Dental calculus
Dental biofilm mineralized by crystals of calcium phosphate mineral salts between previously living microorganisms.
Supragingival calculus
Location: forms on clinical crowns coronal to the margin of the gingiva.
Distribution: heavy on sites opposite to salivary ducts, teeth out of occlusion, nonfunctioning teeth, and teeth that are not cleaned of biofilm daily.
Subgingival calculus
Location: forms apical to the margin of the gingiva and extending toward the clinical attachment on the root surface.
Distribution: generalized or localized. Heaviest deposits are on hard to clean areas. Will typically form at the cementoenamel junction during recession. Darker color because of exposure to blood and blood breakdown products.
Factors in rate of calculus formation
Genetic and individual variation in saliva composition and flow. Diet, individual variations in bacterial load, age, race, gender, more severe periodontal disease, malposition and crowding of teeth, lower levels of s.mutans, inhibitors of calculus formation
Precursor to calculus mineralization
Nonmineralized biofilm is necessary for initiation of calculus formation. In Supragingival biofilm, filamentous microorganisms are orients at a right angel to teh tooth and proved the matrix for the deposition of minerals.
In subgingival biofilm, cocci, rods, and filamentous bacteria do not form a distinct pattern in relation to teh tooth.
Mechanism of calc mineralization
Supersaturation of saliva is teh driving force for mineralization
Dead microorganisms degrade and minerali deposition begins using teh cell walls of teh bacteria.
Calcium phosphate crystals form
Final stable phase occurs around 8 months.
Calculus from sin layers.
Supra calc avg 38%
Sub calc avg 58%
Types of calc deposits
Crusty, spiny, or modular deposits
Ledge or ring
Thin, smooth veneers
finger-and firm like formations
Individual calculus islands or spots.
Formation time
Average time for teh primary soft deposit to change to the mature mineralized stage is about 12 days.
Mineralization can begin within 24-48 hours, 50% mineralized in 2 days, 90% mineralized in 12 days.
Final stable phase of calculus occurs around 8 months.
Attachment by means of an acquired pellicle
In early calculus formation the attachment is superficial because no interlocking with the tooth surface occurs and calculus can be easily removed.
Attachment to minute irregularities in the tooth surface
Dentin irregularities include cracks, resorption, and carious defect.
Cemental irregularities include tiny spaces left and previous locations of sharp’s fibers. Calculus is difficult to remove when it is attached because it becomes locked into the irrregularities.
Attachment by direct contact with the tooth surface
Interlocking of inorganic apatite crystals of the enamel and cementum with the calcium phosphate crystals of the calculus. Research suggests this mode of attachment results in a portion of the calculus that is prone to fracture during removal, but it may leave calculus crystals attached to the tooth surface.
Clinical implications of calculus
Calculus is always covered by a layer of unmineralized viable biofilm and it is likely the biofilm is responsible for the intimidation of teh immune response in gingivitis and periodontitis.
Supragingival characteristics
Color: white, creamy yellow, gray
Shape: amorphous, bulky, form a bridge, extend over the margin of the gingiva, based on anatomy of tooth.
Consistency and texture: moderate hard
Size and quantity: depends of personal oral-self care, diet, individual characteristics, such as salivary flow, position of teeth, use of tobacco
Distribution: coronal to margin of gingiva. Rafted to opening of salivary gland duct.
Subgingival characteristics
Color: light to dark brown
Shape: conforms to root surface, modular, ledge or ring like, smooth veneers, finger and fern like, islands
consistency and texture: harder and more mineralized
Size and quantity: related to personal oral care, age, bacterial load, disease severity
distribution: apical to margin of gingiva, extends to bottom of the pocket. Heaviest on proximal surfaces.
Supragingival examination
Can be seen directly or indirectly using a mouth mirror. Or use of compressed air they can become visible when once hidden by saliva.
Subgingival examination
Visual examination: dark edges bay be seen just below gingival margin or gentle air blast can deflect gingival margin to see
Gingival tissue color change: dark shadow
Tactile examination: wine probing a rough subgingival tooth surface or exploring can detect calculus deposits.
Radiographic: may detect large calculus deposits
Dental endoscopy: detect other wise undetectable calculus.
Prevention of calculus
Personal dental biofilm control: remove by brushing, interdental care, and supplementary methods
Make sure you educate the patient.
What creates disease
A mixed infection of bacteria in biofilm + Host Response = Disease
Composition
Inorganic: primarily calcium, phosphorus, carbonate, sodium, magnesium, trace elements, fluoride, crystals
Organic: dead epithelial cells, Leukocytes, mucin from saliva, lipids, phospholipids, proteins.
Crystal formation
Brushing: new calf
Octoclacium phosphate: Supra
Whitlockite: sub
Hydroxyapatite: final stable phase occurs around 8 months.
Increased calculus formation
Concentration of calcium and phosphate in saliva. Decreased level of home care. Malposition and crowding of teeth. Low levels of pyrophosphates and zinc salts, frequent use of chlorine iodine gluconate, lower levels of S. Mutants, High levels of alkaline foods and silicon (rice and refined carb based diets)
Anti calculus agents
Does not reduce amount of calculus already present. Has no measurable effect on subgingival calculus; may prevent new Supra. Proper toothbrushing alone can reduce calculus levels by up to 50%, use has in some cases caused soft tissue irritation or dentinal hypersensitivity.