ADDITIONAL FACTORS KNOWN TO INFLUENCE DENTAL CARIES
SALIVA
Although saliva was identified in the etiology section earlier as part of the host component and thus a primary part of the caries process, the role of saliva overall is so unique and special that further discussion is warranted here regarding its influence on several aspects of the caries process that may help produce favorable environments to combat the process. Any patient with a salivary deficiency, from any cause, is at higher risk for caries activity.
It is generally accepted that the dental caries process is controlled to a large extent by a natural protective mechanism inherent within the saliva. Many properties of saliva have been investigated to learn their possible role in the caries process. Considerable importance has been placed on the salivary pH, the acid-neutralizing power, and the calcium, fluoride, and phosphorus content. It has long been suggested that in addition to these properties the rate of flow and the viscosity of saliva may influence the development of caries. The normal salivary flow aids in the solution of food debris on which microorganisms thrive. In addition, the saliva manifests a variety of antibacterial and other anti-infectious properties. All known characteristics of saliva seem somehow relevant to the process of dental caries.
Saliva is secreted by three paired masses of cells—the submaxillary, sublingual, and parotid glands. Small accessory glands are also scattered over the oral mucous membranes. Each of these has its own duct.
The salivary glands are under the control of the autonomic (involuntary) nervous system, receiving fibers from both its parasympathetic and sympathetic divisions. Stimulation of either the parasympathetic (chorda tympani) fibers or the sympathetic fibers to the submaxillary or sublingual gland causes a secretion of saliva. The secretion resulting from parasympathetic stimulation is profuse and watery in most animals. Sympathetic stimulation, however, causes a scanty secretion of a thick, mucinous juice. Stimulation of the parasympathetic fibers to the parotid gland causes a profuse, watery secretion, but stimulation of the sympathetic fibers causes no secretion.
Salivary Deficiency
One of the first descriptions of a severe salivary deficiency with its deleterious effect on the dentition was reported by Hutchinson in 1888.34 Since that time, many reports have emphasized the importance of a normal flow of saliva in preventing a breakdown of the dentition. A reduction in the salivary flow may be temporary or permanent. When the quantity is only moderately reduced, the oral structures may appear normal. A pronounced reduction or complete absence of saliva, however, results in an acidic environment with rampant caries (Fig. 10-4). In addition to the rapid destruction of the teeth, there may be dryness and cracking of the lips, with fissuring at the corners of the mouth, burning and soreness of the mucous membranes, crusting of the tongue and palate, and sometimes paresthesia of the tongue or mucous membrane.
ADDITIONAL FACTORS KNOWN TO INFLUENCE DENTAL CARIESSALIVAAlthough saliva was identified in the etiology section earlier as part of the host component and thus a primary part of the caries process, the role of saliva overall is so unique and special that further discussion is warranted here regarding its influence on several aspects of the caries process that may help produce favorable environments to combat the process. Any patient with a salivary deficiency, from any cause, is at higher risk for caries activity.It is generally accepted that the dental caries process is controlled to a large extent by a natural protective mechanism inherent within the saliva. Many properties of saliva have been investigated to learn their possible role in the caries process. Considerable importance has been placed on the salivary pH, the acid-neutralizing power, and the calcium, fluoride, and phosphorus content. It has long been suggested that in addition to these properties the rate of flow and the viscosity of saliva may influence the development of caries. The normal salivary flow aids in the solution of food debris on which microorganisms thrive. In addition, the saliva manifests a variety of antibacterial and other anti-infectious properties. All known characteristics of saliva seem somehow relevant to the process of dental caries.Saliva is secreted by three paired masses of cells—the submaxillary, sublingual, and parotid glands. Small accessory glands are also scattered over the oral mucous membranes. Each of these has its own duct.The salivary glands are under the control of the autonomic (involuntary) nervous system, receiving fibers from both its parasympathetic and sympathetic divisions. Stimulation of either the parasympathetic (chorda tympani) fibers or the sympathetic fibers to the submaxillary or sublingual gland causes a secretion of saliva. The secretion resulting from parasympathetic stimulation is profuse and watery in most animals. Sympathetic stimulation, however, causes a scanty secretion of a thick, mucinous juice. Stimulation of the parasympathetic fibers to the parotid gland causes a profuse, watery secretion, but stimulation of the sympathetic fibers causes no secretion.
Salivary Deficiency
One of the first descriptions of a severe salivary deficiency with its deleterious effect on the dentition was reported by Hutchinson in 1888.34 Since that time, many reports have emphasized the importance of a normal flow of saliva in preventing a breakdown of the dentition. A reduction in the salivary flow may be temporary or permanent. When the quantity is only moderately reduced, the oral structures may appear normal. A pronounced reduction or complete absence of saliva, however, results in an acidic environment with rampant caries (Fig. 10-4). In addition to the rapid destruction of the teeth, there may be dryness and cracking of the lips, with fissuring at the corners of the mouth, burning and soreness of the mucous membranes, crusting of the tongue and palate, and sometimes paresthesia of the tongue or mucous membrane.
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