Dental calculus: recent insights into occurrence, formation, prevention, removal and oral health effects of supragingival and subgingival deposits

Abstract

Dental calculus, both supra- and subgingival occurs in the majority of adults worldwide. Dental calculus is calcified dental plaque, composed primarily of calcium phosphate mineral salts deposited between and within remnants of formerly viable microorganisms. A viable dental plaque covers mineralized calculus deposits. Levels of calculus and location of formation are population specific and are affected by oral hygiene habits, access to professional care, diet, age, ethnic origin, time since last dental cleaning, systemic disease and the use of prescription medications. In populations that practice regular oral hygiene and with access to regular professional care, supragingival dental calculus formation is restricted to tooth surfaces adjacent to the salivary ducts. Levels of supragingival calculus in these populations is minor and the calculus has little if any impact on oral-health. Subgingival calculus formation in these populations occurs coincident with periodontal disease (although the calculus itself appears to have little impact on attachment loss), the latter being correlated with dental plaque. In populations that do not practice regular hygiene and that do not have access to professional care, supragingival calculus occurs throughout the dentition and the extent of calculus formation can be extreme. In these populations, supragingival calculus is associated with the promotion of gingival recession. Subgingival calculus, in "low hygiene" populations, is extensive and is directly correlated with enhanced periodontal attachment loss. Despite extensive research, a complete understanding of the etiologic significance of subgingival calculus to periodontal disease remains elusive, due to inability to clearly differentiate effects of calculus versus "plaque on calculus". As a result, we are not entirely sure whether subgingival calculus is the cause or result of periodontal inflammation. Research suggests that subgingival calculus, at a minimum, may expand the radius of plaque induced periodontal injury. Removal of subgingival plaque and calculus remains the cornerstone of periodontal therapy. Calculus formation is the result of petrification of dental plaque biofilm, with mineral ions provided by bathing saliva or crevicular fluids. Supragingival calculus formation can be controlled by chemical mineralization inhibitors, applied in toothpastes or mouthrinses. These agents act to delay plaque calcification, keeping deposits in an amorphous non-hardened state to facilitate removal with regular hygiene. Clinical efficacy for these agents is typically assessed as the reduction in tartar area coverage on the teeth between dental cleaning. Research shows that topically applied mineralization inhibitors can also influence adhesion and hardness of calculus deposits on the tooth surface, facilitating removal. Future research in calculus may include the development of improved supragingival tartar control formulations, the development of treatments for the prevention of subgingival calculus formation, the development ...

Gingival recession, oral hygiene and associated factors among tanzanian women

“…The association between gingival recession and calculus in this study is in agreement with results for other populations in Tanzania (16,27), Brazil (26) and elsewhere (20). The explanation for this is thought to be due to mechanical displacement of the gingival tissue by calculus deposits as well as toxins from both the viable microbial plaque and that which is harboured within the calculus deposit (28). Also in this study, there was an association between gingival recession and gingival bleeding, which was in agreement with other reports (2,29).…”

Evaluating microfossil content of dental calculus from Brazilian sambaquis

“…Various systemic factors, including disease, affect the amount of deposition as well as the velocity of deposition of dental calculus (Beiswanger et al, 1989, Lieverse, 1999, Poff et al, 1997, Epstein et al, 1980, Mandel, 1995, Scheie, 1994, Shasha et al, 1983, Eigner et al, 1986and Fujimaki et al, 1998. Levels and location of calculi are population-specific and are influenced by ora1l hygiene habits, diet, age, ethnicity, and use of teeth as tools (White, 1997). In this regard, some prehistoric habits that might have limited calculus formation include quid-chewing, abrasive diets, and preparing fibers for cultural uses using the teeth.…”

Patients with dental calculus have increased saliva and gingival crevicular fluid fetuin-A levels but no association with fetuin-A polymorphisms

“…5,6 Other factors that influence calculus formation are age, gender, eating habits, oral care, bacterial composition, host response, systemic diseases and prescribed medications. 7 Futhermore, it is thought that genetic factors can play a role on calcification. Polymorphisms of several protein genes, as fetuin-A and matrix gla protein (MGP), that affect calcium metabolism have been investigated in studies because they may potentially have a critical and key role in the calcification-related diseases.…”