Dental Disease Essay, Research Paper
Dental DiseaseOne significant problem in dentistry is the progression of carious lesions in the teeth. Carious lesions or dental caries is defined as a localized, progressively destructive disease of the teeth that starts at the external surface with an apparent dissolution of the inorganic components by organic acid. The tendency to the development of dental caries depends on specific surfaces of teeth and several other factors which include: type of tooth, location and length of exposure to the oral environment, oral hygiene practices, nutritional status, previous fluoride exposure , and the oral status of the patient. Among the primary teeth, there are many more occlusal cavities than any other type of lesion. Evidence shows that caries is a more common occurrence on two surfaces of a tooth rather than just one surface. Occlusal caries is the most common type of caries on the permanent teeth. Studies show that 43-75% of all caries lesions are on the occlusal surfaces of posterior teeth. In the entire dentition, there are more mesial cavities than distal cavities and there are more buccal cavities than lingual cavities. The cuspal, incisal, buccal, lingual, and palatal surfaces are usually resistant to dental caries. This resistance is related to external factors such as food retention and the formation of dental plaque. The most susceptible areas for dental caries are the fissures and proximal surfaces of the teeth. The occlusal surface will usually start to decay soon after tooth eruption. About 20% of the erupted teeth do not develop decay. The reason for this is due to the anatomical structure or chemical composition of the tooth. These factors could include the shape and condition of the gingival margin and papilla, the nearness of another tooth, the width of the interdental space, and the degree of tooth mobility. Fluoride also plays an important role in the prevention of dental caries. Dental caries is composed of three basic types of diseases: Streptococcus mutans, Streptococcus sanquis, and Lactobacillus species. Each has its own anatomical site on the tooth and particular disease-causing microorganisms. All three cause pit and fissure caries which are bacteria that are forced into the bony structures of the tooth. Streptococcus mutans is an organism that bonds to the tooth surface because of it s ability to produce dextrans which will allow bacteria to bond to tooth surfaces. This microorganism plays an important role in the initiation of dental caries. The leading role of Streptococcus mutans is determined by a composition of biochemical properties which include the capability of growing and producing acids in an acidic environment that initially causes dental caries in enamel. Enamel is defined as the hard substance covering the exposed portion of the tooth. In its mature form, it is composed of an inorganic portion made up of 90% hydroxyapatite and 6-8% calcium carbonate, calcium fluoride, and magnesium carbonate, and the remainder comprising an organic matrix of protein and glycoprotein. The basic unit of structure of enamel is called the enamel rod. This rod is a column of enamel that runs all the way from the dentinoenamel junction to the surface of the tooth. The rod is generally perpendicular to the dentinoenamel junction and to the surface. The ameloblast is round or hexagonal in cross section and the enamel rods, which fit tightly together, are keyhole shaped. The enamel is composed of two parts: the rod and rod sheath. The rod is made up of hydroxyapatite crystals. The rod sheath outlines the rod and contains most of the organic fibrous substance. Caries lesions in enamel can partially remineralize. Differences in the fluoride and carbonate concentrations of the remineralizing solutions are reflected in the composition of the enamel. Fluoride present during the remineralization period inhibits the progression of demineralization. The influence of fluoride is the result of the fact that the mineral deposited contained fluorapatite, which is less soluble than hydroxyapatite. Fluorapatite may be present as a result of remineralization or as a result of transformation reactions occurring during the secondary demineralization. The conclusion was that the resistance to dental decay imparted by fluorine was the result of an increase of fluorine in the tooth structure, particularly the enamel, which added to the ability of the tooth substance to resist decalification by acids. Caries of the enamel can be divided into progressive or acute and arrested or chronic types of disease. Acute enamel caries is characterized clinically by being white or chalky in appearance. Arrested enamel caries is yellow to dark brown in color. Enamel caries depends upon its location. On smooth surfaces the carious lesion tends to develop in a conical form with the apex pointing towards the dentin. In fissural caries, however, the apex points towards the enamel surface. The first sign of dental caries is the presence of white spots. The white spots are demineralized sub-surface areas with a mostly intact surfaces. This is known as hypocalcified enamel and is the result of an insuffient growth of the enamel crystals or an insufficient number of crystals originally deposited in the matrix. “Permanent teeth are more susceptible to hypomineralization or “white spot” defect.”1 Thus a less dense enamel is produced, which may make the enamel decay more rapidly. Cracks in the enamel caused by developmental problems or trauma are called enamel lamellae. The most common types are those caused by trauma. Clinically they appear as hairlike cracks in the enamel. These may extend all the was through the enamel and eventually into the dentin. “The differences between permanent and primary teeth extend to the area of dental trauma.”2 A developmental defect is a less common type of lamella which results in preventing the production of enamel and leaving a space between other enamel rods. These provide an entrance through the enamel for bacteria to enter which makes the tooth more susceptible to dental caries or the early development of a caries lesion. The early lesion of dental caries in permanent enamel is divided into four zones: the translucent zone, the dark zone, the body of the lesion zone, and the surface zone. The translucent zone is the first sign of normal enamel seen in enamel caries . It lies at the beginning p
The dark zone is superficial to the translucent zone. It constitutes a “molecular sieve” in the tissue and the exclusion of large molecules from the micropores, which remain filled with air or vapor. The body of the lesion zone known as the third zone is the bulk of the carious area. It extends superficially from the dark zone but does not include “intact” enamel surface. The surface zone of enamel caries contains the greatest degree of demineralization which occurs at the sub-surface level. The early lesion is in a sub-surface position and remains covered by a surface layer, which is most affected by a caries attack. The structural resistance of teeth to caries lies mainly in the enamel surface since this disease begins on the surface of the enamel and extends to the deeper layers of the tissue and dentin. Dentin is defined as the hard calcified tissue forming the inside of the tooth, underlying the cementum and enamel and surrounding the pulpal tissue. About 20% of the mass is organic matrix, mostly collagen, with some elastin and a small amount of mucopolysaccharide; the inorganic fraction (70%) is mainly hydroxyapatite, with some carbonate, magnesium, and fluoride. Dentin in cross section is composed of three distinct areas microscopically: dentinal tubule, peritubular dentin, and intertubular dentin. A dentinal tubule is a long tube, running from the dentinoenamel junction or dentinocemental junction to the pulp. This tube is filled with a cellular extension of the odontoblast called the odontoblastic process. The dentin that surrounds and is closest to the tubules in the circumpulpal dentin is hypermineralized. This dentin is peritubular dentin because it surrounds the tubule. It has an area of higher crystalline content surrounding the dentinal tubules. This dentin is formed within the existing tubule and the term intratubular dentin is more accurate. It is slightly more calcified than the rest of the dentin. The intertubular dentin is the remainder of the dentin matrix, that lies between the tubules. However, increased formation and mineralization of intratubular dentin, the tubule may eventually become occluded. The resulting dentin is termed sclerotic, transparent, and transluccent dentin. These are all microscopic structures. Dentin deposition begins with the formation of the pulp chamber and continues as long as the pulp remains vital. Primary dentin is developmental dentin that is formed from the beginning of calcification until tooth eruption. Secondary dentin is dentin that is formed throughout the pulp chamber and pulp canal from the time of eruption. There is a considerable variation in the composition of primary and secondary dentine. There is a change in the course of the dentinal tubules in the shift from primary dentin to secondary dentin deposition, the tubules are more irregular in secondary dentin. Secondary deposits contain less calcium, phosphorous, and collagenous matrix per unit volume than the primary dentine. Secondary dentin is less mineralized and contains 6-10 % more mineral than primary dentin. “Unlike secondary dentin, which is formed as a result of normal physiological stimuli, tertiary or reparative dentin is formed as a result of a pathological process, caries.” (3) A carious lesion involves the enamel and eventually can enter into permanent dentinal deposits. These deposits do not always prevent toxins from entering into the dental pulp before becoming a carious lesion. The variations of the mineral deposits are due to the differing proportions of apatite and octocalcuim phosphate crystals in the mineralized matrix of the teeth. Calcifications with calcium/phosphorolar ratios of 1.47-1.68 suggested that octocalcium phosphate crystals were located on collagen fibers within the pulp enduring fibrotic and arteriosclerotic age changes. However, in the mantle zone there are increased amounts of collagen and mineral content of the primary dentine, but were proportionately consistent everywhere else. Secondary deposits contain less calcium, phosphorous, and collagenous matrix per unit volume than the primary dentine. Another type of dental caries, known as root caries may be caused by filamentous organisms including Actinomyces viscosus and Actinomyces naeslundi and Streptococcus mutans. Root surface caries is a soft, progressive lesion that can be found anywhere on the root surface that has lost connective tissue attachment and is exposed to the oral environment. Dental plaque and microbial attack are an essential part of the cause and progression of the caries lesion. The carious lesion of the root is similar to that of enamel, except that the microflora associated with the lesion may be different. Root surface caries are usually associated with filamentous organisms whereas coccal forms are seen in enamel caries. Dental plaque plays a major role in dental caries. Plaque is a group of microbes that stick to the tooth surface. In order for plaque to form it must have a form of energy. The energy used are sugars which is known to be metabolized to lactic acid, which acts as the demineralizing agent in dental caries. As the glucose is metabolized to the lactic acid, the cell transforms the glucose to adenosine triphosphate (ATP), heat and lactic acid. It is these materials in the plaque that cause decalcification and cavitation of tooth structure. Since plaque is the major cause of dental caries, it affects the majority of the population of the United States and other countries of the world. People need to be more educated on the cause and prevention of dental caries to keep there teeth more healthy and their overall oral hygiene status healthy. By educating the population on plaque and dental caries, it could reduce many dental cavities, periodontal disease, and reduce tooth loss. Many people value their teeth and are willing to do what is necessary to maintain a good oral status. The only problem is they do not have the education to ensure the health of their mouth. Since their has been a lot of research and new techniques developed to improve the conditions of the oral status, there should not be any reason why someone should be forced to loose any of their teeth and to develop periodontal disease.