Reduction of Dental Calculus in Humans Through the Use of a Dentifrice Containing a Crystal‐Growth Inhibitor

Sturzenberger, O. P.; Swancar, James R.; Reiter, Gabriel

doi:10.1902/jop.1971.42.7.416

Cited by 49 publications

(13 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, their clinical action is not in reducing the rate of development but in reducing the maximum levels of tartar formation on the teeth. Examples include clinical studies carried out by Suomi et al (1974), Schiff (1987) and Sturzenberger et al (1971). In addition to these clinical effects, research has recently demonstrated that inhibitors have no apparent effect on the long term composition of dental calculus, despite their presumed action in preventing the maturation of calcium phosphates within early deposits.…”

Section: The Importance Of Adhesion/cementation To Calculus Formationmentioning

confidence: 99%

Processes contributing to the formation of dental calculus

White

1991

Biofouling

View full text Add to dashboard Cite

Dental calculus is a petrified plaque biofilm. Calculus removal requires professional scaling procedures as a result of its physical hardness and strong attachment to the teeth. The aim of this paper is to review chemical (MD, Ca, P, F), physical (hardness, adhesive strength), ultrastructural (SEM, TEM), and clinical data on calculus in order to provide perspective on the roles that adhesion and cementation play in tartar development. SEM, TEM and microradiographic analyses of deposits in cross section show that calculus mineralizes in successive layers of varying thickness. Chemical analysis shows that plaque mineralization occurs rapidly (on a clinical time scale, < 2 wks on average) with the formation of calcium phosphate crystals contributing up to 80% of the weight of deposits. Although calculus adheres strongly to the teeth (up to 4,000 kN.m -2 in attachment force) the hardness measures only 10-20% of sound enamel (20-40 Vickers Hardness Numbers). The clinical formation of calculus (measured as the area coverage on the teeth) follows a rapid course, levelling off after 2-3 months. Crystal growth inhibitors reduce the maximum plateau of calculus coverage but do not alter the mineral composition of mature deposits. These findings support the view that calculus formation is strongly affected by the adhesion of mineralizing plaques onto existing deposits. Maximum tooth coverage with supragingival calculus is affected by the time period of cementation of plaque layers (influenced by plaque formation and mineralization rates) and average frictional forces (mastication/ toothbrushing) acting on appositional layers. Tartar control action by current technologies can be thought of as "antiadhesive" in the sense that lengthened time periods of plaque petrification permit cleansing of softer deposits by patients using normal hygiene methods. The development of technologies for the "complete" control of calculus development must take into account the strong role of adhesion/cementation in tartar formation.

show abstract

Section: The Importance Of Adhesion/cementation To Calculus Formationmentioning

confidence: 99%

Processes contributing to the formation of dental calculus

White

1991

Biofouling

View full text Add to dashboard Cite

show abstract

“…The diphosphonate EHDP acts against calculus formation [Sturzenberger et al, 1971;Herforth, 1976], although it does not improve gingival health [Suomi et al, 1974]. The different effect of EHDP on experimental caries in the in vitro as op posed to the ICT system can be explained in the following way.…”

Section: Discussionmentioning

confidence: 99%

“…The effects of the anticalculus agent disodium ethane 1,1-diphosphonate (EHDP) on dental caries are still question able [Sturzenberger et al, 1971;Herforth, 1976], Whereas the general agreement is that EHDP inhibits demineralization in vitro, the reports on the effects of diphos phonate on remineralization are still con troversial. Brineret al [1971], Miihlemann and Aeschbacher [1970], and ten Cate et al [1981], demonstrated, in experimental ani mals and in vitro, respectively, the inhibi tion of enamel maturation and remineral ization by EHDP.…”

mentioning

confidence: 99%

Comparison of Diphosphonate Effects on Enamel in vitro and in vivo

Wöltgens¹,

Koulourides²

1983

Caries Res

View full text Add to dashboard Cite

Enamel was exposed to diphosphonate solutions (EHDP) in vitro and in vivo. EHDP inhibited remineralization in vitro, but increased the resistance against acid when incorporated in the enamel. In vivo EHDP acted differently. This may be explained by additivity of the effect of EHDP on acid formation in plaque and the effect of surface active salivary molecules to the inhibition of EHDP on de- and remineralization as was found in the in vitro experiments.

show abstract

“…These findings suggest that a Percentage of total organic phosphorus (in residue and solution) in the aqueous solution, corrected for presence of diphosphonates, when phosphatidyl serine or complexed lipids are dispersed in 5 ml acetate-buffered (pH 5), Tris-buffered (pH 7.4), or NH4OH-NH4Cl-buffered (pH 9) aqueous solutions. Each "value is the combined average • of measurement for 3 measurements on PS and 3 measurements on Ca-PL-PO4 complex Other bar shows amount of organic P in residue following dispersion of 0.2 mg PS in 10 ml of the various EHDP solutions diphosphonates have been shown to inhibit dental calculus formation in human and animal models (15,(30)(31)(32)(33)(34); it has been postulated that both these systems involve lipids (32,35). In addition, diphosphonates have been found to prevent cholesterol-induced atherosclerotic plaque formation in experimental animals (36).…”

Section: Discussionmentioning

confidence: 99%

Effect of diphosphonates on hydroxyapatite formation induced by calcium-phospholipid-phosphate complexes

1979

View full text Add to dashboard Cite

The diphosphonates disodium ethane-1-hydroxy-1, 1-diphosphonate (EHDP) and disodium dichloromethylene diphosphonate (Cl2MDP) prevent hydroxyapatite (HA) formation in metastable calcium phosphate solutions, induced by calcium-phospholipid-phosphate complexes and by the acidic phospholipids phosphatidyl serine and phosphatidyl inositol. The diphosphonates appear to act not only as HA crystal poisons but also as surfactants which probably change the nature of the lipid micelle and the charge and conformational properties of the lipid molecules. The surfactants sodium dodecyl sulfate (SDS) and Non-Idet P-40 (NP-40), like the diphosphonates, prevent HA formation by the acidic phospholipids and complexed lipids, but do not act as HA surface poisons. The lipid surfactant lyso-phosphatidyl serine did not induce HA formation from solution. The relevance of the ability of the diphosphonates to act as lipid surfactants to the in vivo use of these agents is discussed.

show abstract

Reduction of Dental Calculus in Humans Through the Use of a Dentifrice Containing a Crystal‐Growth Inhibitor

Cited by 49 publications

References 5 publications

Processes contributing to the formation of dental calculus

Processes contributing to the formation of dental calculus

Comparison of Diphosphonate Effects on Enamel in vitro and in vivo

Effect of diphosphonates on hydroxyapatite formation induced by calcium-phospholipid-phosphate complexes

Contact Info

Product

Resources

About