaque takes its final shape.

The whole process is as follows: After tooth eruption, the pellicle forms on its surface that contacts the saliva. This is a thin film that comprises mucin, glyco- and sialoproteins of the saliva and gingival crevicular fluid. It functions as a lubricant for the surfaces and prevents them from drying. It also promotes mineral exchange between the saliva and tooth enamel. The layer has a ridge surface that makes it easier for microorganisms to attach despite the mechanical forces of saliva flow, as well as cheek and tongue movements.

In most cases, gram-positive bacteria, such as Streptococcus mutans and Streptococcus sanguinis, Actinomyces naeslundii, and Actinomyces viscosus, are the first to colonize the tooth surface. These initial colonizers adhere to the pellicle by means of specific adhensins that interact with receptors in the pellicle. Structurally, adhesins can be both surface proteins and fimbriae-associated proteins.

Early gram-positive colonizers (also known as pioneer species) are aerobic bacteria that feed on sugars and decrease the oxidation-reduction potential of the environment. The longer plaque remains on the tooth surface, the thicker it gets, which reduces the amount of oxygen available for bacteria. This creates a prerequisite for anaerobic microbes, primarily gram-negative ones, to multiply. As these microorganisms are asaccharolytic, they get their nutrition from aminoacids and small peptides. On average, dental plaque forms within 48 hours. The plaque community is supplemented by gram-negative rods and cocci (days 2–3), Veillonella and fusobacteria (days 4–5), and spirilla and spirochetes (days 6–9). 

Prevotella intermedia, Prevotella loescheii, Capnocytophaga spp., Fusobacterium nucleatum, and Porphyromonas gingivalis are secondary colonizers. These microorganisms tend to bind to the bacterial cells that have already become part of the plaque. The process of bacterial adhesion is called coaggreagation. It arises due to direct intercellular binding or cellular attachment via polyvalent molecules, such as saliva mucins and glycoproteins. The interactions may also be less specific if based on hydrophobic, electrostatic, or Van der Waals forces. Extracellular glucans generated by Streptococcus mutans, Streptococcus mitis, and Actinomyces naeslundii may also promote interbacterial binding and accumulation.

Dental plaque is pierced by canals filled with fluid where nutrients and bacterial byproducts circulate. 

As the conditions in the sub- and supragingival regions differ, so do the plaque structure and composition in these areas.

Gram-positive cocci and rods dominate in supragingival plaque on the tooth surface, while gram-negative rods and filamentous bacteria, as well as spirochetes, prevail on the external surface of mature plaque. 

If supragingival plaque close to gingival margin persists for long periods of time, it takes a corncob shape. One of the consequences of coaggregation is that the central gram-negative nucleus of rod species (for instance, Fusobacterium nucleatum or Bacterionema matruchotii) wraps around cocci cells (such as streptococci or Porphyromonas gingivalis).

The gingival crevicular fluid is a medium where the metabolism of subgingival plaque bacteria happens. Inflammatory cells and mediators of the host have a major influence on bacterial colonization and growth in this area.

Subgingival plaque attached to the tooth comprises gram-positive rods and cocci (Streptococcus mitis, Streptococcus sanguis, Actinomyces naeslundii, Actinomyces viscosus, Eubacterium spp.), whereas plaque adjacent to the soft tissue is dominated by Streptococcus oralis, Streptococcus intermedius, Peptostreptococcus micros, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus, and Fusobacterium nucleatum.

The number of fusobacteria and filamentous microorganisms, motile rods, and spirochetes increases in case of periodontium diseases. Various factors can influence the rate of dental plaque formation. These may include saliva viscosity, oral cavity microflora, desquamation of epithelial mucosa in the oral cavity, local inflammatory processes, diet, or mastication intensity. 

Self-cleaning properties, depending on tooth anatomy and interactions between adjacent tissues, should also be accounted for.

Not only does dental plaque promote caries, but it also causes irritation and tissue damage due to microbial activity and the toxins they produce, which can eventually lead to gingivitis and periodontitis.

Anatomic Pathology

Macroscopically, dental plaque appears as a white, yellowish, or grayish film.

Initially, it can be observed in the gingival sulcus, interdental spaces, pits, and fissures. It may also accumulate at restoration sites, on dental prostheses, or orthodontic appliances.

Materia alba is a loose, thick mass of white, yellow, or brownish color that resembles fur and is easy to see with the naked eye. 

Plaque can be either supragingival (located at the gingival margin or just above it) or subgingival (primarily found below the gingival margin, between the tooth and the gingival sulcus tissue). 

Subgingival deposits consist of a structured plaque attached to the tooth surface, a free bacterial layer, and a plaque adjacent to the gingival epithelium.

Diagnosis

• Visual examination: Dental plaque is difficult to detect without special equipment. When dried, it has a matte, rough surface. Soft dental plaque is visually identifiable;
• Probing: Dental plaque can be removed by scraping;
• Staining: Dyes in solutions or reagent tablets are used to stain the pellicle, dental plaque, and soft dental deposits. Some dyes may help identify mature and immature plaque by developing different colors when applied;
• Index evaluation: Oral Hygiene Index, Simplified Oral Hygiene Index (OHI-S, Greens — Vermillion), PHP (Podshadley, Haley), PLJ (Silness — Löe). 

Clinical Manifestations

Patients may complain of teeth discoloration, foul breath, and gingival hemorrhage when brushing their teeth.

Dental plaque starts to develop just a few hours after brushing. If personal hygiene is not maintained regularly, the deposits become visible within 1–2 days.

Soft dental deposits are primarily found in the neck areas, interdental spaces, distal surfaces of the outermost teeth in a row, pits and fissures, and surfaces of embedded teeth that are hard to reach and keep clean.

The gingiva typically shows various signs of inflammation linked to deposits — edema, hyperemia, or gingival hemorrhage during probing.

Treatment

You may either control your dental deposits on your own by following an individual oral hygiene routine or have them removed by a professional. In this case, the deposits are broken down and scraped off mechanically.

As dental plaque forms continually, it is crucial to maintain personal hygiene on a daily basis and to know exactly how to brush your teeth correctly. To remove soft dental deposits from the comfort of your own home, you may need a toothbrush, an abrasive toothpaste, interdental hygiene tools such as floss or interdental brushes, a water flosser, and tongue scrapers. Professional dental care employs rotating brushes, specialized pastes, ultrasonic and airflow appliances. Dental plaque can also be controlled with fluoride-based medicinal products that prevent microbial adhesion to the tooth surface, antiseptics that exert bactericidal and bacteriostatic effects, surfactants, and enzyme drugs.

Hard Dental Deposits

Hard dental deposits, or calculus, are mineralized dental plaque that develops in the supra- and subgingival regions. 

Etiology

Dental calculus is 70–90 % of inorganic origin. The minerals identified in its composition are mainly calcium phosphate crystals, encompassing dicalcium phosphate dihydrate (DCPD, brushite), octacalcium phosphate (OCP), substituted hydroxyapatite (HA), and whitlockite. Calcium carbonate, magnesium phosphate, and trace quantities of sodium, barium, zinc, strontium, bromine, copper, silver, aluminum, and iron may also be detected. Bacterial cells (aerobic and anaerobic bacteria, including periodontal pathogens such as Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Treponema denticola), yeasts (Candida albicans), proteins, lipids (fatty acids, triglycerides, glycolipids, phospholipids), and extracellular DNA constitute the organic component of the structure.

Calculus may develop above the gingiva (referred to as supragingival calculus) or below the gingiva (referred to as subgingival calculus). These two types of dental calculus have different characteristics, locations, and mechanisms of formation. Supragingival calculus retrieves its minerals from the saliva, making it a salivary-type formation. The gingival crevicular fluid, which is similar to blood serum, is the primary source of building materials for subgingival calculus. Thus, it can be attributed to serum-type calculus. Supragingival calculus comprises saliva proteins, more brushite and OCP, but less whitlockite and sodium.

Subgingival calculus, on the other hand, is deprived of any saliva proteins, has less brushite and OCP, but more whitlockite and HA in its composition. The deeper the pocket, the more sodium it contains.

Statistically, adults are more prone to dental calculus than children.

Dental calculus theories:

1. According to the salivary theory, the saliva from the ducts of the major salivary glands contains an excess of carbonic acid. Under these conditions, phosphates and calcium carbonates are dissolved. When in contact with air, a part of CO2 evaporates, the saliva pH increases, and salts precipitate. 
2. The epitaxy theory states that the concentration of calcium and phosphate ions in the saliva is not high enough to make them precipitate. However, it may still promote hydroxyapatite crystal growth when the initial nucleus has already formed. A compound similar to hydroxyapatite crystals activates the precipitation of calcium salts from the solution, and small calcification foci start to form. Over time, they grow bigger and may merge together. A carbohydrate-protein complex, which is believed to originate from the extracellular matrix, initiates calcification. It removes calcium from the saliva by means of chelation and binds to nuclei thus stimulating further mineral precipitation.
3. The phosphatase theory is based on the presupposition that phosphatase is released from desquamated epithelial cells, bacterial cells, and dental plaque. It then hydrolyzes organic phosphates in the saliva, which makes calcium phosphate precipitate.
4. Pursuant to the bacteriological theory, mineralization of dental plaque is an extracellular process that takes place around gram-negative and gram-positive microorganisms. However, some bacteria are capable of generating intracellular apatite crystals. It is also assumed that bacteria may play a crucial role in dental plaque mineralization by producing phosphatases that eventually influence the plaque pH.
5. One more theory, the stagnation theory, suggests that colloid proteins in the saliva bind to calcium and phosphate ions, creating an oversaturated solution. When the saliva in the oral cavity becomes stagnant, these colloids accumulate, leading to the precipitation of phosphate and calcium salts.
6. Regarding the transformation theory, calcium octaphosphate is thought to be generated as amorphous deposits and brushite transform. It then turns into hydroxyapatite.

To sum it all up, numerous factors contribute to dental calculus. When assessing the condition, your dentist should take into account your oral hygiene, hypersalivation (the more saliva is produced, the more salts precipitate), inadequate or unilateral mastication, dietary preferences (high-residue food impedes dental calculus formation), and overall health. The rate of dental plaque mineralization may differ. This is explained by interindividual variability; moreover, even different groups of teeth in one individual may not show similar plaque growth.

Dental calculus is a significant factor in periodontium diseases. It does not destroy the tissues itself but provides a suitable surface for retaining nonmineralized dental plaque, which is the key causative agent of gingivitis and periodontitis. The rough surface of dental calculus serves as an ideal growth medium for subgingival bacteria colonies. Its adverse action is purely mechanical: it irritates the periodontium tissues and stretches the walls of the periodontal pockets.

Classification

• Supragingival dental calculus
• Subgingival dental calculus

Anatomic Pathology

Supragingival dental calculus

Supragingival dental calculus is a hard or clay-like mass of white to yellow color (depending on tobacco use or food colorant consumption). It is fragile and can be removed by scraping. Over time, the structure may grow to such an extent that it completely covers the tooth crowns that bear no antagonists. This type of calculus typically affects the dental crown surface above the gingival margin, covered by a layer of soft dental plaque. Its primary localization is next to the excretory ducts of the major salivary glands, including the vestibular surface of the superior molar and the lingual surface of the anterior teeth of the mandible. 

Subgingival dental calculus

Unlike supragingival calculus, this is a brown to greenish-black hard mass that tightly adheres to the tooth surface and is difficult to remove by scraping. This type of calculus tends to accumulate in the area of the gingival sulcus, more apical to the gingival margin, making it impossible to identify upon visual examination. However, it typically develops in small quantities that correspond to the gingival pocket depth.

Diagnosis

• Visual examination: Supragingival dental calculus is easy to detect, whereas a discolored marginal gingiva (a gray shadow below the gingival margin) may indicate subgingival localization.
• Drying: Careful blowing of an air spray into the gingival sulcus to examine the site.
• Transillumination.
• Periodontium probing.
• Index evaluation: Oral Calculus Index (OCI, Greene and Vermilion), Calculus Index (CI), Calculus Surface Severity Index (CSI), Marginal Line Calculus Index (MLC-I), etc.
• Radiography (intraoral contact radiography, bite-wing, DPR, CBCT): In the case of mineralized dental deposits, a radiograph shows radiopaque shadows that protrude into the interdental spaces.

Clinical Manifestations

Patients may complain of tooth discoloration, foul odor, and gingival hemorrhage. Their tooth surface may feel rough, or there may be a sense of a foreign body. Sometimes, during mastication or brushing, pieces of calculus may break off.

When dried with an air spray, supragingival calculus becomes matte white and easier to inspect. Upon transillumination, it appears as a dark shadow on the tooth surface with a low transparency. Subgingival calculus cannot be detected by visual means; the only sign it may be present is a discolored gingival margin. The change in color is due to the inflammation of the gingiva that contacts the calculus. It is characterized by edema, hyperemia, or gingival hemorrhage during probing. The calculus is primarily located on the teeth surfaces that are in constant contact with the saliva coming from the excretory ducts of the major salivary glands, including the vestibular surface of the superior molars and the lingual surface of the inferior teeth. Subgingival deposits are exposed for examination by carefully pulling away the marginal gingiva with an air spray and a periodontal probe. An X-ray can also be employed.

Treatment

Hard supra- and subgingival dental deposits should be removed mechanically by a professional during a special oral hygiene procedure. 

To this end, your dentist may use scalers, curettes, excavators, chisels, ultrasonic and acoustic tools. 

Enzyme- and surfactant-based hygiene products are utilized to control dental calculus. It is also recommended to include pyrophosphate salts, biphosphonates, and zinc salts, which inhibit mineralization processes, into your dental care routine.

Pigmented Dental Deposits

Pigmented dental deposits (extrinsic tooth staining) are a reversible discoloration of the teeth when the pellicle or dental plaque is dyed by external colorants.

Etiology

The tooth color appears altered when a pigment settles in the pellicle or dental plaque on the tooth surface. It is believed that pigments react with pellicle proteins; however, the actual process is still unknown.

Clean enamel does not absorb any colorants, but porous dentin is prone to discoloration.

The factors that influence extrinsic discoloration of the teeth can be classified as follows:

• Direct extrinsic tooth staining: Pigmented substances are inserted into plaque or the pellicle and dye it their primary color;
• Indirect extrinsic tooth staining: This process involves a chemical reaction between a compound on the tooth surface and a substance that has no color or a color that differs from that of the resulting spot.

A spot may also be of metallic or nonmetallic origin.

What causes direct staining?

• Food colorants (tea, coffee, other colored beverages, spices, and vegetables)
• Smoking or tobacco chewing
• Medicinal products, mouthwashes
• Chromogenic bacteria

Polyphenol compounds from foods are thought to determine the spot color. Poor oral hygiene leads to dental deposit accumulation, which eventually increases the intensity of discoloration.

Indirect staining, on the other hand, is associated with cationic antiseptics and metal salts. The mechanism behind indirect staining is associated with anionic food chromogens that settle on absorbed cationic antiseptics or polyvalent metal salts on the tooth surface.

Polyvalent metal salts promote extrinsic tooth staining in individuals who take iron supplements and/or work at plants where they are exposed to metal salts. Iron, manganese, silver, and iodine dye the teeth black. Copper develops a green shade if an oral rinse containing copper salts is used or an individual contacts metal on a regular basis at a production facility. Potassium permanganate in mouthwashes makes teeth purple to black. Silver nitrate salt used by dentists may cause a black to dark gray color, whereas tin fluoride is responsible for golden brown teeth. 

If used over long periods of time (around 7–10 days), cationic antiseptics may cause brown or black spots. They are supposed to have an affinity for sulfate groups present in dental plaque, carious lesions, and the bacterial cell membrane. This is the reason why they remain within dental deposits and discolor the tooth surface.

A special case of pigmented dental plaque is extrinsic tooth discoloration associated with chromogenic bacteria, such as Prevotella melaninogenica, Actinomyces israelii, Actinomyces naeslundii, Capnocytophaga, Leptotrichia, Fusobacterium, Corynebacterium, and Streptococcus. The exact mechanism of the phenomenon known as black staining is still unclear, but scientists suppose that dark discoloration develops due to an insoluble metal salt that forms when hydrogen sulfide generated by bacteria reacts with iron in the saliva or gingival crevicular fluid. Such stains are more likely to develop if an individual drinks water with high iron content or pH. The condition tends to exacerbate if the saliva pH is also high. Linear discoloration consisting of dark brown to black dots is primarily found on the vestibular and oral surfaces of the neck areas of the teeth. This type of plaque is typical in children but may sometimes be seen in adults as well.

Anatomic Pathology and Clinical Manifestations

Patients usually complain of a cosmetic imperfection.

Brown staining

This is a thin, semitransparent pigmented film. Its light to dark brown color depends on pigments found in coffee and tea. 

This type of discoloration is more common on the vestibular surfaces of the superior anterior and lateral teeth and the lingual (sometimes vestibular) surface of the inferior anterior teeth.

Black staining caused by smoking

This is a dense, dark brown to black film that tightly adheres to the tooth surface. It is formed by residues of the tar produced while smoking.

The lingual surfaces of the anterior inferior teeth are more prone to this type of discoloration; however, poor hygiene may lead to all the teeth being affected. Tobacco tar may penetrate deep pits and fissures, enamel cracks, and exposed dentin, making the staining even more resilient.

Black iron staining

This type of discoloration appears as black spots on the anterior teeth of the maxilla and mandible; in some instances, it may affect all the teeth.

Iron-containing mouthwashes, dust at production facilities that handle iron, manganese, silver, and/or iodine, and oral iron supplements may contribute to the condition.

Black staining

Chromogenic bacteria, as the main driver of black staining, tend to settle on the vestibular and oral surfaces of the teeth of the maxilla and mandible.

Initially, linear discoloration consisting of dark brown to black dots is observed in the neck areas of the teeth along the gingival margin. Over time, it spreads and may also affect the middle and coronal portions of the crown. The defect is more pronounced in areas with poor hygiene.

Orange staining

This type of staining may develop due to some species of chromogenic bacteria (Serratia marcescens, Flavobacterium lutescens) or regular exposure to chromic acid vapors.

In the majority of cases, it is observed on the vestibular and lingual surfaces of the anterior teeth of the maxilla and mandible.

Green staining

These are green or greenish-yellow spots that are mostly seen on the vestibular surface of the teeth of the maxilla.

Such staining may develop in children due to chromogenic bacteria, in individuals that use mouthwashes containing copper, and/or in those who are exposed to copper and nickel professionally.

Yellowish-brown staining

Such spots have a yellowish-brown to dark brown and black color.

They are commonly found in the neck areas and on the lateral surfaces of the teeth and may also cover dental plaque and the dorsum of the tongue. One of their common features is that they do not stick to the tooth surface and are easy to remove by scraping. This type of staining is caused by mouthwashes containing cationic antiseptics when used for long periods of time.

Diagnosis

• Visual examination
• Probing
• Index evaluation (OHI-S, MacPherson Stain Index, Tooth Stain Index, etc.)

Treatment

• A dentist should explain to a patient why their teeth are stained and motivate them to add thorough oral hygiene techniques to their self-care routine. This includes correct toothbrushing techniques, flossing, and the use of appropriate personal hygiene products;
• A patient should be encouraged to quit smoking and chewing tobacco, and to alter their dietary habits (e.g., to consume moderate amounts of tea and coffee, use a straw to drink colored beverages, etc.);
• Individuals at high risk of black staining should try to drink bottled or osmotic filtered water as much as possible;
• It is recommended to use mouthwashes only if indicated; antiseptics should be prescribed for short-term use (less than 7–10 days);
• Pigmented plaque may be removed professionally; polishing using an abrasive toothpaste and rotating brushes and/or rubber cups, airflow polishing, and ultrasonic teeth cleaning have proven to be the most effective techniques.