Dental calculus is mineralized, mature plaque covered on its surface with nonmineralized plaque, material alba, desquamated epithelial cells, and formed blood elements The bacterial components are largely branched and unbranched filamentous microorganisms that are usually nonvital or display minimal metabolic activity.
These bacteria probably alay a role in the mineralization of dental calculus as inorganic crystals are frequently found within and around microorganisms. Structurally, calculus retains much of the histologic morphology of its plaque precursor.
Dental calculus may be classified as supragingival or sub gingival cased on location. It may also be classified as salivary or serurnal based on the source of inorganic salts that comprise ajculus. Root calculus is usually more strongly adherent tooth surfaces than that found on enamel surfaces.
The inorganic components of dental calculus deposits are primarily organized into crystalline structures that vary according to the age of the deposit. For instance, in mature calculus (>6 months). the major crystalline structure is hydroxyapatite CaPO4]6(OH) 2) with lesser amounts of octacalcium phosphate (Ca5 [HP04j4), whitlockite (Ca3[P04]2), and brushite CaHPO412H2O). In younger deposits (<3 months), brushite predominates, but with progressive aging, octacalcium phospihate. whitlockite, and finally hyclroxyapatite become more abundant.
Dental calculus deposits have also been described as radiographic apparent The radiographic detection of calculus is positively influence by the thickness of the deposit, the amount of surface area covered by the deposit, and the anatomy of the tooth. Only 40% to 50% of calculus deposits will be radio- graphically apparent.
Therefore, radiographs should not solely be used to measure the presence or absence of calculus.
How Does Calculus Attach to Teeth? Do the Attachment Mechanisms Have Any Clinical Significance?
Dental calculus will attach to tooth surfaces by several mechanisms. The most common mechanism of supragingival calculus attachment to smooth enamel surfaces is salivary pellicle, and it is usually easily removed using ultrasonic or hand instrumentation. The irregularities of unrestored caries and defective dental restorations complicate the removal of supragingival calculus.
The attachment of subgingival calculus is further complicated by microscopic irregularities in cementum such as cemental tears, cemental voids once occupied by Sharpeys fibers, resorption bays, and other surface cemental defects.
It is for these reasons that clinicians will further designate calculus deposits as either coronal or radicular to reflect the relative tenaciousness of radicular and coronal dental calculus, and in the case of radicular calculus, the difficulty they may have in achieving total calculus removal during root planning.
What Is the Pathogenic Potential of Calculus?
The current view is that dental calculus exerts its pathogenic potential as a contributing factor that fosters plaque formation and promotes its retention on teeth. Also, there is little question that the microbial composition of calculus provides bacterial factors that, by themselves, produce an inflammatory reaction in tissue.
Bacterial components (outer membrane besides containing LPS, cell wall material containing Iipoteichoic acids, periplasmic and cytoplasmic enzymes, and bacterial metabolic factors) are all suspect pathogenic factors in dental calculus. The persistent inflammation in gingival tissue predictably seen adjacent to reasonably plaque free calculus is unequivocal evidence of the pathogenic effect of calculus.
Aside from this, the rough surface of dental calculus is usually covered with a layer of plaque biofilm. As such, calculus tends to present plaque to periodontal soft tissues and interfere with efforts to improve plaque control. The physical removal of dental calculus remains a critical component of mechanical periodontal inflammatory disease control.