Internal Modifying Factors Involved in Dental Caries
Introduction
As discussed in chapter 2, many factors modify the prevalence, onset, and progression of dental caries. The major internal (endogenous) modifying risk indicators, risk factors, and prognostic risk factors related to dental caries are reduced salivary secretion rate (SSR), poor salivary quality, impaired host factors, chronic diseases, unfavorable macroanatomy and microanatomy of the teeth, and the stage of eruption, all of which favor plaque retention, poor quality and maturation of enamel, and exposed root cementum or dentin. Impaired salivary function, particularly an
inadequate SSR, is of utmost importance.
Role of Saliva
Introduction
The secretion rate and quality of saliva are important not only in caries development but also for remineralization.
Function of saliva
Saliva serves as a first line of both nonspecific and specific defense in the oral cavity against infectious diseases, erosion, attrition, and traumatic lesions of the oral mucosa.
Saliva is vital to the integrity of the mineralized tissues (teeth) as well as the soft tissues; to the selection, ingestion, and preparation of food for digestion; and to the ability to communicate. Maintenance of the integrity of the oral tissues is primarily a function of the unstimulated (resting) basal secretions; the functions related to digestion are served by salivary flow stimulated by the intake of food. Saliva has manifold functions in protecting the integrity of the oral cavity from food residue, debris, and bacteria:
1. Saliva has some buffering effect against strong acids and bases.
2. Saliva provides the ions needed to remineralize the teeth.
3. Saliva has antibacterial, antifungal, and antiviral capacities.
Components of saliva also facilitate the motor functions of chewing, swallowing, and
speaking, as well as sensory and chemosensory functions in the oral cavity. These
functions are summarized in Table 12.
Secretion of saliva
The normal daily volume produced by the salivary glands is about 0.5 to 1.0 L, of
which only about 2% to 10% is produced during sleep. About 80%, stimulated by
chewing, is produced during meals; that is, the mechanisms of salivary production are
capable of rapid response to physiologic demand. About 90% of the total volume is
produced by three major pairs of symmetrically located salivary glands: glandulae
parotidea, glandulae sublingualis, and glandulae submandibularis (Fig 80).
In humans, salivary glands are classified, according to the nature of their secretion, as
serous, mucous, or mixed. Serous glands, for example, the parotids, produce a thin,
watery secretion rich in enzymes. Mucous glands, for example, the minor glands of
the soft palate, produce a viscid secretion. In mixed salivary glands, such as the
submandibular and sublingual glands, the secretory product varies, depending on the
proportion of mucous to serous cells within the gland. The submandibular glands are
mainly serous, and the sublingual glands are mainly mucous.
Salivary glands can also be classified as simple or compound, according to their duct
system. The glands comprise mainly ducts and acini (Fig 81). The duct system of the
submandibular and parotid glands is well developed and branched, containing
intercalated, striated, and excretory ducts. In sublingual glands, the intercalated and
striated ducts are sparsely distributed. The minor salivary glands are classified as
simple branched tubular glands.
Of the major salivary glands (see Fig 80), the parotids are the largest, weighing 20 to
30 g each. The parotid duct (Stensen’s duct) is about 5 cm long and opens into the oral
cavity opposite the buccal surface of the maxillary second molar (the parotid papilla).
The submandibular glands are smaller than the parotids and are surrounded by a welldefined
capsule. The main duct (Wharton’s duct) is about 5 cm long and opens at the
summit of the sublingual papilla just lateral to the frenulum of the tongue. The
sublingual gland is composed of several smaller glands; the main duct (Bartholin’s
duct) opens close to the duct of the submandibular gland.
The minor salivary glands, numbering between 200 and 400, produce about 10% of
the total volume of saliva. They occur throughout the oral mucosa, with the exception
of the gingivae and anterior part of the hard palate. They are named, according to their
location, as labial, buccal, palatine, lingual, glossopalatine, and minor sublingual
glands.
Salivary secretion from major and minor glands is controlled by both parasympathetic
and sympathetic stimuli. Depending on the nature of the stimulus, this also affects the
composition of saliva. In general, parasympathetic stimuli increase the output of water
and electrolytes, whereas sympathetic stimuli enhance protein synthesis and secretion.
Clinically, this difference may have relevance, because both the volume of fluid and
the concentration and nature of salivary proteins are important for protection against
microbial diseases, such as dental caries: In the clearance process, the waterelectrolyte
fraction is important, and the actual antimicrobial activity is determined by
the protein fraction.
Saliva is secreted in response to neurotransmitter stimuli. For most of the day,
neurotransmitter release is low and salivary flow is basal, or unstimulated. During
food ingestion, in response to gustatory and masticatory stimuli (via mechanical
stimulation of the nerves in the periodontal ligaments), there is a pronounced increase
in neurotransmitter release, and secretion is stimulated. Resting secretion is
considered to be mainly protective, while the larger volume of stimulated saliva is
needed to facilitate ingestion (formation and swallowing of a food bolus) and
communication. The bulk of the stimulated saliva is secreted by the parotid gland,
which is estimated to contribute about 10% of unstimulated and more than 50% of
stimulated whole saliva.
Salivary secretion rate (SSR)
“Normal” values and thresholds. Of the many studies of SSRs in presumably healthy
individuals in different countries, the most remarkable finding is the enormous
variability; the SSR ranges between 0.08 and 1.83 mL/min, a 23-fold range, for
resting whole saliva and between 0.2 and 5.7 mL/min, an almost 30-fold range, for
stimulated saliva. Throughout these vast ranges, individuals are generally free of
subjective complaints and objective signs of salivary gland dysfunction. These studies
show that normal oral function can be maintained with wide individual ranges in
saliva production.
Because of this heterogeneity, it is difficult to assess the status of a patient’s salivary
gland function from a single measurement of SSR. In the absence of complaints or
signs, it is difficult to determine the presence of a salivary gland disorder.
Furthermore, it is evident that caution should be exercised in comparing a single SSR
with a population standard. Changes in a patient’s SSR over time are probably a more
reliable indicator of oral health. If clinicians routinely assessed saliva production in all
their patients, they would be able to establish a patient`s normal SSR and be alert to
any decline. This would allow early intervention to prevent or limit the deleterious
consequences of salivary gland dysfunction.
“Whole saliva,” the fluid present in the mouth, comprises not only pure secretions
from the major and minor salivary glands but also gingival exudate, microorganisms
and their products, epithelial cells, food debris, and, to some extent, nasal exudate.
Whole saliva is of clinical relevance for susceptibility to caries and carious activity.
However, there is no linear association between SSR and carious activity, but rather a
“threshold effect.” Although, for clinical purposes, there is consensus on the
thresholds presented in Table 13, this is clearly an oversimplification, particularly at
the individual level.
The so-called normal values for unstimulated and stimulated SSR exhibit a large
biologic variation, which should be considered in relation to sex, body weight, and
age. For example, 3- to 4-year-old children, with limited experience of different
tastes, seem to have an extremely high SSR per kilogram of body weight, about five
times as high as that of 10 year olds. On the other hand, in healthy adults, there is only
a limited decline in stimulated SSR with age.
Studies by Heintze et al (1983) established the gender-related ranges of unstimulated
whole SSR (Fig 82) and stimulated SSR (Fig 83) in adults, with peaks at about 0.3 to
0.4 mL/min and 1.5 mL/min, respectively. However, the secretion rates for both
unstimulated and stimulated saliva were significantly lower for females than for
males. In most studies, the reported mean value for stimulated SSR is about 1.5
mL/min in females and 2.0 mL/min in males; the difference is attributed mainly to the
greater body weight of males. When the secretion rate is evaluated, body weight
(reflecting glandular size) should be taken into account. Although Heintze et al (1983)
found a significant correlation between unstimulated (resting) and stimulated SSRs,
the individual variations were so large that one type of SSR could not readily be
predicted from the other.
A study by Percival et al (1994) compared the SSR of unstimulated whole saliva and
stimulated saliva from the parotid gland in relation to age and gender in “healthy”
adults (without medication). The mean values were lower in females than in males.
However, while the unstimulated whole SSR (Fig 84) was significantly lower in the
older age groups (80 or older) than in the younger groups (20 to 39 years), there was
no correspondingly significant difference for the stimulated parotid SSR (Fig 85).
Randomized samples of adults will, however, include both healthy and unhealthy
individuals. Particularly among the elderly, there is widespread regular use of
pharmaceuticals that have systemic depressive effects on SSR as well as the quality of
the saliva. Loss of teeth is also strictly age related; because of total or partial
edentulousness, chewing stimulation is reduced in a relatively high percentage of the
elderly (about 20% to 50% of 65 to 90 year olds).
In a randomized sample of about 1,000 50, 65, and 75 year olds, one of many clinical
and anamnestic variables evaluated was stimulated whole SSR (Axelsson et al, 1990).
Figure 86 shows the percentage of individuals with 0.0 to 0.7 mL/min, 0.8 to 1.4
mL/min, and more than 1.5 mL/min in the three age groups.
Link to caries risk. The relationship between stimulated SSR and the development of
carious lesions has been studied extensively. Although caries risk is extreme in the
absence of saliva or in the presence of very low secretion rates, there does not seem to
be a strictly linear correlation. An inverse relationship between stimulated SSR and
caries incidence, for both enamel and root caries, is found in most studies, and
statistical significance has also been demonstrated in some cross-sectional
investigations. Stimulated SSR values of less than 0.7 mL/min are regarded as a
threshold for considerably increased risk of further caries development. Therefore, it
is interesting that in randomized samples of 50, 65, and 75 year olds, such low values
were recorded in as many as 15%, 20%, and 25%, respectively, about one subject in
five over the age of 50 years (see Fig 86) (Axelsson et al, 1990).
However, SSR cannot be assessed qualitatively. As the most important clinical
variable of saliva affecting susceptibility to dental caries, simple quantitative
assessment of stimulated whole saliva should be a routine clinical procedure in the
adult population. The same saliva sample can also be used to measure salivary
buffering capacity and the levels of salivary mutans streptococci and lactobacilli.
In clinical practice, measurement of saliva (sialometry) is particularly indicated:
1. As part of the initial examination of a new patient to be treated for dental caries.
2. During evaluation of preventive and restorative treatment of dental caries, to assess
how the overall treatment has affected oral health.
3. In elderly patients who take regular medication, and/or have exposed root surfaces.
4. As part of the investigative procedures for suspected hyposalivation associated
with, for example, regular use of medicines with systemic depressive effects on SSR,
Sjogren’s syndrome and other diseases associated with reduced SSR, or irradiation to
the head and neck region.
The data gathered by Axelsson et al (1990) were used to analyze the relationship
between SSR and dental health. Figure 87 shows the mean values of stimulated whole
SSR in dentate and edentulous individuals. Figure 88 shows the mean stimulated
whole SSRs related to sex, regular medication, and edentulous versus dentate. Figure
89 shows the mean number of teeth (third molars excluded) in 50, 65, and 75 year
olds with low and high stimulated SSRs (0.0 to 0.7 and more than 1.5 mL/min,
respectively). The results indicated that the stimulated SSR values may influence the
number of teeth lost. Figure 90, from the same study (Axelsson et al, 1990), shows the
percentage of intact, decayed, filled, and missing surfaces among 50-, 65-, and 75-
year-old dentate individuals and all individuals with low and high stimulated SSRs.
In a more recent cross-sectional study of a randomized sample of more than 600 50 to
55 year olds, among many clinical and anamnestic variables caries prevalence was
related to stimulated whole SSR and regular use of medicines with known systemic
effects on SSR (Axelsson and Paulander, 1994). Twenty-nine percent of the subjects
were taking medication regularly, and 22% used medicines that impair SSR. Figure
91 compares the frequency distribution of intact, decayed, missing, and filled surfaces
in subjects with a stimulated SSR of less than 0.7 mL/min, versus subjects with an
SSR of greater than 1.5 mL/min, and in subjects using drugs that impair salivary
function versus subjects not taking any medication.
These data show conclusively that the SSR is an important factor in caries severity
and should be considered when caries risk is assessed. Very low stimulated SSR
(hyposialosis) (less than 0.7 mL/min, and particularly less than 0.4 mL/min) results in
a high risk of caries. Clinically, it is therefore important to determine whether SSR is
normal or impaired.
