Eur J Oral Set 1997: 105: 508-522 Copyright C' Stunksi'uurd }997

Primed in UK. All rif^lils ri-servcd EUROPEAN JOURNAL OF

ORAL SCIENCES
ISSN 0909S836

Donald J. White
Dental calculus: recent The Procter and Gamble Company, Health
Care Research Center, Mason. OH, USA

insights into occurrence,

formation, prevention,
removal and oral health
effects of supragingival and
subgingival deposits
White DJ: Dented calculus: recent insights into occurrence, formation, prevention,
removal and oral health effects of supragingival and subgingival deposits. Eur
J Oral Sci 1997: 105: 508-522. Munksgaard, 1997

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 lo inability to clearly dilTerentiate 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 inliammation. Research suggests that
subgingival calculus, at a minimum, may expand the radius of plaque induced
periodontal injury. Removal of subgingival plaque and calculus remains lhe Donald J. White, The Procter and Gamble
cornerstone of periodontal therapy. Calculus formation is the result of Company, Health Care Research Center,
petrification of dental plaque biofilm. with mineral ions provided by biithing 8700 Mason-Montgomery Road, Mason,
OH 45040-9462, USA
saliva or crevicular fluids. Supragingival calculus formation can be conlrolled
by chemical mineralization inhibitors, applied in toothpastes or mouthrinses. Telefax: +1-513-6220413
These agents act to delay plaque calcification, keeping deposits in an E-mail: White.DJ.1@PG.com
amorpho^us non-hardened state to facilitate removal with regular hygiene.
Key words: calculus; tartar; plaque; biofilm;
Clinical eflicacy for these agents is typically assessed as the reduction in tartar mineralization
area coverage on the teeth between dental cleatiing. Research shows that
Accepted for publication July 1997
 Dental ealculus: current understanding 509

topically applied mineralizalion 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 of improved methods for
root detoxification and dcbridement and the development and application of
sensitive diagnostic methods to assess subgingival debridement efficacy.

the many substances present in mature calculus

Dental calculus: definition, localization,
composition
The definition, localization and composition of
dental calculus are well known {see 1-5). Calculus
is mineralized dental plaque which forms both
above (supragingival) and below (subgingival) the
gumline. Once highly mineralized, calculus can
become cement-like in terms of both physical hard-
ness (Vickers Hardness averaging 30-40 units,
maximum observed ^ 190) (6) and adhesive
strength (7-8). We have recorded developed forces
up to 2.0 kg required for calculus removal during
scaling (9). While the substrate for subgingival
calculus is hmited to root surfaces, supragingival
calculus can occur on enamel surfaces, dentin or
cementum. depending upon exposure o( the latter
two surfaces through recession or attachment loss
(10). The composition of calculus and adhesive
aspects are influenced by the location of its forma-
tion as well as its age (1 -3 ). The mineral component
of dental calculus predominates in formed,
hardened deposits. Minerals found in human calcu-
lus are typically calcium phosphate salts, including
variable amounts of dicalcium phosphate dihydrate
(DCPD), octacalcium phosphate (OCP). substi-
tuted hydroxyapatite (HAP) and magnesium sub-
stituted tricalcium phosphate (Whitlockite),
Evidence suggests that the proportion of mineral
phases is affected by kinetic aspects of calcification
initiation and transformation (1-3, 5, 11-15). In
addition to mineral components, calculus contains
a variety of inorganic and organic species from
bacterial, salivary and dietary origin (1. 4, 16).
These can be incorporated either during mineraliz-
ation or following calcification, as calculus is quite
porous. Mineral deposits are found to be distrib-
uted both between and within organisms,
depending upon deposit age (1).
Recent studies have applied sophisticated analyt-
ical and biochemical methods toward the analysis
of dental calculus in an effort to expand under-
standing of its composition and properties (17-26).
The porosity properties of calculus makes it an
attractive substrate for study in a variety of fields.
Oxalic acid (27). porphyrins (28) and osteopontin
(29) have recently been newly identified as some o(
deposits. PARSCHE et al. (30) analyzed calculus
from skeletal remains to assess dietary aspects of
ancient Bavarian and Egyptian civilizations.
ABDAZIMOV (31) analyzed heavy metal levels in
calculus from production workers as a quantitative
and simple means to assess occupational exposure
to these toxins. KAWANO et al. (32) successfully
extracted DNA from calculus and used this for the
forensic assessment of gender.
Epidemiology of calculus
An understanding of the prevalence and incidence
o( both supragingival and subgingival calculus is
important, as it provides perspective not only on
the health, but on treatment and professional ser-
vice requirements of populations (33-34). There
are a multitude of recent reports available on
calculus prevalence from throughout the world. A
Medline survey against key words "dental calculus
and epidemiology" revealed over 50 iniliviilital stud-
ies published in the 199O's. These studies have
included a number of national surveys for the U.S.
(36-39) and various countries in Europe (40-41).
as well as many surveys from geographies reported
for the first time. Invariably, these surveys revealed
a high prevalence of calculus (70-100%) in virtually
every population studied. Unfortunately, most of
these surveys provide insufficient detail to differen-
tiate actual levels of supragingival versus subgingi-
val deposits. Many studies from around the world
evaluated calculus while applying the CPITN index
(34) for assessing population need for periodontai
care. In studies applying the CPITN, supra- and
subgingival calculus are not difl'erentiated, although
calculus formation is assigned a higher score (# 2)
than gingivitis. Additional sttidies which assist in
defining the epidemiology o( supragingival calculus
include BEISWANGER et al. (42), MACPHERSON et al.
(43) and ANERUD ei al. (44). Overall, the results of
these three surveys support that both supragingival
and subgingival calculus are commonly found in
most populations. Regardless of scoring indices
used, it is clear that calculus levels observed within
populations are affected by numerous variables.
These include, for example, subject age (36-42,
510 White
43-44) gender (38, 42,44), ethnic background and
diet (1, 36, 38,45-47), oral hygiene {43-44,48-50),
access to (and time since) last professional cleaning
(42, 43-44, 48-50) the presence of mental or phys-
ical handicaps (51), diabetes (52) and use of com-
monly prescribed medications (53-54).
Considering all factors, it would appear that the
bulk of data on calculus prevalence support the
conclusions cited by ANERUD and co-workers (44)
- summarized as follows.
Calculus development must be considered in
light of hygiene practiced by populations and
access of these individuals to professional
services.
In populations with regular oral hygiene and
regular access to professional care (Western
Model):
Supragingival calculus forms in the vast major-
ity of adults 0 50-100%);
Supragingival calculus is observed in early teen
years and rate of accumulation does not signi-
ficantly increase with age:
Supragingival calculus is restricted primarily to
''VMF' teeth (55) - mandibular lingual surfaces
of anterior teeth and buccal surfaces of maxil-
lary molars;
Subgingival calculus is also widely prevalent
(>50 -100%);
Subgingival calculus occurs throughout the den-
tition - particularly on proximal surfaces;
In populations without access to regular profes-
sional care and/or those who do not practice regular
hygiene (Non-Western Model):
Supragingival and subgingival calculus is found
in 100% of subjects
Supragingival and subgingival calculus forma-
tion occurs throughout the dentition;
Supragingival calculus formation starts soon
after tooth eruption and continues to a max-
imum at age 30;
Subgingival calculus is formed within a decade
of tooth eruption and both affected teeth and
quantity of calculus increase with age - until
age 30.
Association of calculus with disease
pathology
The association of dental calculus with periodontal
health has probably been one of the most studied
topics in dental research. For several millennia
prior to 1960. dental calculus was considered to be
a primary etiologic factor in the initiation and
progression of periodontal diseases (1, 4). In the
decade of the 1970s, the improved understanding
of the microbiological contribution to periodontal
disease decreased interest in calculus as a specific
etiologic agent. As documented by TEN CATE (56)
and MANDEL & GAFFEN (4, 57), the last decade
has seen renewed interest in supra- and subgingival
calculus effects on disease processes, on the one
hand, due to the commercial success of toothpastes
sold for the control of supragingival calculus, and
on the other hand, due to the success of phase I
periodontal therapy (scaling and root planing, with
subgingival calculus debridement) in treating early
periodontal disease.
Supragingival calculus
The location of supragingival calculus precludes its
direct participation in advanced periodontal dis-
ease. Researchers have, however, considered
whether calculus deposits can enhance gingivitis
along the gingival margin as a precursor toward
more advanced periodontal disease. ENZER (58)
reported that only 11%. of examined tooth surfaces
containing calculus (supragingival or subgingival)
exhibited gingivitis, while 75yo of the surfaces harb-
oring plaque exhibited gingival inflammation.
FRENCKEN et al. (59), in a longitudinal study of
Morogoro school children from 1984-1988 in
Tanzania, observed that dental calculus increased
with increasing age while gingival bleeding
remained the same, suggestive of no correlation
between calculus and gingival condition. BADER
et al. (60-61) made the observation that tooth
crowns produced decreases in dental calculus and
increases in gingivitis, suggestive of an inverse
relation of calculus to disease. ANERUD et al. (44)
observed that supragingival calculus in the
Norwegian populations produced little effect on
local attachment loss. DONG et al. (62) recently
carried out expanded analysis of CPITN survey
data (differentiating supra- and subgingival calculus
measures) and demonstrated that supragingival cal-
culus levels did not correlate with gingival bleeding.
In spite of these specific results, it is not uncom-
mon to find significant correlations between plaque,
calculus, debris and gingival disease levels in epide-
miologic studies. The mixture of epidemiologic
results illustrates of the difiiculty in separating
effects of plaque versus calculus as etiologic factors
in disease initiation and progression. In fact, the
design of most epidemiologic surveys does not
permit the delineation, on a site basis, of the relative
effects of calculus versus "plaque on calculus", on
disease promotion. Clinical studies, however, can
in principle provide researchers with a belter means
to delineate the proportionate contributions of
supragingival calculus to disease processes, owing

10 the controlled conditions (oral hygiene, treat-
ment etc.) possible in these experiments.
A pivotal study examining the disease promoting
potential of supragingival calculus versus that of
dental plaque was conducted by GAARE and
co-workers employing a novel clinical design (63).
136 Indonesian soldiers exhibiting substantial levels
of calculus were recruited for participation. In one
half of the subjects, a full prophylaxis was per-
formed, while in the remaining subjects, calculus
was allowed to remain on the teeth. At the initiation
of the study, all subjects, prophylaxis and control,
were given a commercial fluoridated dentifrice
(Pepsodent, 1500 ppm fluoride, alumina abrasive),
a new toothbrush, and oral hygiene instructions
directing twice daily toothbrushing with the
assigned paste. Subjects were recalled at one month
for clinical regrading at which time oral hygiene
was reinforced. At two months, subjects returned
for a final clinical grading. Results showed no
differences in gingivitis and gingival bleeding
between the subjects who had, and had not received
an initial prophylaxis. The authors interpreted these
results to suggest that supragingival calculus does
not produce increased gingival inflammation. These
conclusions were supported by the fact that subjects
carrying out oral hygiene without the benefit of an
initial prophylaxis would have been expected to
have been restricted in their ability to cleanse
plaque from the oral cavity. This plaque would
have been expected to produce more gingivitis.
Instead, any eflect of calculus on plaque build up
was obviously not of sufficient magnitude to affect
gingivitis measures in these individuals. The results
ofthe study are made more powerful by considering
that the high level of calculus formation in the
Indonesians and the pronounced response of gin-
gival indices to oral hygiene were illustrative oi
excellent clinical sensitivity.
Additional support for the lack of gingival
"pathogenicity" of supragingival calculus includes
studies of the clinical eflects of agents proven
eflective in reducing calculus mineralization.
Diphosphonate crystal growth inhibitors have been
investigated for their potential to simultaneously
reduce calculus formation and gingivitis in two
long-term chnical investigations. In the first, SUOMI
et al. (64) examined the clinical effects of a denti-
frice containing 3yo ethane hydroxy diphosphonate
{EHDP - disodium etidronate) on both calculus
formation and gingivitis development in 244 adults
in San Francisco over 18 months. The diphosphon-
ate toothpaste produced between 27.1 and A1A%
reductions in supragingival calculus as compared
to a control (non-diphosphonate dentifrice) at the
three clinical measuring points; 6, 12 and 18
months. At these same treatment intervals, subjects
Dental calculus: current understanding 511
utilizing the active dentifrice experienced no signi-
ficant changes in gingival indices. These results
suggest that the clinical benefits of supragingival
calculus reduction are not accompanied by gingiv-
itis improvement.
In a second study, KOCH et al. (65) examined
changes in gingival bleeding among - 1035 children
participating in a 3-year caries clinical study com-
paring the eflects of three fluoride toothpastes to
two "fluoride-I-anticalculus" toothpastes, one con-
taining \% EHDP as the active tartar control
ingredient, and the other containing l"4ofa diphos-
phonate analog { AHP-azocyciohept\lidene 1.1
diphosphonic acid). Clinical examinations demon-
strated no differences in gingival bleeding for any
oi the five toothpastes over the 3 year clinical
period, although improved oral hygiene produced
an overall reduction in gingival bleeding in all
children. The use of the tartar control dentifrices
also produced directionally improved caries reduc-
tions to fluoride controls. Again, these results sup-
ported the lack of a strong correlation between
supragingival calculus and gingival bleeding and
gingivitis in a population practicing routine oral
hygiene.
Similar findings have also been observed in clin-
ical studies of currently marketed tartar control
formulations in the U.S. (66). In a 6 month double-
blind parallel design clinical study involving 454
subjects, the efl"ects of Crest Tartar Control^ denti-
frice containing 5.0'Mi soluble pyrophosphate was
compared with effects produced by a similarly
formulated placebo control dentifrice containing
no anticalculus ingredients. During the treatment
period, subjects using the commercial tartar control
active dentifrice were observed to produce signific-
antly less supragingival calculus than subjects using
control dentifrice, with reductions averaging
^ 30'/<i. In contrast, the tartar control dentifrice
produced no therapeutic benefits for reducing gin-
givitis or gingival bleeding in comparison to placebo
dentifrice over the clinical period.
MANDEL (4) has speculated that the lack of
gingivitis effect for chemical agents proven to
reduce supragingival calculus may be related to the
modest antitartar efficacy of agents tested to date.
In support of this, MCNABB et al. (67) observed
that professional cleaning of supragingival plaque
and calculus, 3 x times a week for 12 weeks resulted
in shitts in pathogenic bacteria sampled from
4-6 mm pockets. These results suggest that rigorous
control of supragingival plaque and calculus can
potentially effect improved health in individuals
presenting with existing early stages of periodon-
titis. Despite these findings, it is difficult to imagine
a chemical antitartar agent producing clinical
512 White
effects comparable to thrice a week professional
dental cleaning.
Additional clinical evidence supporting the lack
of pathogenic potential for supragingival calculus
is provided by clinical studies of chlorhexidine
mouthrinses. In long-term clinical studies. LOE et al.
(68) have observed increases in supragingival calcu-
lus formation complemented with decreases in
dental plaque and gingivitis during the use of
chlorhexidine. It would appear that chlorhexidine
bactericidal actions can act to promote mineraliz-
ation of plaque substrates with no pathological
consequence. These results have been replicated in
a number of recent studies (69-71).
The combination of epidemiologic and clinical
observations suggest lack of an effect for supragin-
gival calculus deposits in promoting gingivitis.
However, recent data suggest that in populations
with heavy supragingival calculus deposition these
deposits are not without consequence. RUSTOGI
et al. (72) demonstrated a correlation between
gingival recession and supragingival calculus levels
in 260 children and teenagers in Thailand. The
effects of calculus on gingival recession were most
pronounced in subjects exhibiting VMI calculus
levels (55) >35mm. (For reference, the average
levels in a U.S. population, just prior to a dental
cleaning, are between 7-10 mm). JOSHIPURA et al.
(73) and LOE et al. (74) have also observed a direct
correlation between levels of supragingival calculus
and gingival recession in surveys. Authors have
noted that while gingival recession in populations
which did not practice regular hygiene correlated
with supragingival calculus, this correlation was
less clear or absent in "Western" type populations
who practiced regular oral hygiene. In populations
practicing regular oral hygiene, it would appear
that gingival recession correlates most strongly with
improper toothbrushing technique.
Subgingival calculus
As with the case of supragingival calculus and
gingivitis, epidemiologic studies quite typically find
statistical correlations between subgingival calculus
levels and loss of attachment and other measures
of periodontal disease progression. A wealth of
literature also supports the benefits of subgingival
scaling and root planing (with concomitant calculus
removal) as highly efi'ective in resolving periodontal
disease. Scaling and root planing are taught as
phase I therapeutic options in periodontal treat-
ment (10). However, it can be fairly asked whether
these correlations produce evidence of an etiologic
association of subgingival calculus with periodontal
disease processes, or whether calculus is merely a
"by-product" of periodontitis. On the one hand, it
is known that while calculus itself contains few
viable bacteria, a dental plaque virtually always
covers the calculus surface, and that this plaque
contains periodontal pathogens (1. 75-78). On the
other hand calculus, like dentin and cementum. is
a porous substrate and can therefore adsorb a
variety of substances from saliva and gingival exud-
ate, including fiuoride and bacterial by-products.
Subgingival dental calculus has been demonstrated
to retain significant levels of endotoxin. and these
mineral deposits have been shown to effect tissue
damage in controlled experiments (79-87). The
separation of "cause and effect" for subgingival
calculus and periodontal disease has continued to
be elusive and remains the subject of extensive
research and debate (10, 57, 88-91). Recent studies
contribute further data to this controversy.
A number of contemporary studies (92-97) pro-
duced data which could be interpreted as suggesting
a relation between subgingival calculus and bone
and/or tissue attachment loss. CHRISTERSON et al.
(97) observed that race and age were additional
factors correlated to both subgingival calculus
formation and periodontal status. In their expanded
study of category 2 CPITN scores, DONG et al.
(62) noted a positive correlation between subgingi-
val calculus and pocket bleeding status. In a 6-year
longitudinal study in China, BAELUM et al. (98)
observed an association of subgingival calculus
level with periodontal disease progression. In a
study of Leukemia patients. BERGMANN et al. (99)
observed that scaling procedures were better than
plaque removal alone in alleviating pocket bleeding.
BROWN et al. (100) observed that black pigmented
bacteriodes and spirochetes were found more often
in pockets with calculus than in pockets without.
This suggests that subgingival calculus can alter
microbial manifestations of periodontal disease.
TAKAHASHI et al. (101) studied the influence of
local oral hygiene, e.g. plaque and calculus depos-
ition, on pocket formation (in excess of 4 mm) in
615 manual workers aged 18-49. The authors
reported a substantial difference in pocket foiTna-
tion for teeth with subgingival plaque vs. subgingi-
val plaque free. Further, the authors reported a
smaller yet discernible increase in pocket formation
for teeth with subgingival plaque and calculus vs.
teeth with subgingival plaque alone. These results
would support the controlling feature of subgingi-
val plaque in promoting disease progression and in
the potential for subgingival calculus to expand (he
radius of damage associated with plaque. WOUTERS
et al. (102) observed an association between subgin-
gival calculus and alveolar bone height - although
oddly these authors did not see a relation between
plaque and bone height. In a series of studies in
diabetes patients, a strong correlation between

subgingival calculus level and periodontai disease
progression was found, but again, the proportional
elTects of plaque versus mineralized deposits could
not be separated (103-106). Data obtained in the
Sri Lankan population studied by ANERUD et al.
(44) suggested that untreated calculus formation
resulted in significant attachment loss over time. In
contrast to these studies, others (107-112) pro-
duced findings suggesting bone loss and attachment
loss were not directly associated with subgingival
calculus per se. The studies cited above must be
considered along with the multitude of surveys
employing CPITN indices (see earlier section),
which invariably show elevated periodontai disease
status paralleling calculus (subgingival) levels. In a
practical context, researchers (109, 112, 113-116)
have commented that calculus enumeration in the
CPITN (community periodontai index of treatment
needs) may overestimate treatment needs in popula-
tions due in part to the indirect causative relation
between calculus and disease progression.
Studies showing a positive epidemiologic associ-
ation between the presence of subgingival calculus
and periodontai disease progression are, of course,
supplemented with a continuing stream of reports
on the health benefits associated with calculus and
plaque removal, supplied by scaling and root plan-
ing (117-119). Interestingly, however, the debate
over the etiologic role of subgingival calculus has
recently prompted significant levels of research
toward the definition of the amount of subgingival
debridement required to restore health to perio-
dontai sites (88-90, 120). The rationale in this
research is that scaling and root planing are typic-
ally highly elective in promoting healing, even
though it is well known that the procedure is not
completely effective in removing subgingival calcu-
lus (88-90. 121). Experts now speculate that a
smooth root surface denuded of calculus, cementum
and superficial dentin is not requisite for the promo-
tion of healing. MOMBELLI et al. (122) showed that
pocket depth reduction without calculus removal
altered clinical course of periodontitis. CHIEW et al,
(123), in an in vitro study, examined LPS remaining
on root surfaces with moderate or extensive mineral
removal (with ultrasonic scaling) and saw marked
reductions in LPS levels with both techniques.
BiAGiNi et al. (124) demonstrated growth of perio-
dontai fibroblasts on cementum that had attached
calculus. LiSTGARTHN & ELLGAARD (125). as early
as 1973. noted gingival epithelial reattachment to
calculus deposits sterilized by 2Vu chlorhexidinc.
More recently. FUJIKAWA et al. (126) demonstrated
that periodontai health in dogs could be maintained
in the presence of subgingival calculus deposits.
Clearly, the debate over the etiologic role of
subgingival calcuhis in periodontai disease does not
Dental calculus: current understanding 513
look like it will be solved in the near future. In
fact, it may be impossible to completely clarify the
cause or effect relation of calculus to pocket
inflammation and disease progression. The removal
of subgingival calculus, with overlying plaque how-
ever, remains the cornerstone of phase I periodontai
therapy. As a result, research continues on ways to
increase the thoroughness and efficacy of scaling
and root planing procedures (e.g., 127-148) and
improved means for the in vivo assessment of
cleaning efficacy (149-151). With respect to
improvements in tactile sensitivity of subgingival
cleaning efficacy, it is possible that the application
of new technologies such as the transducer-modified
sealers and periodontai probes (9. 149-150) may
provide considerable potential for both professional
training and therapy.
Mechanisms of calculus mineralization
The steps in calculus fonnation have been well
characterized on both a chemical and ultrastruc-
tural level (1-5). Although calculus can be induced
in germ free animals (152). human calculus devel-
opment invariably involves plaque bacteria! calci-
fication. Following tooth eruption or a dental
prophylaxis, a mixture of pellicle proteins rapidly
adsorb onto the enamel surface (153-154).
Bacterial adhesion and development of a plaque
biofilm proceeds (155 156) with the characteristic
microbial maturation of initial gram positive coc-
coidal organisms followed by outgrowth o{ fila-
mentous bacteria. Plaque absorbs calcium and
phosphate out of saliva (for supragingival calculus)
and out of crevicular fiuid for subgingival calculus.
Areas prone to supragingival calculus fonnation
include maxillary molar and mandibular incisor
surfaces adjacent to the saliva ducts (1). In these
locations, researchers report more rapid uptake of
calcium and phosphate than within plaque at non-
calcifying sites ( 157). The supersaturation of plaque
fluid is prerequisite to mineralization of partially
soluble calcium phosphate minerals within calculus
(5). Supersaturation can also be acquired through
ureolytic action of bacterial plaque organisms rais-
ing local pH (158). Although mature calculus dem-
onstrates mineralization both within and between
micro-organisms, ultrastructural studies show that
mineral formation typically initiates with nucle-
ation at localized regions of the dental plaque -
usually within the matrix between micro-
organisms ( I ) .
A number of factors may afTect the initial mineral
nucleation and subsequent calcium phosphate crys-
tal growth within dental plaque. These have been
reviewed in detail by SCHEIE (159) and include both
potentiating and inhibiting factors. Factors which
514 White
may enhance initial calcification processes include
the sensitivity of specific bacteria (159-161) and
bacterial proteolipid membrane components to
mineralization (162-163). While mineralization
may occur around and within vital micro-
organisms, it is nevertheless clear that organisms
readily calcify upon death (164-165). (The rapid
calcification of expired organisms can be explained
as a result of deactivation of ATP dependent sys-
tems of the bacteria for controlling intracellular
calcium - once cells cease metabolic control, the
high intracellular phosphate concentrations
encounter external calcium levels m excess of
calcium phosphate saturation - and intracellular
mineralization results). Endogenous factors con-
tributing to calculus mineralization may include
salivary mineral ion levels (166), protein (167) and
lipids (168). Exogenous factors which may affect
tartar formation may include dietary components
such as silicon, which may act to promote mineral
nucleation (169-171). While both vital and dying
bacterial cells, and by-products, may serve as nucle-
ating centers, numerous salivary and plaque com-
ponents may counteract calcification by acting as
inhibitors of plaque mineralization. These may
include salivary phosphoproteins (5), saliva pyro-
phosphate (172) and plaque lipoteichoic acid (173 ).
In addition to specific inhibition of mineraliz-
ation, enzyme systems in plaque and saliva, includ-
ing phosphatases and proteases may contribute to
the degradation of protective inhibitor species
(174-175). Recently, LOSTORTO et al. (176)
reported on the localization of phosphatases in
plaque using cytohistochemical techniques. Both
acid and alkaHne phosphatase were found in intra-
and intercellular components of plaque. In extracel-
lular matrix, phosphatases were often associated
with small vesicles of apparent microbial origin.
Acid phosphatase was found to be concentrated on
the cell walls of gram positive and negative bacteria.
The localization of phosphatases could affect both
natural inhibition of plaque calcification by pyro-
phosphate and phosphorylated proteins, and the
clinical action of tartar control toothpastes con-
taining pyrophosphate.
Once mineralized, crystals in calculus are char-
acteristically found in aggregates with individual
crystallites measuring 10-300 nm in length and
2-30 nm in width (1). Based upon x-ray diffraction
analysis of calculus deposits of varying age, it has
been suggested that calculus mineralization begins
with the deposition of kinetically favored precursor
phases of calcium phosphate, such as OCP and
DCPD, and that this is followed over time by the
maturation into less soluble hydroxyapatite and
whitlockite mineral phases (11-13). This is sup-
ported by more recent observations (15). Crystal
habits vary considerably within calculus - with
needle-shaped and plate-like morphologies
observed (1. 14. 20).
The variability of calculus mineral composition
and structure is the likely result of the numerous
factors which can affect mineral nucleation and
growth. Whatever the mineral composition, the
surface of mature calculus always remains covered
with a matte of dental plaque (75-78). Mineral
crystals within the calculus are presumably coated
with various proteins - presumably similar to those
of enamel pellicle - acquired following mineraliz-
ation. TEM and SEM studies of calculus show that
the mineralization process can occur in layers,
ranging in thickness from 20-400 fim. These layers
are often separated by incremental lines of elevated
organic content resembling pellicle ( 1 ). These stri-
ations suggest periods of active mineralization fol-
lowed by quiescent periods with increased organic
inhibitor uptake.
Obviously, there are a large number of variables
present within the oral cavity and in the calculus
matrix which can influence mineralization and
hence the fate of bacterial plaque. While the inde-
pendent studies of these variables is useful, the
study of the overall mineralization of dental plaque,
considered as a biofilm, continues to attract interest.
The study of plaque mineralization from a biofilm
perspective takes into account many unique aspects
which may affect plaque mineralization, including
the permselective and concentrating effects of extra-
cellular matrix on the penetration and reactivity
within these deposits. The study of plaque calcifica-
tion in biofilm based models dates back to the
1950^s (177-178). SISSONS et al. (179) have most
recently developed a biofilm model which closely
simulates the bacterial colonization and maturation
in dental pkique ecosystems. The system permits
controlled manipulation of pH, mineral ions, and
important metabolic intermediates (like urease)
which can control plaque calcification. In our
laboratories (180), we have also recently adopted
a biofilm model for both mechanistic evaluations
of factors affecting biofilm calcification. The model
is used for the study of factors affecting plaque
calcification and the mechanism of action of anti-
tartar inhibitors.
Tartar control - current strategies for
prevention and removal; expanded benefits
for antitartar formulations
Previous attempts at tartar control have included
strategies directed toward the solubilization of min-
eral components, solubilization of organic matrix,
interference with calculus adhesion, interference
with initial plaque formation, and interference with

plaque mineralization. To this point, chnical success
has been largely achieved with agents directed
toward the inhibition of plaque mineralization
(181-183) including pyrophosphate salts, diphos-
phonates and zinc salts. Two observations on the
clinical efficacy of these agents are worth expanded
discussion. First, mineralization inhibitors have
been proven effective only for the control of suprag-
ingival calculus. Efficacy for the control of subgingi-
val calculus has in large part not been measured -
and would be expected to be minimal due to the
difficulty in transporting topically applied materials
into the gingival pocket. Second, the efficacy of
commercial toothpastes and mouthwashes for the
control of supragingival calculus is directed at
prevention of deposit formation. After a dental
cleaning, these agents provide efficacy in slowing
the rate of calculus build-up. Commercial agents
containing mineralization inhibitors have not been
shown to remove or dissolve existing deposits. The
clinical effects of mineralization inhibitors are typic-
ally assessed by the area coverage of tartar on the
teeth by the Volpe-Manhold index (55).
Although multiple mmeralization inhibitors have
been proven clinically effective, their precise mech-
anism of action is not completely understood. All
effective inhibitors studied to date have in common
the ability to inhibit calcium phosphate nucleation
and or crystal growth processes and the transforma-
tion of precursor calcium phosphate mmeral phases
into more stable calcium phosphates (184). These
agents also show the ability to slow initial plaque
mineralization in biofilm models (180. 185).
Interestingly, the concentration of mineralization
inhibitor required for clinical effectiveness is one to
three orders of magnitude higher than that required
to inhibit mineral growth and nucleation in vitro
(180). In an in vivo pilot study involving calculus
formation on intraoral appliances mounted in lin-
gual mandibular surfaces, samples of immature
calculus qualitatively appeared to contain larger
proportions of precursor calcium phosphate min-
eral phases such as DCPD when treated with
antitartar toothpaste containing pyrophosphate
(15). Analysis of mineral content of mature calculus
however, has revealed no major differences in cal-
cium, phosphate and fluoride concentrations in
samples collected from individuals using placebo
versus antitartar dentifrice (6). It is possible that
mineralization inhibitors provide substantial activ-
ity within the earliest stages of biofilm mineraliz-
ation - and once sufficient calcification is achieved,
modification of physical characteristics (hardening
and adhesion) is irreversible and the plaque layer
effectively becomes "calculus".
Recent studies on chemical agents for tartar
control have included;
Dental calculus: current understanding 515
confirmatory evaluation of clinically proven
formulations
evaluation of tartar control efficacy for composi-
tions containing combinations of mineralization
inhibitors along with antimicrobial (plaque gin-
givitis) or antihypersensitivity ingredients
evaluation of new tartar control systems
evaluation of a gel composition designed to
soften calculus
evaluation of additional benefits of tartar con-
trol fonnulations to patients, including the
potential reduction of gingival recession (in
populations with limited access to professional
care) and the facilitation of easier dental clean-
ings (in populations with access to profes-
sional care).
Table I lists recently completed studies examining
the efficacy of tartar control formulations for the
prevention of new calculus formation (see 181-183
for reviews of prior studies). As shown, a number
of clinical studies included the combination oi
effective tartar control inhibitors, such as pyro-
phosphate. gantrez acid copolymer. and zinc cit-
rate, with antimicrobial ingredients, such as
triclosan or stannous fluoride. The combination of
antigingivitis, antiplaque and antitartar technology
within a single fonnulation is attractive to the
general public due to the simplification which is
provided in selection of toothpastes and mouthrin-
ses for oral hygiene. Also shown in the table are
reports on a number of new agent combinations
tested for effects on tartar development, including
a calculus solubilizmg dentifrice (citroxain; a com-
bination of papain enzyme and citrate chelate)
(186-187), an "antiadherance" rinse (formulated
with delmopinol; a surface anti-adherance agent)
(200) and a calcium lactate dentifrice (192). All of
these formulations were reported to have efficacy
for calculus prevention.
A number of the recently published clinical
reports have examined the efficacy o{ tartar control
dentifrices toward providing new and unique bene-
fits and the efficacy of new multibenefit tartar
control combination products. In a series of studies,
researchers reported on the efficacy of pyrophosph-
ate tartar control dentifrices toward the reduction
of gingival recession in both teenage and adult
populations in Thailand (204-206). As mentioned
earlier, the tartar levels in these populations are far
outside western experience (>35 mm of calculus in
many subjects). However, the results did show that
supragingival tartar control, provided in some
unique setting, may provide additional benefits to
the public. GAFFAR et al. published a series of
studies documenting the clinical efficacy of com-
binations of tartar control inhibitors (pyrophosph-
516 mute
Table I ate and ganlrez acid polymer) with potassium
Recent clinical studies af antitartar dentifrices and mouthrinse^^ nitrate. These formulations demonstrated efficacy
for the combined prevention of both supragingival
Study Formulation/treatment Observed effects calculus formation (195) and desensitization of
(186)
hypersensitive dentin (207-208). WHITE et al.
citrate/enzyme (papain) + tartar reduction
combination dentifrice
(209-212) published a series oi studies docu-
(187) citrate/enzyme (papain) + tartar reduction menting the efficacy of tartar control dentifrices in
combination dentifrice promoting easier calculus debridement. presumably
(188) pyrophosphate dentifrice + tartar reduction through structural modifications of calculus during
(189) "Rembrandt" dentifrice 4-tartar reduction mineralization. In these studies, development of a
(70) chlorhexidine gel tartar increase unique electromechanical transducer modified
(190) pyrophosphate, triclosan + tartar reduction for
dentifrice all formulations
dental sealer permitted the clinical study of calculus
zinc citrate/triclosan adhesion to the teeth and the clinical effects of
dentifrice tartar control formations in facilitating regularly
Gantrez triclosan scheduled tartar removal.
dentifrice
(191) zinc citrate/triclosan In addition to the study of new agents for the
dentifrice + tartar reduction chemical prevention of tartar development and new
(192) calcium lactate dentifrice + tartar reduction benefits for existing tartar control tbtTnuiations.
(193) pyrophosphate dentifrice + tartar reduction research has also recently been reported on attempts
(194) water irrigation with + tartar reduction toward the development of convenient in-ofRce
magnetic device
(195) pyrophosphate/Gantrez/ + tartar reduction techniques to assist in softening dental calculus,
KNO3 dentifrice thus facilitating professional removal. A commer-
(196) pyrophosphate/Gantrez 4-tartar reduction cial scalmg gel. SofScale'. has been developed and
dentifrice marketed worldwide. Components of the gel
Gantrez/triclosan include calcium chelators and surfactants. Initial
dentifrice
zinc citrate/triclosan
published studies reported efficacy for the gel in
dentifrice making calculus easier to remove from teeth and
(70) chlorhexidine dentifrice tartar increase in extracting endotoxin from calculus, possibly
(69) chlorhexidine dentifrice + tartar reduction - rendering deposits less pathogenic (213-214). More
chlorhexidine + zinc compared to CHX control recent studies, including human and animal studies,
dentifrice suggest that the clinical eflects ofthe gel in facilitat-
(197) pyrophosphate + triclosan + tartar reduction
rinse
ing calculus removal may have been due to exam-
(198) chlorhexidine rinse + + tartar reduction - iner bias (215-218). Because the QC dental sealer
pyrophosphate dentifrice compared to CHX control is ideally suited to the study of this type of efficacy,
(199) pyrophosphate/ Gantrez -1-tartar reduction a double blind clinical study was carried oul to
dentifrices examine the efface of SofScale gel in enhancing
(200) delmopinol dentifrices + tartar reduction
(201) zinc citrate triclosan + tartar reduction
calculus removal. Study results showed no betielits
rinse for the scaling gel in facilitating calculus removal
(203) pyrophosphate/Gantrez + tartar reduction (219).
dentifrices
(204) pyrophosphate/Gantrez + tartar reduction
dentifrices
(205) pyrophosphate/Gantrez + tartar reduction Future research on calculus
dentifrices
(206) pyrophosphate/Gantrez + tartar reduction It is probable that the high prevalence of calculus,
dentifrices marketplace dynamics and the focus of the dental
(209) pyrophosphate dentifrice + tartar reduction profession on calculus removal will demand con-
(210) pyrophosphate/triclosan + tartar reduction tinued research interest by academic and commer-
dentifrice cial researchers alike. Considering the foregoing,
pyrophosphate dentifrice
(212) pyrophosphate dentifrice + tartar reduction areas of continued interest may include the develop-
pyrophosphte/Gantrez ment of:
dentifrice
(202) pyrophosphate/triclosan + tartar reduction improved understanding of the mechanism of
dentifrice plaque biofilm mineralization (both in the
zinc citrate/trielosan supra- and subgingival environments) with the
dentifrice
Gantrez triclosan improved mechanistic understanding of the
dentifricepyroph impact of tartar control inhibitors on these
processes;
ill p
For clinical efficacy studies prior to 1991, see refs. (181-183 improved tartar control formulations;

Ireatmenls with efficacy in preventing subgingi-
val tartar development;
improved methods treatments aimed at root
detoxification;
improved methods and treatments facihtating
calculus debridement; and
sensitive diagnostic methods to assess subgingi-
val debridement efficacy.
We can hope that the successful culmination of
this research will help to rid mankind of the calculus
plague which has beset him for these many years.
described by Albucasis prophetically:
'There accumulates on the roots of the teeth
from the inside and outside and between the
gtims, rough and ugly scales which may be black.
yellow or green. As a result there is corruption
of the gums and suppuration around the teeth.
Scrape the teeth that have the scales or the sand
hke substance until nothing remains of them..."
References
ScHROEDER HH. The formation and inhibit ion of dental
cakuhi.s. Hans Huber: Berne, 1969: 10-208.
LEGEROS R Z . Calcium phosphates in oral biology and
medicine. Karger: Basel. 1991; 130-153.
DRIESSENS F M C . Mineral aspeets of dentistry. Karger:
Basel, 1982: 154-158.
MANDEL I D . Calculus formation and prevention: an over-
view. The compendium of continuing education in dentistry
(1987): 8 (suppl.): S235-241.
NANCOLLAS G H . JOHNSSON MAS. Caleulus formation and
inhibition. Adv Dem Res 1994: 8: 307-311.
WHITE DJ. Processes contributing to the formation of
dental calculus. Biofouling 1991: 4^209-218.
BusscHER HJ, UYEN H M W . JONGEBLOED WL. VAN DIJK
LJ. Adhesional aspects of dental calculus formation. In:
TEN CATE JM (ed): Recent advances in ihe study of dentul
calculus. Oxford, England: IRL Press. 1989: 87-96.
WATTS T L P , COMBE EC. An estimation of the strength of
attachment of subgingival calculus to extracted teeth.
J Clin Periodontol 1981: 8: 1-3.
WHITE DJ, Cox ER, ARENDS J, NIEBORG JH. LEYDSMAN
H. WiERiNGA DW, DiJKMAN AG, RuBEN JR. Instruments
and methods for the quantitative measurement of factors
affecling hygienist/dentist efforts during scaling und root
planing oi the teeth. J Clin Dent 1996: 7: 32-40.
WiLKiNs EM. Clinical praetice of the dental hygienist. 7th
edition. Baltimore: Williams and Wilkins, 1994: 273.
RowLEs SL. The inorganic composition of dental ealculus.
In: Blackwood HJJ (ed): Bone and tooth: proceedings of
First European Symposium. London. Pergamon Press,
1964: 175-183.
RowLES SL. Biophysical studies on dental calculus in
relation to periodonlal disease. Dent Pnict Dent Rec
1964: 2-7.
RowLis SL. The composition of supragingival calculus.
J Dent Res 1967: 46 (suppl. 1): 114.
KODAKA T. OHOHARA Y , DEBARI K . Scanning electron
microscopy and energy dispersive x-ray microanalysis
studies of early dental ealculus on resin plates exposed to
human oral cavities. Scanning Microscopy 1992: 6:
475^485.
15 FEATHERSTONE JDB, ZERO D T , SHARIATI M , WHITE DJ.
Dental calculus: current understanding 517
Intraoral models for the study of calculus fonnation and
control. J Dent Res 1992: 71: 234 (#1026).
16. EMBERY G . The organic matrix of dental calculus and its
interaction with mineral. In: TEN CATE JM (ed): Recent
advances in the study of denial calculus. Oxford. England:
IRL Press, 1989: 75-84.
17. HAYASHI Y . High resolution electron microscopy of the
initial mineral deposition on enamel surfaces. / Electron
Microscopy Tokyo 1993: 42: 342-345.
18. HAYASPn Y. High resolution electron microscopy of the
junction between enamel and dental calculus. Scanning
Microscopy 1993: 7: 973-978.
19. MANDEL ID. LEVY BM. Studies on salivary caleulus. I:
Histochemical and chemical mvestigations of supra and
subgingival calculus. Oral Surg Oral Med Oral Path 1957:
10: 874-878.
20. HAYASHI Y : High resolution electron microscopy of the
interface between dental calculus and denture resin.
Scanning Microscopy 1995: 9: 419-425.
21. KoDAKA T, DEBARI K , YAMADA M . Heterogeneity of
crystals attached to the human enamel and cementum
surfaces after caleulus removal in vitro. Scanning
Microscopy 1991: 5: 713-721.
22. KoDAKA T. MiAKE K. Inorganic components and the fine
structures of marginal and deep subgingival calculus
attached to human teeth. Bull Tokyo Dental Coll 1991:
32:99-110.
23. TsuDA H. ARENDS J. Raman spectra of human dentai
calculus. J Dent Res 1993: 72: 1609-1613.
24. Tst_iDA H. MicroRaman spectroscopy in dentul research: a
study on enamel, dentine, hydroxyapatite and calculus. PhD
Thesis, State Univ. of Groningen, The Netherlands. 1996:
211pp.
25. OKUMURA H , NAKAGAKI H . KATO K , ITO F . WEATHERALL
JA. ROBINSON C . Distribution of fluoride in human dental
calculus. Caries Res 1993: 27: 271-276.
26. HUANG S, NAKAGAKI H , OKUMURA H , MORITA I, STRONG
M, ROBINSON C . PEARE E. Fluoride distribution in human
dental caleulus obtained from different sites on the tooth
surface. J Periodontal Res 1996: 31: 149-156.
27. WAHL R , KALLEE E . Oxalic acid in saliva, teeth, and tooth
tartar. Ew J Clin Chem Clin Bioelwn 1994: 32: 821-825.
28. DoLOWY w e , PARKER JD, BRANDES ML. GOUTERMAN M .
Porphyrins in canine and feline dental calculus and
Patuerella multocida cultured from calculus. / Anier let
Med Assoe 1995: 206: 26-27.
29. KiDO J, KASAHARA C , OHISHI K , NISHIKAWA S, ISHIDA H .
YAMASHITA K . KITAMURA S. KoHRr K, NAGATA T .
Identification of osteopontin in human dental calculus
matrix. Arch Oral Biol 1995: 40: 967-972.
3(1. PARSCHE F. WILLERSHAUSEN-ZONNCHEN B . HAMM G.
Trace elements on the dental calculus of individuals from
historical populations. Diseh Zalm Muml Kieferheilkd
Zentralbl 1991:79:219-223.
31. ABDAZIMO\ A D . Changes in the trace clement composition
of the hard dental tissues, dental calculus, saliva and
gingival biopsies in workers under the influence of unfav-
orable factors in the manufacture of Cu, Zn and Pb,
Stomatohgiia Mosk 1991: 70: 22-25.
32. KAWANO S, TSUKAMOTO T . OHTAGURO H . TUSTSUMI H ,
TAKAHASHI T , MIURA 1, MUKOYAMA R , ABOSHI H ,
KoMURO T. Sex determination from dental calculus by
polymerase chain reaction. Nippon Hoigaku Zasshi 1995:
49: 193-198.
33. PFiErER MR, PFIEFER JS. Dental prevention: the oral
prophylaxis. Clin Prev Dent 1988: 10: 18-24.
34. AiNAMO J, BARMES D . BEAGRIE G . CUTRESS T . MARTIN J.
SARDO-INFIRRI J. Development of the World Health
518 White
Organization (WHO) Community Periodontal Index of
Treatment Needs (CPITN ). Int Dent J 1982: 32: 281-291.
35. MANDtL ID. Calculus update: Prevalence, pathogenicity
and prevention. J Amer Dent Assoe 1995; 126: 573-580.
36. MILLER A J . BRUNELLE JA. CARLOS J P , BROWN LJ, LOE
H. Oral health in United States adults. National findings.
The national survey of oral health in US employed adults
and seniors: 1985-1986. NIH Publication No. 87-2868.
Washington DC: US Department o^ Health and Human
Services, 1987.
37. Fox CH. JETTE AM. MCGUIRE SM. FELDMAN HA.
DOUGLASS CW. Periodontal disease among New England
elders. J Periodontol 1994; 65: 676-684.
38. BHAT M . Periodontal health of 14-17 year old US school-
children. J Public Health Dentistry 1991; 51: 5-11.
39. BROWN LJ, BRUNELLE JA, KJNGMAN A. Periodontal status
in the United States. 1988-91: prevalence, extent, and
demographic variation. J Dent Res 1996: 75: 672-683.
40. PILOT T , MIVAZAKI H . Periodontal conditions in Europe.
J Clin Periodontol 1991; 18: 353-357.
41. PILOT T . MIYAZAKI H, LECLERCQ MH. BARMES DE.
Profiles of periodontal conditions in older age cohorts,
measured by CPITN. Int Dent J 1992; 42: 23-^30.
42. BEISWANGER B B . SEGRETO VA, MALLATT ME. PFEIFFER
HJ. The prevalence and incidence of dental calculus in
adults. J Clin Dent 1989; 1: 55-58.
43. MACPHERSON L M D , GIRARDIN DC. HUGHES N J , STEPHEN
KW, DAWES C . The site specificity of supragingival calcu-
lus deposition on the lingual surfaces of the six permanent
lower anterior teeth in humans and the effects of age, sex,
gum chewing habits and the time since the last prophylaxis
on calculus scores. J Dciii Res 1995; 74: 1715-1720.
44. ANERUD A, LOE H , BOYSEN H . The natural history and
clinical course of calculus formation in man. J Clin
Periodontol 1991; 18: 160-170.
45. GARRE D , ROLLA G , VAN DER OUDERAA F . Comparison
of the rate of formation of supragingival calculus in an
Asian and European population. In: TEN CATE JM (ed):
Reeent advances in lhe study of dental calculus. Oxford,
England: IRL Press, 1989: 115-122.
46. WEI SHY, YAN S, BARNES DE. Needs and implementation
of preventive dentistry in China. Comin Dent Oral Epid
1986; 14: 19-23.
47. LOE H , ANERUD H , BOYSEX H , MORRISON E . Natural
history of periodontal disease in man. Rapid, moderate
and no loss of attachment in Sri Lanken laborers 14 to
46 years age. J Clin Periodontol 1986; 13: 431-445.
48. LANG W P , RONIS D L , FARGHALY MM. Preventive
behaviors as correlates of periodontal health status.
/ Puhlie Health Dent 1995; 55: 10-17.
49. MuLLALY BH, LINDEN G H . The periodontal status of
irregular dentai attenders. J Clin Periodontol 1994; 21:
544-548.
50. BLANK L W . RULE J T . COLANGELO GA, COPELAN N S ,
PERLICH M A . The relationship between first presentation
and subsequent observations in heavy calculus formers.
/ Periodontol 1994; 65: 750-754.
51. SHIP JA. Oral health of patients with Alzheimer's disease.
JADA 1992; 123: 53-58.
52. EMRICH LJ, SnLOSSMAN M, GENCO RJ. Periodontal disease
in non-insulin dependent diabetes mellitus. J Periodontol
1991; 62: 123-131.
53. BREUER M M . MBOYA SA, MOROI H , TURESKY SS. Effect
of selected beta blockers on supragingival calculus forma-
tion. J Periodontol 1996; 67: 428-432,
54. TURESKY S, BREUER M , COFEMAN G . The effect of certain
systemic medications on oral calculus formation.
J Periodontol 1992; 63: 871-875.
55. VoLi't AR. MANHOLD JH. HAZEN S P . In vivo calculus
assessment part 1. A method and its examiner reproducibil-
ity. J Periodontol 1965; 36: 292-298.
56. TEN CATE JM. Research on dental calculus: Why? In; TEN
CATE JM (ed): Recent advances in the study of dental
calculus. Oxford, England: IRL Press. 1989; 1-4.
57. MANDEL ID, GAFFAR A. Calculus revisited. J Clin
Periodontol 1986; 13: 249-257.
58. ENZER MI. Some clinical observations on marginal gingiv-
itis. Northwest Univ Bull 1960; 61; 9-11.
59. FRENCKEN JE, TRUIN G J , VAN'T HOF MA. KONIG KG,
LEMBARITI B S . MULDER J, KALSBEEK H . Plaque calculus
and gingival bleeding and type of tooth cleaning device
in a Tanzanian child population in 1984. J Clin Periodontol
1991; 18: 592-597.
60. BADER J. ROZIER R G . MCFALL WT JR. The effect of
crown receipt on measures of gingival status. J Dent Res
1991: 70: 1386-1389.
61. B.U3ER JD. RozrER RG, MCFALL WT JR. RAMSEY DL.
Effect of crown margins on periodontal conditions in
regularly attending patients, J Prosthetic Dent 1991; 65:
75-79.
62. DONG Y J . LEE MM. PAI L , PENG T K . Relationship of
gingival calculus and bleeding on probing in CPITN code
2 sextants. Community Dent Oral Epidemiol 1994; 22:
294-297.
63. GAARE D . ROLLA G . ARYADI F J , VAN DER OUDERAA F .
Improvement of gingival health by toothbrushing in indi-
viduals with large amounts of calculus. J Clin Periodontol
1990: 17: 38-41.
64. SuoMi JD, HOROWITZ H S , BARBANO JP. SPOLSKI V W ,
HEIEETZ SB. A clinical trial of a calculus inhibitory
dentifrice. J Periodontol 1974; 45: 139-145.
65. KOCH G. BERGMANN-ARNADOTTIR I. BJARNASON S.
FiNNBOGASON S, HosKULDSsoN O. KARLSSON R . Caries
preventive effect of fluoride dentifrices with and without
anticalculus agents: a 3-year controlled clinical trial. Curies
Res 1990; 24: 72-79.
66. WHITE DJ. Data on file. 1994. Procter and Gamble.
67. MCNABB H , MOMBELLI A. LANG N P . Supragingival clean-
ing three times a week. The microbiological effects in
moderately deep pockets. J Clin Periodontol 1992; 19:
348-356.
68. LOE H . RINDOM-SCHIOTT C , GLAVINT) L . KARRING T . TWO
years of chlorhexidine use in man. J Periodont Res 1976;
II; 135-144.
69. SANZ M , VALLCORBA N. FABREGUES S, MULLER I.
HERKSTROTER F . The effect of a dentifrice containing
chlorhexidine on plaque, gingivitis, calculus and tooth-
staimng. J Clin Periodontol \99A\ 21: 431-437.
70. YATES R , JENKINS S, NEWCOMBE R . WADE W , MORAN J,
ADDY M . A 6-month home usage trial of a 1"\. chlorhexid-
ine toothpaste (1). Effects on plaque, gingivitis, calculus
and toothstaining. J Clin Periodonlol 1993; 20: 130-138.
71. STIEFEL DJ, TRUELOVE EL. CHIN MM. MANDEL L S .
Efficacy of chlorhexidine swabbing in oral health care for
people with severe disabilities. Spec Care Dent 1992;
12: 57-62.
72. RUSTOGI K N , TRIRATANA T . LINDHE J. KIETPRAJUK C,
VOLPE AR. The association between supragingival calculus
deposits and the extent of gingivai recession in a sample
of Thai children and teenagers. J Clin Dent 1991; (suppl.
B); 6-11.
73. JosHiPUR^\ KJ. KENT R L , DEPAOLA P F . Gingival reces-
sion: intra-oral distribution and associated factors.
J Periodontol 1994; 65: 864-871.
74. LOE H , ANERUD A. BOYSEN H . The natural history of

periodontal disease in man: Prevalence, severity and extent
of gingival recession. J Periodontol 1994; 63: 489-495.
75. FRISKOPP J. HAMMARSTROM L . A comparative scanning
electron microscopic study of supragingival and subgingi-
val calculus. J Periodontol 1980; 51: 553-562.
76. FRISKOPP J. HAMMARSTROM L . An enzyme histochemical
study of dental plaque and calculus. Acta Odontol Scand
1982: 40: 459-456.
77. FRISKOPP J. Ultrastructure of nondecalcified supragingival
and subgingival calculus. J Periodontol 1982: 54: 542-550.
78. HowELL A. Rizzo F. PAUL F . Cultivable bacteria in
developing and mature human dental calculus. Arch Oral
Biol 1965; 10: 307-313.
79. ALEO JJ. DERENZIS FA. FARBER PA. CARBONCOEUR AP.
The presence and biological activity of cementum-bound
endotoxin. J Periodontol 1974; 45: 672-675.
80. ALEO JJ, DERENZIS FA. FARBER PA. In vitro attachment
of human gingival fibroblasts to root surfaces.
J Periodontol f975; 46: 639-645.
81. BAUMHAMMERS A . ROHRBAUGH EA. Permeability of
human and rat dental calculus. J Pcriodotitol 1970; 41:
39-42.
82. HATFIELD CG. BAUMHAMMERS A. Cytotoxic effects of
periodontally mvolved surfaces of human teeth. Arch Oral
Biol 1971; 16: 465-468.
83. ITO K . HINDMAN RE. O'LEARV TJ. KAFRAWY AH.
Determination of the presence of root bound endotoxin
using the Local Shvvartzman Phenomenon (LSP).
J Periodontol 1985:56: 8-17.
84. JONES WA. O'LEARV TJ. The etTcctiveness of root planing
in removing bacterial endotoxm from the roots of perio-
dontally involved teeth. J Periodontol 1978; 49: 337-342.
85. MORRIS ML. The subcutaneous implantation of perio-
dontally diseased roots. J Periodontol 1972; 43: 737-747.
86. MORRIS ML. An inhibitory principle in the matrix of
periodontally diseased roots. J Periodontol 1975: 46:
33-39.
87. PATTERS MR. LANDESBERG R L . JOHANSSON LA. RUMMEL
CL. ROBERTSON PB. Baeteriodes gingivalis antigens and
bone resorbing activity in root surface fractions of perio-
dontally involved teeth. 7 R'/'W/WJ/^t-.v 1982; 17: 122-130.
88. DRISKO C L . KILLOY WJ. Scaling and root planing:
removal of calculus and subgingival organisms. Curr Opin
Dent I99I; 1: 74-80.
89. ZAPPA U E . Factors determinmg the outcome of scaling
and root planing. Can Dent Hyg Probe 1992; 26: 152-159.
W. BADKR H I . Scaling and root planing: Its role in contempor-
ary periodontal therapy. Cump Cont Ed Dent 1993; 14:
436-449.
91. RoBF.RTsoN PB. The residual calculus paradox.
J Periodontol 1990: 61: 65-66.
92. CLEREHUGH V, LE>fNON MA. WORTIIINGTON H V . 5-year
results of a longitudinal study of early periodontitis in 14-
to 19- year old adolescents. J Clin Periodontol 1990;
17: 702-708.
93. DAHLLOF G . BJORKMAN S. LINDVALL K . AXIO E. MOOEER
T. Oral health in adolescents with immigrant background
in Stockholm. Swed Dent J 1991; 15: 197-203.
94. ISMAIL AL. MORRISON EC. BURT BA. CAFFESSE R G .
KAVANAGH M T . Natural history of periodontal disease in
adults: findings from the Tccumsah PcriodoiUu! Disease
Study. 1959 1987. ./ Dent Res 1990; 69: 430 435.
95. KALLESTAL C . MATSSON L . Marginal bone loss in 16-year
old Swedish adolescents in 1975 and 1988. ./ Clin
Periodontol 1991; 18: 740 743.
96. SJ6DIN B, MATSSON L . Marginal bone loss in the primary
denlilion. A survey of 7-9 year old children in Sweden.
./ Ctin rcriodontol 1994; 21: 313-319.
Dental calculus: current understanding 519
97. CHRISTERSSON LA. GROSSI SG. DUKFORD RG. MACHTEI
EE. GENCO RJ. Dental plaque and calculus: Risk indic-
ators for their formation. 7 >/ Res 1992: 71: 1425-1430.
98. BAELUM V. WEN-MIN L . DAHLEN G . FE^RSKOV O . XIA
C. Six year progression of destructive periodontal disease
in two subgroups of eiderly Chinese. J Periodontol 1993:
64: 891-899.
99. BERGMANN O J . ELLEGAARD B . DAHL M . ELLEGAARD J.
Gingival status during chemical plaque control with or
without prior mechanical plaque removal m patients with
acute myeloid leukemia. J Clin Periodontot 1992; 19:
169-173.
100. BROWN CM. HANCOCK EB. O LEARV TJ. MILLER CH.
SHELDRAKE MA. A microbiological comparison of young
adults based on relative amounts of subgingival calculus.
J Periodontol 1991: 62: 591-597.
101. TAKAHASHI Y . OKAWA Y . MATSUKUBO T . TAKAESU Y .
SASAKI Y . IHIL T {1990): Epidemiological analysis for the
influences of plaque and calculus deposition on prevalence
of pocket formation. Dent Jpn Tokyo 27: 155-160.
102. WouTERs FR. SALON-EN LW. FITHIOF L. HELLDEN LB.
Significance of some vanables on interproximal bone
height based on cross-sectional epidemiologic data. J Clin
Periodontol 1993; 20: 199-206.
103. OLIVTZR RC. TERVONEN T . Periodontitis and tooth loss:
comparing diabetics with the general population. J Am
Dent Assoe 1993: 124: 71-76.
104. TERVONEN T . OLIVER RC. Long term control of diabetes
mellitus and periodontitis. J Clin Periodontol 1993: 20:
431-435.
105. OLIVER RC. TERVON'EN T . Diabetes a risk factor for
periodontitis in adults? J Periodontol 1994; 65: 530-538.
106. KARJALAINEN KM. KNUUTTILA ML. VON DICKHOFF K J .
Association of the severity of periodontal disease with
organ complications in type 1 diabetic patients.
J Periodontol 1994; 65: 1067-1072.
107. BAELUM V. MANJI F . FEJERSKOV O . WANZALA P. Validity
of CPITN's assumptions of hierarchical occurrence of
periodontal conditions in a Kenyan population aged
15-65 years. Community Dent Oral Epidemiol 1993: 21:
347-353.
108. MACHTEI EE. CHISTERSSON LA. ZAMBON JJ, HALSMAS'N
E. GROSSI SG, DUNFORD R . GENCO RJ. Alternative
methods for screening periodontal disease in adults. J Clin
Periodontol 1993; 20: 81-87.
109. ALBANDAR JM. Juvenile periodontitis - pattern of progres-
sion and relationship to clinical parameters. Comnnnutv
Dent Oral Epidemiol 1993; 21: 185-189.
110. NuNN JH. WELBURY R R , GORDON PH, STRETTON-DOWNES
S. ABATE CG. The dental health of adults in an integrated
urban development in Addis Ababa. Etliiopia. //(/ Dent J
1993; 43: 202 206.
111. KALLESTAL C . MATSSON L. Periodontal conditions in a
group of Swedish adoleseents. UI). Analysis of data.
J Clin Periodontol 1990; 17: 609-612.
112. SoNGPAiSAN Y. D A V I E S G N . Periodontal status and treat-
ment needs in the Chianmai/Lamphun provinces of
Thailand. Community Dent Oral Epidemiol 1989; 17:
196-199.
113. LEWIS JM. MORGAN M V . WRIGHT FA. The validity of
the CPITN scoring and presentation method for measur-
ing periodontal conditions. J Clin Periodontol 19^)4; 21:
1-6.
114. MILLER NA. BENAMGHAR L, ROLAND E , PENAIII) J.
MARTIN G . An analysis of the community periodontal
index of treatment needs. Studies on adults in France. V.
Presentation of CPITN data in cross-tabulations. Comm
Dent Health 1991; 8: 349-355.
520 White
115. BAELUM V. FEJERSKOV O . MANJI F . WANZALA P. Influence
of CPITN parlial recordings on estimates oi" prevalence
and severity of various periodontal conditions in adults.
Community Dent Oral Epidemiol 1993; 21: 354-359.
116. BAELUM V, MANJI F . WANZALA P, FEJERSKOV O.
Relationship between CPITlsl and periodonta] attachment
loss findings in an adult population. J Clin Periodontol
1995; 22: 146-152.
117. RAWLISON A . WALSH T F . Rationale and techniques of
non-surgical pocket management in periodontal therapy.
Br Dent J 1993; 174: 161-166.
118. DRISKO CL. Scaling and root planing without over instru-
mentation: hand versus power driven sealers. Curr Opin
Periodonlol 1993; XX: 78-88.
119. MAGGIORE E . FRANCETTI L . WEISTEIN R . An update on
nonsurgieal periodontal therapy. A review of the literature.
Minerva Siomatol 1992; 41: 515-522.
120. BADER H . Scaling and root planing. Evolution or
Revolution? Dent Today 1991: (December). 54-56.
121. CORBET E F . VAUGHAN AJ, KIESER JB. The periodontally
involved root surface. J Clin Periodontol 1993; 20:
402-410.
122. MoMBELLi A. NYMAN S, BRAGGER U . WENNSTROM J. LANG
NP. Clinical and microbiological changes associated with
an altered subgingival environment induced by perio-
dontal pocket reduction. J Clin Periodontol 1995: 22:
780-787.
123. CHIEW S Y . WILSON M . DAVIES EH, KIESER JB. Assessment
of ultrasonic debridement of caleulus-associated perio-
dontally-involved root surfaces by the limulus amoebocyte
lysate assay. An in vitro study. J Clin Periodontol 1991;
18: 240-244.
124. BiAGiNi G, CHECCHI L. PELLICCIONI G A , SOLMI R . In
vitro growth of periodontal fibroblasts on treated
cementum. Otiintess Int 1992: 23: 335-340.
125. LiSTGARTEN MA. ELLEGAARD B . Electron microscopic
evidence of a cellular attachment between junetional epi-
thelium and dental calculus. J Periodont Res 1973: 8:
143-150.
126. FUJIKAWA K , O'LEARY TJ. KAFRAWY AH. The effect of
retained subgingival calculus on healing after flap surgery.
J Periodunlol 1988; 59: 170-175.
127. QuiRYNEN M, BoLLEN CM, VANDEKERCHKHOVE B N ,
DEKEYSER C . PAPAIOANNOU W . EYSSEN H . Full vs. partial-
mouth disinfection in the treatment of periodontal infec-
tions: short-term clinical and microbiological observa-
tions. / Dent Res 1995; 74: 1459-1467.
128. PARASHIS A O . ANAGNOU-VAELTZIDES A, DEMETRIOU N .
Calculus removal from multiiooted teeth with and without
surgical access. I. Eflicacy on external and furcation
surfaces in relation to probing depth. J Clin Periodontol
1993; 20: 63-68.
129. PARASHIS AO. ANAGNOU-VARELTZIDES A, DEMETRIOU N .
Calculus removal from multirooted teeth with and without
surgical access II. Comparison between externLil and furca-
tion surfaces and effect of furcation entrance width. J Clin
Periodontol 1993; 20: 294-298,
130. TAKACS V J , LIE T . PERALA D G , ADAMS D F . Efficacy of 5
machining instruments in scaling of molar furcations.
J Periodontol 1993; 64: 228-236.
131. CHAVES E , COX C F , MORRISON E . CAFEESSE R . The effect
of citric acid application on periodontally involved
root surfaces (II). An in vitro scanning electron micro-
scopic study. Int J Periodont Restorative Dent 1993: 13:
188-196.
132. REED KL. Sonic sealers: a review. Gen Dent 1992; 40:
34-36.
133. RADVAR M , CREANOR SL, GILMOUR WH, PAYNE AP,
M C G A D E Y J FOYE R H , WHITTERS CJ, KINANH DF. An
evaluation ofthe effects of an Nd: YAG laser on subgingi-
val calculus, dentine and cementum. An in vitro study.
J Clin Periodontol 1995; 22: 71-77.
134. AoKi A. ANDO Y , WATANABE H , ISHIKAWA I. In vitro
studies on laser scaling of subgingival calculus with and
erbium: YAG laser. / Periodontol 1994; 65: 1097-1106.
135. DANESH-MEYER MJ. Current applications of lasers in
periodontics. J N Z Soc Periodontol 1992; I I : 17-21.
136. MENGEL R . BU-NS C , STELZEL M , FLORES-DE-JACOBY L.
An in vitro study of oscillating instruments for root
planing. J Clin Periodontol 1994: 21: 513-518.
137. LEE A, HEASNIAN' PA, KELLY PJ. An in vitro comparative
study of a reciprocating sealer for root surface debride-
ment. J Dent 1996: 24: 81-86.
138. LARNER J R . GREENSTEIN G . Effect of calculus and irrigator
tip design on depth of subgingival irrigation. Int
J Periodont Restorative Dent 1993; 13: 288-297.
139. JoTiKASTHiRA NE, LiE T. LEKNES K N . Comparative in
vitro studies of sonic, ultrasonic and reciprocating scaling
instruments. J Clin Periodontol 1992; 19: 560-569.
140. PLAZA JC. DE-LA-SOTTA R . Microscopic analysis of the
effects of ultrasonic instrumentation on the root surface
of molar furcations. Rev Dent Chile 1991; 82: 41^W.
141. EscHLER BM, RAPLEY JW. Mechanical and chemical root
preparation in vitro: efficiency of plaque and calculus
removal. J Periodontol 1991; 62: 755-760.
142. NAGY RJ. OTOMO-CORGEL J. STAMBAUGH R . The effect-
iveness of scaling and root planing with curettes designed
for deep pockets\ J Periodontol 1992; 63: 954-959.
143. DRAGOO MR. A clinical evaluation of hand and ultrasonic
instruments on subgingival debridement. 1. With unmodi-
fied and modified ultrasonic inserts. //(/ / Periodont
Restorative Dent 1992; 12: 310-323.
144. ANDERSON GB. PALMER J A . BYE F L , SMITH B A . C.\FFESSE
RG. Effectiveness of subgingi\al scaling and root plan-
ing: smgle vs. multiple episodes of instrumentation.
J^Periodontol 1996: 67: 367-373.
145. ANDERSON GB. PLOTZKE A E . MORRISON EC, CAFEESSE
RG. Effectiveness of an irrigation solution utilized during
ultrasonic scaling. Ouintess Int 1995: 26: 849-858.
146. WYLAM JM, MEALEY BL, MILLS MP, WALDROP T C ,
MoDKOWicz DC. The clinical effectiveness of open vs.
closed scaling and root planing on multi-rooted teeth.
J Periodontol 1993: 64: 1023-1028.
147. NiEMiNEN A, SIREN E , WOLE J, ASIKAINEN S. Prognostic
criteria for the efficiency of non-surgical periodontal
therapy in advanced periodontitis. J Clin Periodontol 1995;
22: 153-161.
148. ScHOEN DJ. Instrument effects on smoothness discrimina-
tion. J Dent Educ 1992; 56: 741-751.
149. JEEFCOAT M K . JEEECOAT RL. CAPTAIN K . A periodontal
probe with automated cemento-enamel junction detection-
design and clinical trials. IEEE Tran Biorned Eng 1991:
38: 330-333.
150. ZAPPA U . CADOSCH J, SIMONA C , GRAF H . CASE D . In
vivo scaling and root planing forces. J Periodontol 1991;
62: 335-340.
151. PIPPIN DJ. FEIL P. Interrater agreement on subginguai
calculus detection following scaling. J Dent Educ 1992:
56: 322-326.
152. TuEiLADE J, FITZGERALD RJ, SCOTT D B , N \ T E N MU.
Electron microscopic observations of dental calculus in
germ-free and comcntional rats. .4/(7? Oral Biol 1964:
9: 97-101.
153. AL-HASHIMI I, LEVINI-: MJ. Characterization of the in vivo
salivary-derived enamel pellicle. Arch Oral Biol 1989;
34: 289- 295.

154. MAYHALL CW. concerning the composition and source of
the acquired enamel pellicle of human teeth. Arch Oral
Biol 1970; 15: 1327 1341.
155. SniiEin A A A . Mechanisms of dental plaque formation.
Adv Dent Res 1994; 8: 246-253.
156. McHuGH WD. Role of supragingival plaque in oral
disease initiation and progression - State-of-the-Science
review. In: Loe H. Kleinman DV (eds); Dental plaque
eontrol measures am! oral hygiene praetiees IRL Press,
Oxford. 1986. 1-12.
157. MANDEL ID. Biochemical aspects of calculus fonnation:
Comparative studies of plaque in heavy and light calculus
formers. J Periodont Res 1974: 9: 10-17.
138. ScnAMSCHULA RG. PEARCE EIF. U N P S H , COOPER MH.
Immediate and delayed effects of an enzyme dependent
mineralizing mouthrinse on dental plaque. J Dent Res
1985; 64: 454 456.
159. SCHEtE A A A . The role of plaque in dental calculus
formation. In: TEN CATE JM (ed): Recent advances in the
study of dental calculus. Oxford, England: IRL Press.
1989; 47-55.
160. SoucHAY A. PouEZAT JA. MENANTEAU J . Mineralization
of streptococcus mutans in vitro. An ultrastructural study.
Oral Surg Oral Med Oral Path Oral Radiol Endod 1995;
79: 311-320.
161. BoYAN BD. SWAIN LD, BOSKEY AL. Mechanisms of
microbial calcification. In: TEN CATE JM (ed): Recent
advances in the study of dental calculus. Oxford. England:
IRL Press. 1989: 29-35.
162. SWAIN L D , BOYAN BD. Ion-transport properties of mem-
brane proteins associated with microbial calcification. In:
TEN CATE JM (ed): Recent advances in the study of dental
caleulus. Oxford, England; IRL Press, 1989: 37-44.
163. VOGEL JJ. BOYAN-SALYERS B , CAMPBELL MM. Metah Bone
Dis Rcl Res 1978; 1: 149-153.
164. SiDAWAY DA. A microbiological study of dental calculus
(II). The in vitro calcification of micro-organisms from
dental calculus. J Periodont Res I97S; 13: 36U 366.
165. SiDAWAY DA. A microbiological study of dental calculus.
Ill A comparison of the in vitro calcification of viable
and non-viable micro-organisms. J Periodont Res 1979;
14: 167-172.
166. MANDEL ID. Biochemical aspects of calculus fonnation.
II: Comparative studies of saliva and heavy and light
calculus formers. J Periodont Res 1974; 9: 211-221.
167. MANDEL ID, THOMPSON RH. Chemistry of parotid and
submaxillary saliva in heavy calculus formers and non-
formers. ./ Periodontol 1967; 38: 310-315.
168. SLOMiAm' A, SLOMIANY BL, MANDEL ID. Lipid composi-
tion of human parotid saliva from light and heavy dental-
calculus formers. Arch Oral Biol 1981; 26: 151-152.
169. RoLLA G, GAARE D , LANGMYHR F J . HELGELAND K .
Silicon in calculus and its potential role in calculus
formation. In: TEN CATE JM (ed): Recent advances in the
study of dental calculus. Oxford, England: IRL Press,
1989: 97-103.
170. DAMEN J J M . TEN CATE JM. Calcium phosphate precipita-
tion is promoted by silicon. In: TRN CATE JM (ed): Recent
advances in the study of dental caleulus. Oxford, England:
IRL Press, 1989: 105-114.
171. HiDAKA S, OKAMOTO Y , ABE K . Possible regulatory roles
of silicic acid, silica and chiy minerals in the formation of
calcium phosphate precipitates. Arch Oral Biol 1993 38:
405-413.
172. VOGEL JJ, AMDUR BH. Inorganic pyrophosphate in
parolid saliva and its relation to calculus formation. Arch
Oral Biol 1967; 12; 159-163.
Dentul calculus: current understanding 521
173. BERGMANN JE, GULZOW HJ. LEWANDOWSKI T . Oral strep-
tococci affecting Ca-phosphate precipitation. Dtsch
Zalmarztl Z 1991; 46: 561-562.
174. WATANABE T , MORITA M . Relation between calculus
formation and the protease activity of saliva plaque. In:
TEN CATE JM (ed); Recent advances in the study of dental
calculus. Oxford. England: IRL Press, 1989: 65-74.
175. DRAUS FJ, TARBET WJ. MIKLOS F L . Salivary enzymes
and calculus formation. J Periodont Res 1968; 3; 232-235.
176. LO-STORTO S. SILVERSTRINI G , BONL'CCI E . Ultrastructural
localization of alkaline and acid phosphatase activities in
dental plaque. J Periodont Res 1992; 27: 161-166.
177. DRAUS E J . LESMEWSKI M , MIKLOS FL. Pyrophosphate
and hexametaphosphate effects in in vitro calculus forma-
tion. Arch Oral Biol 1970; 15; 898-896.
178. LEUNG SW. The effect of silicones and lactones on syn-
thetic calculus formation. 7 D t / ; / K o 1956; 33: 670. ()^70).
179. SISSONS CH, CUTRESS T W . HOFFMAN M P . WAKEFIELD
JSTJ. A multistation dental plaque microcosm (artificial
mouth) for the study of plaque growth, metabolism. pH.
and mineralization. J Dent Res 1991: 70: I409-I4I6.
180. WHITE DJ. Cox ER. Factors affecting calculus inhibition.
Time Concentration of CGI application. J Dent Res 1992;
71: 173 (abstract #543).
181. VoLPE AR. PETRONE ME. D A V I E S R M . A review of calculus
clinical efficacy studies. J Clin Dent 1992; 4; 71-81.
182. STOOKEY G K . JACKSON RD. BEISWANGER B B , STOOKEY
KR. Clinical efficacy of chemicals for calculus prevention.
In; TEN CATE JM (ed): Recent advances in the study of
dental calculus. Oxford. England: IRL Press. 1989:
235-258.
183. ADAMS D . Calculus inhibition agents: A review of recent
clinical trials. Adv Dent Res 1995: 9: 410 418.
184. WHITE DJ, BOWMAN WD, NANCOLLAS GH. Physical-
ehemical aspects of dental calculus fonnation and inhibi-
tion: in vitro and in vivo. In; TEN CATE JM (ed): Recent
advances in the study oj dental calculus. Oxford. England:
IRL Press, 1989; 175-188.
185. WHITE DJ. Cox ER. Effects of inhibitors on plaque
calcification at various stages in vitro. J Dent Res 1992;
71: 173 (abstract #544).
186. K R A N Z S , BOFFA J . FRANKL S N , GLASER C . A comparative
clinical study of two anticalculus dentifrices for efficacy
in the inhibition and removal of surface stain and calculus.
Praet Periodontics .4e.sthet Dent 1991; 3: 28-31.
187. LYON T C JR, PARKER WA. BARNES GP. Evaluation of
effects of application of a ci(roxain containing dentifrice.
J Esthet Dent 1991; 3: 51-53.
188. KuRBAD A, GANGLER P , HOFFMAN T . KIRCHNER T ,
WEINERT W . Inhibiting effect ofa pyrophosphate dentifrice
on calculus formation. Dt.seh Zahnarztl Z 1991; 46:
277-280.
189. EMLrNG RC, LEVIN S. SHI X, WEINBERG S. YANKELL S.
Rembrandt toothpaste stain pre\cntion with and without
use of Peridex. J Clin Dent 1992; 3: 59-65.
190. SvATUN B. SAXTON CA. HUNTINGTON E . CUMMINS D . The
effects of three silica dentifrices containing triclosan on
supragingival plaque and calculus formation and on gin-
givitis, int Dent J 1993; 43: 441-452.
191. SvATUN B, SAXTON CA, HUNTINGTON E , CUMMINS D . The
effects of a silica dentifrice containing triclosan and zinc
citrate on supragingival plaque and calculus formation
and the control of gingivitis. Int Dent J 1993; 43: 431-439.
192. SCHAEKEN MJ, VAN DER HoEVEN JS. Control of calculus
formation by a dentifrice containing calcium lactate.
Caries Res 1993; 27: 277-279.
193. GAENGLER P , KURBAD A. WFINERT W . Evaluation of anti-
calculus cllicacy. An SEM method of evaluating the
522 White
effectiveness of pyrophosphate dentifrice on calculus
formation. J Clin Periodontol 1993; 20: 144-146.
194. WATT DL, ROSENFELDER C . SUTTON CD. The effect of
oral irrigation with a magnetic water treatment device on
plaque and calculus. / Clin Periodontol 1993; 20: 314-317.
195. COHEN S, SCHIFF T . MCCOOL J, VOLPE A. PETRONE ME.
Anticalculus efficacy of a dentifrice containing potassium
nitrate, soluble pyrophosphate, PVM/MA copolymer. and
sodium fluoride in a silica base: a twelve week clinical
study. J Clin Dent 1994; 5: 93-96.
196. BANOCZY J . SARI K , SCHIFF T , PETRONE M . DAVIES R .
Antiealculus efficacy of three dentifrices. Am J Dent 1995;
8: 2O5-20S.
197. TRIRATANA T , KRAIVAPHAN P , TANDHACHOON K , RusTOGt
K, VOLPE AR, PETRONE M . Effect of a pre-brush
mouthrinse containing triclosan and a copolymer on calcu-
lus formation: a three-month clinical study in Thailand.
J Clin Dent 1995; 6: 139-141.
198. BoLLMER BW. STURZENBERGER O P . VICK V. GROSSMAN
E. Reduction of calculus and Pcridex stain with tartar
control crest. J Clin Dent 1995; 6: 185-187.
199. KATALIN S, SCHIFF T . THOMAS G . KATALIN G , ILDIKO T ,
JOLAN B. Clinical comparison of the calculus inhibiting
effect of three commercially available toothpastes. Forgorv
Sz 1995; 88: 393-398.
200. CLAYDON N . HUNTER L , MORAN J. WADE W . KELTY E .
MovERT R. ADDY M . A 6-month home-usage trial of
0.1% and 0.2% delmopinol mouthwashes. I, Effects on
plaque, supragingival calculus and tooth staining. / Clin
Periodontol 1996; 23: 220-228.
201. ScHAEKEN MJ. VAN DER HOEVEN JS, SAXTON CA. CUMMINS
D, The effect of mouthrinses containing zinc and triclosan
on plaque accumulation, development of gingivitis and
fonnation of calculus in a 28-week clinical test. J Clin
Perioiinntol 1996: 23: 465-470.
202. FAIRBROTHER KJ, KOWOLIK MJ. CURZON M E J , MULLER
I. MCKEOWN S. HILL CM. HANNIGAN C . BARTIZEK R D .
WHITE DJ, The comparative clinical efficacy of pyro-
phosphate/triclosan. copolymer/triclosan, and zinc citrate/
triclosan dentifrices for the reduction of supragingival
calculus formation. / Clin Dent 1997: 8: 62-66.
203. TRIRATANA T , KIETPRAJUK C , BANDITSING P. KRAIWAPHAN
P. Clinical comparison of antiealculus dentifrices: a three-
month study of Thai children and teenagers. ./ Clin Dent
1991; 3: 23-25,
204. TRIRATANA T , KRAIWAPHAN P. RUSTOGI KN, LINDHE J,
VOLPE AR. The effect of an anticalculus dentifrice on
calculus formation and gingival recession in Thai children
and teenagers: one year study. Study #1. An anticalculus
dentifrice containing 3.3% soluble pyrophosphate and
1.0';^, of a copolymer. / Clin Dent 1991; 3: 26-30.
205. RUSTOGI K N . TRIRATANA T , TIMPAWAT S, NAKORNCHAI 8,
VOLPE AR. The effect of an anticalculus dentifrice on
calculus formation and gingival recession in Thai children
and teenagers: one year study. Study 2. An anticalculus
dentifrice containing 1.3% soluble pyrophosphate and
1.5% of a copolymer. J Clin Dent 1991; 3: 26-30.
206. TRIRATANA T . RUSTOGI KN. VOLPE AR. The effect of an
antiealculus dentifrice on supragingival calculus formation
and gingival recession in Thai adults: a one year study.
J Clin Dent 1991:3: 22-26.
207. AYAD E. BERTA R . DEVIZIO W . MCCOOL J, PETRONE ME.
VOLPE AR. Comparative efficacy of two dentifrices con-
taining 5% potassium nitrate on dentinal sensitivity: a
twelve week clinical study. J Clin Den! 1994; 5: 97-101.
208. CRAWFORD RJ. COLLINS MA. CLIPPER D W . PRENCIPE M .
Fluoride and potassium availability in a new dentifrice
that treats hypersensitivity and controls tartar. J Clin Dent
1994: 5: 80-82,
209. WHITE DJ, Cox ER. ARENDS J. NIEBORG JH, LEYDSMAN
H. WEIRINGA DW. DIJKMAN AG. RUBEN JR. Crest tartar
control benefits assessed by Quanticalc: Clinical method
and three month results. J Clin Dent 1996; 7: 41 45.
210. WHITE DJ, BOLLMER BW, BAKER RA, Cox ER, PERLICH
MA. MCCLANAHAN S F . BEISWANGER BB. MAU M . TUOHY
M. AREXDS J, Quanticalc assessment ofthe clinical scaling
benefits provided by pyrophosphate dentifrices with and
without triclosan. J Clin Dent 1996; 7: 46-49.
211. WHITE DJ. Cox ER. BACCA L, LANZALACO AC,
MONTGOMERY R M . COYLE-REES M . BEISWANGER BB. MAU
M. ARENDS J, A quanticalc clinical comparison of profes-
sional efficiency in manual supragingival calculus debride-
ment. J Clin Dent 1996; 7: 54-57.
212. WHITE DJ. MCCLANAHAN SF, LANZALACO AC, Cox ER.
BACCA L , PERLICH MA. CAMPBELL SL. SCHIFF T . STAINS
A. The comparative efficacy of two commercial tartar
control dentifrices in preventing calculus development and
facilitating easier dental cleanings. ,/ Clin Denl 1996;
7: 58-64.
213. JABRO M H . BARKMEIER W W . LATTA MA. A clinical evalu-
ation of the effects of a periodontal sealing gel. J Clin
Dent 1992; 3: 43-46.
214. NOLL K A , CHADWICK DE. Endotoxin reduction by
SofScale gel in an in vitro model system. J Dent Res 1992;
71: 579(511),
215. MAYNOR GB. WILDER RS. MITCHELL S C . MORIARTY JD.
Effectiveness of a calculus scaling gel. J Clin Periodontol
1994; 21: 365-368.
216. HARDING CD. COBB CM. SCHULZ PH. WILLIAMS KB,
BRA^" KK. BROWN AR. Effectiveness of a prescale gel on
subgingival calculus. J Clin Periodontol 1996; 23; 147-152.
217. SMITH S R . FOYLE DM. DANIELS J. An evaluation of a
prescaling gel (SofScale) on the ease of supragingival
calculus removal. J Clin Periodontol 1994; 21: 562-564.
218. MILLER BR. HARVEY C E . SHOFER F . Effectiveness of
SofSeale calculus scaling gel as an aid during dental
scaling of teeth of dogs. J let Dent 1994; 11: 14-17.
219. AREN-DS J , DUKM^N AG. WHITE DJ. Cox ER. Effeets of
a scaling gel on forces developed in debridement of
supragingival calculus determined by means of a trans-
ducer modified dental sealer: the Quanticalc. / Clin Dent
1996; 7: 50-53,