Calculus update: prevalence, pathogenicity and prevention

Calculus Update: Prevalence, Pathogenicity and Prevention IRWIN D. MANDEL, D.D.S.

CALCULUS: ITS EARLY HISTORY Does reduction of supragingival

A

stute observers in several ancient societies noted

calculus provide only a cosmetic effect, or does it benefit oral

the association between tooth deposits and oral

health as well? The author dis-

problems. Hippocrates (460-377 B.C.) referred to

cusses the causes and effects

of calculus development and reviews methods of calculus

the deleterious effects on the gums and teeth of pituita or

calculus, which "insinuates itself under the roots of the

control.

teeth." The Romans, concerned with personal grooming,

developed instruments for scaling the teeth and advocated scaling and polishing as important features of oral care. But it was the Arabian physician-surgeon Albucasis (9631012 A.D.) who most clearly enunciated the relationship

between calcified deposits and "corruption of the gums and

suppuration around the teeth." Convinced of the need for meticulous removal of "rough and ugly scales," he

designed a special set of 14 instruments-the progenitors of our modern armamentarium-and described in detail the process of removal. Indeed, his specific instructions are

applicable to this day.' JADA, Vol. 126, May 1995 573

-CO

YVER STORY joints, Paracelsus considered tartar the principal causative

Figure 1. Calculus in U.S. employed population.8

factor of certain maladies he termed "tartaric diseases."2 Until the middle of the 20th century, calculus was the king of the etiological hierarchy in periodontal disease. Like most 20th century monarchs, however, it was deposed-by an unruly mix of microorganisms, the bacterial plaque. From 1960 to 1985, calculus was relegated to a supporting role at best, and plaque was pursued as the primary cause of periodontal disease. In the last 10 years, however, researchers have reconsidered the effect of supragingival calculus on gingival recession3"4 and of subgingival calculus on the extension and progression of periodontal disease.5 Research documents the importance of regular removal of calcified deposits in periodontal therapy and of the clinical value of anti-calculus dentifrices.5'6 Calculus has regained respectability and status. PREVALENCE AND INCIDENCE OF CALCULUS

Figure 2. Calculus in U.S. adults older than 65 years ,8

Paracelsus, a Swiss-German physician and alchemist, introduced the term "tartar" as a designation of a variety of stone-like concretions that form in various organs in about 1535. He noted the physical resem574 JADA, Vol. 126, May 1995

blance between these deposits and those that form at the bottom of wine casks from potassium bitartrate. Observing that these tophi could be found about the teeth, in the urinary and gall bladders and in gouty

I n the mid-1980s, the National Institute of Dental Research conducted large-scale epidemiologic surveys of the oral health status of U.S. school children and adults.78 These studies serve as a reliable indication of the prevalence of supra- and subgingival calculus in the U.S. population. In the survey of school children, supragingival calculus was noted in 34 percent of 14-to 17-year-olds and subgingival deposits in 23 percent.9 In the National Survey of Oral Health in U.S. Employed Adults (ages 18 to 65) conducted from 1985 to 1986, only 13 percent of the

COVER STORY employed males and 20 percent of the employed females had no calculus. Among those who formed calculus, supragingival deposits were found in 25 percent to 30 percent and subgingival deposits in 40 percent to 55 percent (Figure 1). In the senior

population

(those older than 65), 20 percent had supragingival calculus and 60 percent to 65 percent had subgingival calculus (Figure 2). In a more recent prevalence study involving 1,426 adult males and females in Indiana, researchers used a more quantitative index than that employed in the national surveys. The general findings were similar: males have more calculus than females and calculus formation was directly related to age for both sexes.'0 Researchers also studied the incidence of supragingival calculus among a panel of 980 subjects in Texas by quantitating deposits on the lingual surfaces of the six mandibular anterior teeth, six months after professional prophylaxis. The same general pattern prevailed for incidence as for prevalence: the males had higher scores than females, and the scores were directly related to age. In the incidence study, about 5 percent of subjects of both sexes formed no calculus over the six-month period, and about 5 percent of either sex had extremely high calculus scores."° The prevalence of calculus in

any population, in large measure, reflects the oral hygiene habits of the group members and the frequency of professional care. In a longitudinal study of Norwegian men who had received regular dental care and had been examined from 1969 to 1988, the calculus findings were comparable to the findings in the U.S. SurX i |National vey.'1 In a companion study of Sri Lankan tea plantation laborers who had virtually no oral hygiene or dental care, researchers found that all of the study participants had calculus on almost all tooth surfaces by the age of 40.1"

<0

ETIOLOGY OF CALCULUS

Systemic factors. A number of systemic situations can affect the amount and rate of calculus formation. Patients on dialysis usually form calculus in large quantities due to the elevated pH of their saliva, which in turn is caused by the high urea content between treatments.'2 In studies involving tube-fed patients, calculus formed at a significantly higher rate compared to non-tube-fed control subjects when oral hygiene levels were comparable,'3 or even when oral hygiene was superior in the tube-fed group.14 This most likely results from the lack of mastication in the tubefed patients. Calculus development is similarly elevated in patients who have open bites and those who have teeth without opponents.

An interesting recent finding-very apropos for an aging population-was that people being medicated with beta blockers, diuretics, anticholinergics, synthroid and allopurinol had a statistically significant reduction in calculus, compared to their non-medicated counterparts, despite the presence of a high quantity of plaque."5 The mechanism of this effect remains to be established. Calculus-caries relationship. Although an inverse relationship between calculus and caries has long been postulated (and anecdotally reported)since the plaque environments conducive to the two processes would appear to be mutually exclusive (caries occurring in an acid environment and calculus in an alkaline one)-the actual supporting data have been inconclusive. Over the years, typical studies have shown only a slight inverse relationship'6 or no relationship at all.17 Several recent reports document the same disparity. For example, an analysis of eight three-year caries clinical trials involving 11- and 12-year-olds compared the DMFS increments for calculus formers and non-formers."8 At baseline, the DMFS increment was 20 percent to 30 percent less among calculus formers in seven of the eight trials, and 6 percent less in the eighth, than that of nonformers. On the other hand, a study involving 439 11- to 13year-olds in Thailand found no significant association between calculus status and caries occurrence.19 Apparently, the association is so modest that it requires a very large sample size to demonstrate a statistically significant relationship, if one does in fact exist. JADA, Vol. 126, May 1995 575

-COVER SIORY PATHOGENIC POTENTIAL OF SUPRA- AND SUBOINGIVAL CALCULUS

upragingival calculus. Before 1960, calculus was

considered

a

L 1 pathogenic factor in periodontal disease because of its rough outer surface, which mechanically irritated the adjacent tissues. We now recognize that calculus-mineralized plaque-is covered on its external surface by unmineralized plaque, the prime etiologic agent of periodontitis. Calculus, however, can promote and retain plaque accumulations. Additionally, calculus is porous and can retain toxic substances.52022

The issue, therefore, is whether calculus with its overlying plaque is more damaging than plaque alone. The answer is not clear. The equivocation is the result of the experimental design of most epidemiologic and therapeutic studies: mean soft deposit and mean hard deposit scores are related to mean gingivitis scores. These studies do not show a significant association between calculus and gingivitis.5 Because only a small percentage of the surfaces exhibit supragingival calculus, however, the opportunity to assess a site-specific, depositrelated gingival impact is lost. In a study in which different sections of the mouth were evaluated and a retentive calculus index was employed, researchers documented "a linear increase in the gingival index with increasing per tooth index values of retentive calculU

.s 2

The prevailing view is that supragingival calculus enhances gingival inflammation by promoting and retaining new 576 JADA, Vol. 126, May 1995

plaque accumulations.5'24 The presence of

TABLE

I

supragingival

calculus limits natural selfcleaning mechanisms, makes oral hygiene more difficult and reduces drainage from crevicular

Acids, spring salts Sodium ricinoleate

areas.'524

Recent clinical studies have shown that there is a statistical relationship between the amount of calculus and total gingival reces-

TABLE 2

sion.3 4

Subgingival calculus. Considerable data support the view that subgingival calculus contributes to the chronicity and

Pyrop

progression

Pyrophosphates, Nap,

of

op

hates azic-4X-

Galtrez

c

(methoxyethelene/imaleic acid) periodontal disease.5 CliniCitroxain and sodium citrate cal studies Calcium lactate attest to the importance of Mechas;im nt establis'hed. frequent and thorough removal of root deposits by scal- phological studies that showed that calcified deposits are ing and root planing to prevent attachment loss.25 Diabetics porous and could act as a reservoir for irritating substances with good, moderate or even that affect disease progrespoor glucose control had minision. 19.21 mal periodontitis when there Experimental studies estabwas no calculus. Poor-control lished the permeability of subpatients, however, developed gingival calculus to endotoxin27 extensive periodontal pocketing as well as the presence of high when calculus was present.26 levels of toxic stimulators of This could be explained by mor-

COVER STORY bone resorption and antigens from Bacteroides gingivalis in calculus deposits.28 This, combined with the increasing buildup of plaque on the surface of calculus, has the potential for increasing the displacement rate of the adjacent junctional epithelium and extending the radius of bone destruction beyond that of plaque alone.5 Thorough removal of the porous, toxin-retentive subgingival calculus is key in periodontal therapy. For the most graphic description of the destructive capacity of calculus, we can turn to the novelist Gunter Grass in his book "Local Anesthetic." He writes, "Your tartar is your calcified hate. Not only the microflora in your oral cavity, but also your muddled thoughts, your obstinate squinting backward, the way you regress when you mean to progress, in other words, the tendency of your diseased gums to form germ-catching pockets, all that-the sum of dental picture and psyche-betrays you: stored up violence, murderous designs."29 PREVENTIVE STRATEGIES

Given the widespread presence of calculus, and the labor intensity, expense and discomfort of its mechanical removal, there have been many attempts at developing chemical approaches to calculus removal and inhibition. Until the mid-1950s, virtually all of the many anticalculus agents introduced were directed toward the dissolution or softening of the established deposits. Most of the substances were decalcifying, complexing or chelating agents. Unfortunately, these damaged the tooth sub-

stance, especially cementum and dentin, because of the comparable nature of the inorganic components and had to be abandoned.5'30 A few agents were aimed at affecting the calculus matrix, the bacterial and interbacterial scaffolding that maintained the mineralized structure. One agent, sodium ricinoleate-the salt of fatty acids from castor oil-showed promise in reducing early calculus deposits but failed because of its unacceptable taste (Table 1).5

In the 1960s, the emphasis changed from attempting to alter the mature deposits to preventing the buildup of the early mineralized plaque. Researchers employed two major strategies: altering the attachment of the organic matrix to the tooth; and modifying the nature of the plaque by affecting its metabolic activities or chemical characteristics.30 The attempts to modify plaque attachment, primarily through the use of silicones or sulfonated polystyrene ionexchange resins, were unsuccessful because they were easily abraded and lasted only a short time. Modifying the plaque seemed to be more

promising. Researchers next attempted to alter plaque to limit its ability to calcify. The agents

employed included antiseptics and antibiotics, a number of enzymes and enzyme combinations, and other matrix disrupting agents such as Ascoxal, a non-specific mucous depoly-

merizing agent combined with ascorbic acid, sodium percarbonate and copper sulphate; and 30 percent urea, a protein denaturant. Although some of these studies initially indicated potential for reducing calculus formation, none of the

agents were

effective or safe enough to warrant continued research, at least as far as the supporting companies were concerned. For example, the macrolide antibiotic niddamycin (CC 10232), used as a mouthrinse at a concentration of 0.01 percent, was effective against calculus as well as plaque.31 Research was discontinued, however, because of concern about development of cross-resistance to other antibiotics. The major anti-calculus strategy developed in the 1970s was inhibiting crystal growth and thus preventing development of mineralized plaque. This remains the approach of choice in most of the current anti-tartar products. Research initially focused on pyrosphosphate, because of its important role in the mineralization process,32 but preliminary studies indicated rapid breakdown in the oral cavity by bacterial and, to a lesser extent, host phosphatases and pyrophosphatases. Therefore, researchers developed an analog, diphosphonate, in which substitution of two oxygens by carbon yielded a molecule less susceptible to bacterial hydrolysis. Studies involving 200 adults who used a dentifrice JADA, Vol. 126, May 1995 577

p-COVER STORY containing 3 percent sodium etidronate (the diphosphonate used) and 0.22 percent sodium fluoride over an 18-month period documented the clinical effects.33 At the end of the study, there was a 42 percent reduction in the amount of supragingival calculus. This formulation was never marketed nationally. It's notable that despite the dentifrice's considerable effect on calculus, it did not reduce

gingivitis. During the

1970s, considerable interest developed in the use of zinc salts as anti-calculus (as well as antiplaque agents)34 because of their ability to affect crystal growth. This interest continued into the 1980s and 1990s, and a number of clinical studies have been conducted. In one study with an experimental dentifrice containing 2 percent zinc chloride and 0.22 percent sodium fluoride, there was a significant reduction in calculus at the end of six months.35 Several other studies showed reductions in supragingival calculus in the 35 percent to 50 percent range.36 Despite the high level of effectiveness of 2 percent zinc chloride, commercialization was limited because of the difficulty in masking the disagreeable taste. When researchers replaced the 2 percent zinc chloride by 0.5 percent zinc citrate to improve 578 JADA, Vol. 126, May 1995

the taste in several subsequent studies, reductions of only 0 percent to 14 percent were noted.36 However, when 0.5 percent zinc citrate is combined with 0.2 percent triclosan (an effective antibacterial agent), reductions of up to 50 percent in

supragingival calculus have been report* n the * 1980s, C lflthere was a ~ resurgence of interest >~in the pyrophosphates. A series of clinical studies demonstrated the anti-calculus effect of dentifrices that contained various combinations of pyrophosphate salts combined with sodium fluoride. These initial studies have been reviewed by Lobene and Volpe.39 Apparently, the sodium fluoride is in sufficient concentration to serve as an anti-enzyme and at least partially inhibit the bacterial pyrophosphatases, allowing the relatively high concentrations of pyrophosphate salts to inhibit crystal growth and reduce calculus formation. The addition of 1 percent of a copolymer of methoxyethelene and maleic acid (Gantrez, GAF Corp.) in some products seems to enhance the inhibiting effect on the pyrophosphatases and improve the effectiveness of anti-tartar products containing pyrophosphate salts. As previously noted, several studies of

12-month duration with soluble pyrophosphate and the copolymer also have shown a significant reduction (17 percent to 25 percent) in gingival recession as well as in supragingival calculus, when compared to a placebo.34 Promising initial results have been reported for several other anti-calculus formations. A dentifrice containing Citroxain, a mixture of the enzyme papain, alumina and sodium citrate, showed significant reductions in plaque and calculus when compared to a standard pyrophosphate tartar control dentifrice in two three-month studies.40'4 Long-term safety data is needed because of concern that the sodium citrate, a calcium-complexing agent might affect normal mineral in exposed cementum and dentin of root surfaces. Papain, the enzyme ingredient in the product, potentially could affect the collagen in the root surface area.42 After promising preliminary studies,4344 a recent three-month clinical trial with a calcium lactate-containing dentifrice45 showed a significant reduction of about 45 percent in calculus accumulation when compared to a control paste. This reduction occurred despite an increase in plaque calcium levels, contrary to the conventional expectation. The mechanism is as yet unexplained. Plaque accumulation was not affected. Although an agent is effective in reducing plaque, there is no guarantee that it will reduce calculus. Chlorhexidine mouthwash, for example, can reduce plaque significantly, but it also can cause an increase in supragingival calculus deposits.46 Researchers have observed that good toothbrushing can

COVER STORY slow the rate of calculus deposition. Using a quantitative scoring procedure, Villa47 was able to demonstrate that thorough,

of calculus reduction are major determinants of a purely cosmetic vs. a combined cosmetic and health effect. What is

habitual tooth-

unambiguous -----

brushing alone could reduce calculus formation by as much as 50 percent on the lingual surfaces of the lower anterior teeth. However, given the inadequate nature of oral hygiene as practiced by most people, an anti-calculus reenforcement with effective dentifrice formulations is a welcome addition to preventive dentistry.

at this time is that we now have an array of anti-calculus agents, combinations and products that

-

CONCLUSION

hile the importance of

subgingival

cal-

culus in the chronicity and progression of periodontal disease is becoming increasingly evident, supragingival calculus still languishes in pathogenic limbo. Does reduction in supragingival calculus provide only a cosmetic effect or does it affect oral health as well? Part of the difficulty resides in the limitations of the scoring methods most frequently employed. When the traditional methodologies are used, statistically significant reductions in supragingival calculus usually are not associated with significant reductions in gingivitis. Recent studies, however, have shown a reduction in gingival recession accompany-

ing the reduction in calculus scores. It may be that the length of a study and the degree

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