Calculus Flashcards
Prevelance and systemic factors
Calculus is common amongst adult population and much less common in under 18s.
It’s occurance appears to increase with age and over 65 it’s high.
Presence more common in males than in females.
SYSTEMIC FACTORS
- patients in renal dialysis form calculus in large amounts. Due to elevated PH levels in saliva.
- in tube fed patients it’s formed at a higher rate compared to non tube fed patients. Due to lack of masticatory forces.
- patients taking beta blockers have reduction in calculus despite high levels of plaque. Also noted in patients on diuretics.
General points
- mineralised / calcified dental plaque. Hard and tenacious.
- example of extra osseous calcification meaning calcification outside the bone tissue. Also an example of dystrophic calcification which means in dead or decaying matter.
- matrix into which minerals are deposited and this is plaque.
- mineral content of supra gingival calculus derived from saliva and for sub gingival it’s derived from crevicular fluid.
- most prevalent near openings of salivary ducts ie lower anterior lingually and upper molars buccally.
- rough outer surface attracts plaque.
Supra gingival calculus
Tooth coloured so white/yellowish but as its rough it easily becomes stained, usually brown.
Hardness depends on degree of calcification. Often in thick layers usually relatively easy to remove compared to subgingivally. More rapid deposition of supra compared to sub.
Prior to 1960 it was considered the main pathogenic factor to periodontal disease and that its rough outer surface mechanically irritated adjacent gingival tissues.
Now it’s known that plaque is primary agent. However as calculus always covered in plaque therefore closely linked in many ways. Additionally calculus is porous and therefore retains toxic substances in close proximity to tissues.
The mechanism of supra gingival calculus will limit the self cleansing mechanisms as well as making OH procedures more difficult.
Amorphous and bulky. Oh, diet, individual tendencies and function and use can affect it. Forms interproximally between teeth or over gingival margins and may cover crown of tooth. Can be found on malpositioned teeth, hypo function, abrasion , openings of ducts.
Subgingival calculus
Found subgingivally often extending to base of a pocket. Sometimes sub becomes supra due to recession. Distribution of subgingival tends to be more generalised and no specific site however it’s presence is related to periodontal inflammation and disease.
Mineral content derived from crevicular fluid. Mineral salts in crevicular fluid precipitate into subgingival plaque forming hard deposit. This fluid is greatly increased in disease and inflammation meaning more calculus.
Often stated sub gingival calculus is a by product of disease.
Surface is very rough and attracts plaque. Colour tends to be very dark relating to blood pigments from damaged capillaries in the pocket depositing into calculus.
Subgingival calculus tends to be much harder and more difficult to remove than supra. Due to: greater mineralisation giving deposit brittle consistency, the nature of the mode of attachment of deposit to tooth surface and the fact you can’t see it.
Data supports the view that subgingival calculus contributes to chronocity and progression of periodontal disease. Clinical studies highlight importance of frequent and thorough removal through RSD in order to prevent attachment loss.
Permeability of calculus encourages high levels of toxins , notably high levels of toxic stimulators of bone resporption.
These factors along with increasing build up of plaque on the deposit has potential for increasing the displacement rate of the adjacent junctional epithelium and extending the radius of bone destruction beyond that of plaque alone.
Brittle, harder and dense , below gingival margin and extends to pocket. Sub gingival related to development of periodontal disease. It tends to be flattened due to pressure.
Preventive strategies
Many attempts to find other ways of removing calculus have been done. Until 1950s virtually all the calculus agents introduced were directed towards dissolution or softening of the deposit but were too damaging to tissues.
1960s focused on altering attachment of the organic matrix to the tooth by effecting it’s metabolic activities or chemical characteristics.
Researchers looked at altering plaque to limit its ability to calcify ie antiseptics and antibiotics. But none were safe enough.
Major anti calculus strategy in recent years is inhibiting crystal growth of deposit. This focuses on pyrophosphates which is now found in many anti calculus products and use of zinc salts although issue with taste.
Mineral content
Various salts including calcium and phosphates , magnesium and carbonates plus trace elements of zinc, iron etc found.
At least 2/3rds of inorganic content of calculus is in crystalline form.
Predominating crystal is hydroxyapatite. Other crystalline structures can be found including:
- calcium whitlockite
- octocalcium phosphate
- calcium brushite
Proportions of salts and crystals varies with the individual and area of calculus formation. Variation accounts for different appearances.
Theories of calculus formation
Basic theory must rely on deposition of minerals into an organic matrix as hard tissue. Most theories relate to physical , chemical and bacterial that exist in the mouth and several theories related to supersaturated mineral salts suspended in solution ie saliva or crevicular fluid. These salts held in solution by delicate mechanism of buffers and electrolytes.
PHYSIO-CHEMICAL THEORY
Applies to supragingival calculus only. Saliva secreted into the mouth and once it enters CO2 is released. This changes localised PH , it increases and becomes more alkaline and mineral salts from saliva precipitate out of saliva into plaque.
BACTERIAL-ENZYMATIC THEORIES
Could apply to supra and sub.
A. Filament type bacteria in plaque thought to produce an enzyme that produces localised alkaline reaction therefore creating precipitation of salts from either saliva or crevicular fluid and enter plaque.
B. Enzyme Phosphotase thought to be released by breakdown of epithelial cells and this will create a localised alkaline medium and precipitation of salts.
SERUMNAL THEORY
Applies to sub. Plaque causes inflammation and an increase in crevicular fluid which is released into the pocket. Bacterial by products create a localised alkaline medium which encourages precipitation of salts from the fluid and they therefore become available for deposition into subgingival plaque.
NUCLEATION THEORY
Most believe this is the most likely theory. Can apply to both supra and sub. Certain bacteria in plaque believed to be capable of bringing the mineral salts into a solution into the correct relationship with each other for formation of a salt crystal. This initial crystal then acts as a nucleus for further salt crystal formation. This process is often compared to seeding of an oyster with a grain of sand to form a pearl.
Structure
Calculus formation is 3 basic steps, acquired pellicle formation , plaque formation and maturation and mineralisation.
Formation of sub and supra is same apart from source of minerals. Colonies of bacteria grow together to form plaque layer and that mineralisation begins close to underlying tooth surface.
Mineralisation of plaque can proceed rapidly and may start a few hours after maturation. Concentrations of calcium and phosphate increase daily and bacteria serves as place of deposition.
Supra gingival calculus forms in layers parallel to tooth surface, layers are separated by a line microscopically which would appear to be the pellicle that deposited over calculus first layer.
Subgingival follows different path , it still forms layers but appears as small island of calculus in more random pattern.
Observed under electron microscope calculus appears as mountain like with peaks.
Organic framework of calculus is mostly bacteria along with epithelial cells , LEUCOCYTES , keratin and mucin, fatty acids, amino acids, carbohydrates etc.
Average time for plaque to become calculus is 12 days. However it’s possible it could form in 48 hours. Some people might never get calculus despite poor OH and heavy plaque.
How is calculus attached to the tooth
Calculus removed from some surfaces more easily than others and this could be how it’s attached.
ACQUIRED PELLICLE ATTACHMENT - often happens supra gingivally on enamel but can happen sub. Superficial mode and calculus would be easily removed.
ATTACHMENT TO IRREGULARITIES ON TOOTH OR ROOT
Inc cracks, carious defects etc
May be cementum fragmentation, tiny spaces left after loss of periodontal fibres. These would allow interlocking of deposit and be more difficult to remove.
ATTACHMENT DIRECTLY TO ROOT SURFACE
Interlocking of mineralising plaque with inorganic crystals of the root surface. May include penetration of bacteria into structure of the root and as deposit mineralises the bacteria become embedded and form connection between tooth and deposit. Direct interlocking would make very hard to remove.
Detection of calculus
Supra - clinical inspection. Use air to dry area, run a probe over, feel gritty.
Sub - tactile exam. WHO probe. Pick up roughness on root surface.
Other ways include dark edge round gingival margins, dark calculus may reflect through gingival tissue, radiographs.
Significance
Relationship to plaque - mineralised plaque so plaque prevention prevents calculus. Rough so attracts plaque.
Relationship to pocket - sub calculus always covered by active plaque which is in direct contact with crevicular epithelium. Sub calculus is secondary to pocket formation. With inflammation in pocket wall cause by plaque products more crevicular fluid therefore more minerals for calculus.
Limitation of self cleansing activity - calculus deposits alters shape of teeth. Eg pocket wall may be stretched out and bulky over sub calculus or supra may fill inter dental area. This interferes with self cleansing.
Relationship to plaqu control - plaque over calculus is too rough to remove with toothbrushing. ID calculus will shred floss.
Permeability - rough outer surface and permeable structure calculus acts as a reservoir for toxic microbial and tissue breakdown products .. inflammation therefore persists.
Drainage from diseased pocket - calculus can reduce drainage from those sites by helping trap bacteria and debris and healing will be prevented .periodontal abscess may result.
