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Radiology of the jaws: Diseases involving the teeth
Radiology of the Jaws : Diseases Involving the Teeth F. VIA, JR., D.D.S., M.S.
By WILLIAM
D
ENTAL CARIES and periodontal disease (pyorrhea) are two of man’s most prevalent diseases and are mentioned throughout all of recorded history. It is only recently, however, that the etiologic factors of these diseases have emerged. It is curious to note that both of these diseasesseem to have a common etiologic agent: the dental plaque. This is not to say that the plaque is a simple entity and is always the same, but rather that it contains the microorganisms and provides the environment in which these processesmay fluorish.3 DENTAL
CARIES
Radiologists have long recognized that caries appears in the teeth in three different forms. These were first thought to differ only in location on the tooth. Caries associated with the pits or crevices in teeth is called pit and fissure caries. That found on proximal and other smooth surfaces is termed smooth surface caries. The lesion found in older individuals in areas of root surface exposed by gingival recession is called root or cemental caries. Under carefully controlled experiments, it has been possible to produce in animals each type of caries independent of the others, indicating that different bacteria (substrate combinations ) may be required to produce each type.3 Certain streptococci appear to be associated with all types of caries+6 lactobacilli apparently can produce only pit and fissure caries;’ root caries may be caused by streptococcal strains, some of which are responsible also for periodontal disease.537 Certain age differences have been noted in caries susceptibility. Pit and fissure and smooth surface caries are found at all ages but appear more frequently and progress most rapidly in younger people. Cemental caries (root caries) is a disease of the elderly, in whom it may occur de novo.5 However, there can be no cemental caries without gingival recession first exposing the root surface. The various types of carious lesions and severity of cavitation are illustrated in Figs. 1-6. Progression of dental caries through the calcified parts of the tooth into the inner (pulpal) part of the tooth follows rather regular patterns. Pit and fissure caries starts as a point in the enamel. At the depth of a pit or fissure it spreads along the dentino-enamel junction, forming a triangle-shaped radiolucent area in the enamel with the base toward the dentino-enamel junction and the apex toward the tooth surface. A radiolucent triangle may appear in the dentin with the apex disposed toward the pulp of the tooth as the caries spreads at the dentino-enamel junction (Fig. 3).
WILLIAM F. VIA, JR., D.D.S., MS.: Professor and Chairman, nosis, Uniuersity of North Carolina School of Dentistry, Chapel
370
SEMINARS
IN ROENTGENOLOGY,
Department of Oral Hill, N. C. 27514.
Diag-
VOL. 6, No. 4 (OCTOBER), 1971
371
DISEASESINVOLVINCTHETEETH
Smooth surface caries seen in profile appears as two triangles. The enamel triangle base is at the tooth surface and its apex at the dentino-enamel junction, The dentin triangle has its base on the dentino-enamel junction and the apex toward the pulp ( Fig. 1) . Cemental caries resembles a semicircular radiolucency with the widest part at the root surface (Fig. 6). Progression of the lesion proceeds along the same patterns with enlargement of the radiolucency in all planes. It must be remembered that the bacteria progress in the dentin at a rate more rapid than the appearance of the radiolucency. The pulpal tissue of the tooth will exhibit histologic signs of inflammation long before the caries-caused radiolucency reaches the pulpal tissue. Bacterial invasion may result in death of the pulpal tissue and infection of the periapical tissues. PULPAL
CHAMBER
CHANGES
The dental pulp is the mature form of the organ which forms the dentin of the tooth. It serves as the nutritional and nerve supply for the dentin. As a matter of fact, the dentin may be considered a part of the pulpal tissue because the protoplasmic processes of the odontoblast penetrate the dentin to the dentino-enamel junction. The pulpal tissue contains the odontoblasts which form secondary dentin as a response to stimulation of the odontoblast processes. The pulp further contains fibroblasts, undifferentiated mesenchymal cells which may differentiate into osteoblasts, odontoblasts, or osteoclasts. In addition, pulpal tissue contains a circulatory system, including lymphatics, and the appropriate elements of nervous tissue. The pulpal tissue reacts to stress in a manner quite similar to periosteum or endosteum of bone, This is characterized by resorption of damaged calcified tissue followed by repair. There is a buildup of calcified areas in the pulpal tissue in response to external stimuli to the dento-enamel junction from caries, occlusal wear, or minor trauma to the tooth. Calcification may take the form of pulp stones or may be laid down on the walls of the pulp chamber by the odontoblast in response to a small carious lesion, a dental restoration, or a fracture of enamel and dentin, as in the breaking off of a corner of an incisor tooth (Figs. 7, 8, and 9). Resorption of the pulp chamber wall may take place as a response to an overwhelming bacterial invasion which may cause metaplasia of the pulpal tissue to granulation tissue. Trauma to the tooth can cause interference with the blood supply of the pulp. The odontoblastic layer of the pulpal tissue may be lost. This cellular breakdown may stimulate the undifferentiated mesenchymal cells of the pulp to form osteoclasts (odontoclasts) and result in resorption of the dentin wall of the pulp chamber (Fig. 10 and 11). PERIRADICULAR
CHANGES
When the defense mechanisms in the pulpal tissues are unable to contain the bacterial invasion or have been sufficiently damaged by trauma, periapical inflammation may result. There are one or more openings in the apex of the tooth through which blood vessels, lymphatics, and nerves enter or leave the
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JR.
pulpal tissue. Through these openings, a noxious agent that has overwhelmed the pulp or breakdown products of pulpal degeneration may escape the pulpal cavity and enter the periradicular tissues. The tissue immediately surrounding the apex of the tooth is the periodontal ligament or membrane. This ligament contains all of the elements of periosteum, in addition to some specialized cementum cells. Cementum is similar to cortical bone in many respects, but lacks a haversian system. Cementum is the tissue that connects the fiber bundles of the periodontal ligament to the tooth root surface. It responds to stress in essentially the same manner as periosteal bone. An inflammatory process starting in the periradicular tissue causes resorption of the lamina dura, or tooth socket, surrounding the apex of the root. The first change of periradicular inflammation seen radiographically is thickening of the periapical portion of the periodontal ligament caused by resorption of the lamina dura (Figs. 12 and 13). As the lesion progresses, it tends to become spherical and surround the apex of the tooth (Fig. 14). Numerous studies have shown that one cannot determine the character of a periapical lesion by its radiographic appearance. Granuloma, cyst, and abscess exhibit See figures on facing page. Fig. L-Smooth surface caries. Small enamel and dentin carious lesion (white arrow). The black arrow showsa large smooth surface lesion involving enamel and penetrating deep into the dentin. Fig. 2.-Smooth
surface caries. The arrow indicates enamellesions.
Fig. 3.-Pit and fissure caries. The pit and fissurecaries triangles have a common base upon the dentino-enamel junction. The enamel triangle of caries has its apex in the central pit of the rotated bicuspid (top arrow). The apex of the dentin extension of the cariesis indicated by the bottom arrow. Fig. 4.-Extensive smooth surface and pit and fissure caries. The pit and fissure lesion is in the mandibular secondmolar. The lesions in the distal portions of the first molar and second premolar (arrow) are smooth surface type caries. The latter involves the pulpal tissue. Fig. 5.-Medium sized carious lesion (A) is seenin the distal portion of the mandibular secondmolar. Note also the normal appearing pulp chamber in the mandibular first molar. B. Eighteen months later. Note the exposure of the pulp tissue in the mand!bular secondmolar by caries (right arrow) and internal resorption in the pulp chamber walls in the first molar (left arrow). Internal resorption results from loss of the odontoblastic layer of cells in the pulp chamber and their replacement in part by osteoclasts,as a responseto inflammation. Fig. 6.-Cemental caries. The carious lesion (arrow) is confined to the cementum and dentin of the root and doesnot affect the enamel. Fig. ‘I.-Severely abraded teeth. They have been worn down almost to the neck of the tooth. The pulp chambers (arrow) have become smaller by apposition of secondary dentin in responseto the mechanical stimulation of the abrasion. Fig. 8.-Pulp stone, probably the result of irritation to the pulpal tissue from the restorationsplaced in the tooth.
DISEASES
INVOLVING
THE TEETH
373
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the same radiographic characteristics .7 Histologic examination of the tissue removed from a periapical lesion is the only sure way of differentiating them. Figures 15 and 16 illustrate other simulators of periapical infection. In addition to radiolucencies, chronic inflammation of the periradicular tissues
or complete healing after a minor pulpal infection may cause periapical response in the form of certain patterns of calcification. The usual reaction is one of calcification in the marrow spaces surrounding the apex of the root. This may take the form of an enostosis (Fig. 17). These calcifications often indicate healing of the periradicular tissues, If, however, a thickened periodontal ligament space about the apex of the tooth is in evidence, the health of the tooth is still open to question ( Fig. 18). PERIODONTAL
DISEASE
Periodontal disease may be defined as a bacterial process resulting from accumulation of baclerial plaques about the teeth that cause loss of the supporting structures with loosening and exfoliation of the teeth as the end result in severe cases.There is a great body of evidence presented by Keyes to support the hypothesis that periodontal disease is the result of bacterial invasion into the gingival crevices surrounding the teeth. 3-s The disease starts with the See figures on facing page. Fig. 9.-Secondary dentin and sclerotic dentin. The white arrows indicate areas of sclerotic dentin. The black arrow shows filling in of the pulp chamber with secondary dentin. Both are normal and desirable reactions. Fig. I&-Internal resorption pulpal blood supply.
resulting
from trauma
Fig. Il.-Internal resorption in a primary pulp chamber of this tooth in response to B. The opposite side, same patient. The (arrow) and root canals is a result of trauma absence of the permanent successor should
causing
interference
with
the
tooth. A. Note the diminutive size of the irritation from the caries and restoration. internal resorption in the pulp chamber or bacterial invasion. Bilateral congenital be noted.
Fig. le.-Early periapical changes of periradicular inflammation. Thickening of the periodontal ligament space due to resorption of cementurn of root and lamina dura indicates chronic inflammation of these tissues from bacterial invasion from the infected pulpal tissue. Fig. IX-Chronic periapical infection resulting in thickened periodontal ligament and thickened lamina dura as evidence of enostosis of the marrow spaces surrounding both roots (white arrow). This is a response to chronic inflammation of the pulpal tissue which followed pulp exposure and capping (black arrow). Fig. 14.-P&apical infection. The distofacial root shows a large area of periapical radiolucency (arrow) which may be a granuloma, cyst, or abscess. Such lesions are indistinguishable from each other on the radiograph. Fig. IS.-Incomplete root formation (arrowheads) simulating periapical This normal stage of root development must be distinguished from periapical
infection. infection
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F. VU,
JR.
DISEASES
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See figures on facing page. Fig. 16.-Postoperative defect simulating periapical infection. An apicectomy has been recently performed on this endodontically treated tooth. This can be differentiated from periapical infection by history. Fig. 17.-Root resorption and development of enostosis (arrows), pulpal inflammat’o I n. Note also the pulpal calcification.
a result of chronic
Fig. 18.-Periapical radiolucency and root resorption of long-standing. Compare the puIp chamber sizes. The right incisor (right arrow) has a large pulp chamber, the left incisor (left arrow) has a normal thin pulp chamber as seen in the elderly, This indicates that the pulp in the right incisor was devitalized, probably many years prior to the time of this radiograph. Periapical radiolucency and root resorption (bottom arrow) are also a result of the long-standing chronic irritation caused by necrosis of the pulpal elements. Fig. 19.-Periapical arrows). The lesion (lower white arrow). Fig. 20.4ocalized
infection as an extension of a periodontal pocket (upper is complicated by cemental caries exposing the pulpal The black arrow indicates dental calculus. periodontal
disease. The arrow
indicates
an infrabony
white tissue
pocket.
Fig. 21.-Severe generalized periodontal disease and calculus accumulation (horizontal arrow). Note loss of alveolar bone to apical third of roots (vertical arrows). Fig. 22.~Severe localized periodontal disease causing loss of alveolar bone down to the apex of the root of the second molar (arrows) and extending horizontally to the middle third and interradicular area of the first molar. Fig, 23.~Early cates periodontal
periodontal disease. A moderate loss of alveolar bone height indi.. disease (upper arrow). Note also the large accumulation of calculus about the necks of the teeth (lower arrow).
Fig. 24.-Periodontal disease.A. Infrabony pockets in an interproximal view (black arrows). B. Normal side. White arrow shows narmal alveolar bone contour. Note that the bone crest in the interproximal area is parallel to a line connecting the enamel edges of the approximating teeth (parallel lines).
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attachment of bacteria to the surface of a tooth. They propagate and form gelatinous plaques which invade the gingival crevice and initiate the periodontal disease. This results in inflammation and subsequent loss of the crevicular epithelium and invasion of the soft tissue of the gingiva and periodontal ligament by the advancing bacterial colonies. The bacteria attach themselves to the cementum of the root and may cause root caries in addition to the periodontal disease (Fig. 19). The organisms which are most frequently implicated are diphtheroids which have been shown to develop filamentous branching forms in some in vitro and in vivo studies.4 Calculus, the calcified material seen on radiographs as spurs or convex concretions on the root and crown surfaces of teeth, has also been considered a cause of periodontal disease. Calculus occurs at two sites, above the gingiva or below, that is, within the gingival crevice. It is composed of organic matter, water, and inorganic salts. The inorganic component is mainly calcium phosphate with small amounts of magnesium and carbonate. There is no logical basis for postulating different etiologies for the two types of calculi. They have a common origin, saliva. Rather than causative, calculus may be a protective reaction of the host to the onslaught of periodontal disease. Bacteria are not essential in the formation of calculus8 (Figs. 19, 21 and 23). Periodontal disease may be localized or generalized; that is, it may affect the entire dentition equally or it may affect only a single or a group of teeth. The loss of alveolar bone may be general about the crown of the tooth, or a pocket may extend down the wall of the tooth interproximally (Figs. 20-23). The outer wall of this pocket may be bony, the inner wall of course being the
Fig. 25.-Root
resorption.
Blunting of the roots is an occasionalfinding following
orthodontic treatment. Fig. 26.-Retained primary canine tooth with root resorption. There is no permanent successorto the primary tooth to cause the type of resorption one seesduring the normal shedding process.The resorption (arrow) here is a result of occlusal trauma becausethe root surface area in a primary root is much smallerthan in a permanent tooth. The periodontal ligament is stressedto the point of blood supply interference, resulting in resorption of the root and repair with alveolar bone.
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DISEASESINVOLVlNGTHETEETH
Fig. 27.-Damage to unerupted permanent tooth, resulting from trauma to a primary tooth. A. Age 2. An accident had intruded his primary incisor (arrow) causing interruption of blood supply to the developing permanent central incisor. B. The location of the lesion datesthe time of the incident, Note the hypoplastic lateral incisor (arrow) and compare it to the normal lateral incisor of the opposite side (C).
cementum of the root, hence the term infrabony pocket. It is necessary to differentiate infrabony pockets from difference in height of alveolar bone caused by tooth tipping or resulting from developmental stages in young individauls. The crest of the alveolar bone generally parallels a line drawn between the cemento-enamel junction of adjacent teeth ( Fig. 24). MINOR TOOTH TRAUMA
Throughout the course of an individual’s life, his maxillary and mandibular incisor teeth may be subject to frequent trauma. The incident may be minor, involving only slight loosening of a tooth due to stretching of the periodontal ligament, or may result in complete exfoliation of the tooth. With respect to the damage to the pulpal tissue following trauma, both primary and permanent teeth react much the same way. If the blood or nerve suppIy to the pulpal at the apical foramen, the amount of damage may be tissue is interrupted severe. Slight injury generally results in stimulation of the pulpal tissue to lay down calcified material and eventually the entire pulp chamber is filled with this calcified “‘scar tissue.” If the blood supply is interrupted completely, the tissue within the pulpal chamber may degenerate and the normal maturation of the pulp chamber, i.e., diminution in size over the years, may not take place (Fig. 18). Injury to a tooth may also produce root resorption. Even the minor trauma caused by orthodontic tooth movement may sometimes do this (Fig. 25). Root resorption can also result from overstressing the periodontal ligament ( Fig. 26). Trauma to primary teeth during the developmental stages of the permanent
380
WILLIAMF.VLA,JR.
teeth poses certain special problems. When an injury involves, for instance, a maxillary primary central incisor at age 2, there is a good chance that the developing permanent tooth, whose crown is only half formed, will be damaged. If in the movement of the primary tooth root there is interference with the blood supply of the cells forming enamel on the permanent tooth, or if there is contact between the moving tooth root and the developing permanent tooth, an area of enamel hypoplasia will result on the crown of the permanent tooth, This may take many forms (Fig. 27). It may be a single pit in the enamel surface or it may be a ring of enamel hypoplasia about the crown of the developing tooth.rr One can predict the time at which the traumatic incident took place by the position of the defect on the permanent tooth if he consults any of the growth and development charts that are available.9, 11 When a permanent tooth is damaged to the extent that the pulp degenerates completely, an acute inflammatory response seldom follows; rather, there is a chronic inflammatory response at the apex and, of course, the narmal laying down of secondary dentin, with narrowing of the pulp chamber does not take place (Fig. 18). REFERENCES 1. Fitzgerald, R. J., Jordan, H. V., and Archard, H. 0.: Dental caries in gnotobiotic rats infected with a variety of Lactobacillus acidophilus. Arch. Oral Biol. 11:473, 1966. 2. Frostell, G., Keyes, P. H., and Larson, R. H.: Effect of various sugars and sugar substitutes on dental caries in hamsters and rats. J. Nutr. 93:65, 1967. 3. Keyes, P. H.: Research in dental caries. J. Amer. Dent. Ass. 76:1357, 1968. 4. --: Are periodontal pathoses caused by bacterial infections on cervicoradicular surfaces of teeth? J. Dent. Res. 49:223, 1970. 5. -, and Jordan, H. V.: Periodontal lesions in the Syrian hamster. III. Findings related to an infectious and transmissible component. Arch. Oral Biol. 9:377, 1964. 6. Larson, R. H., and Fitzgerald, R. J.:
Caries development in rats of different ages with controlled flora. Arch. Oral Biol. 9:705, 1964. 7. Mehta, F. S., and Shroff, B. C.: Aspects of dental diseases in the Indian aborigines, Int. Dent. J. 15:182, 1965. 8. Review article: The inhibitions of calculus. Dent. Abstr. 12:539, 1967. 9. &hour, I., and Massler, M.: Studies in tooth development: growth pattern of human teeth. J. Amer. Dent. Ass. 27: 1178, 1940. 10. Via, W. F., Jr.: Enamel defects induced by trauma during tooth formation. Oral Surg. 25:49, 1968. 11. Wuehrmann, A. H., and MansonHing, L. R.: Dental Radiology. fed. 2). St. Louis, Mosby, 1969, p. 279.
By WILLIAM
D
ENTAL CARIES and periodontal disease (pyorrhea) are two of man’s most prevalent diseases and are mentioned throughout all of recorded history. It is only recently, however, that the etiologic factors of these diseases have emerged. It is curious to note that both of these diseasesseem to have a common etiologic agent: the dental plaque. This is not to say that the plaque is a simple entity and is always the same, but rather that it contains the microorganisms and provides the environment in which these processesmay fluorish.3 DENTAL
CARIES
Radiologists have long recognized that caries appears in the teeth in three different forms. These were first thought to differ only in location on the tooth. Caries associated with the pits or crevices in teeth is called pit and fissure caries. That found on proximal and other smooth surfaces is termed smooth surface caries. The lesion found in older individuals in areas of root surface exposed by gingival recession is called root or cemental caries. Under carefully controlled experiments, it has been possible to produce in animals each type of caries independent of the others, indicating that different bacteria (substrate combinations ) may be required to produce each type.3 Certain streptococci appear to be associated with all types of caries+6 lactobacilli apparently can produce only pit and fissure caries;’ root caries may be caused by streptococcal strains, some of which are responsible also for periodontal disease.537 Certain age differences have been noted in caries susceptibility. Pit and fissure and smooth surface caries are found at all ages but appear more frequently and progress most rapidly in younger people. Cemental caries (root caries) is a disease of the elderly, in whom it may occur de novo.5 However, there can be no cemental caries without gingival recession first exposing the root surface. The various types of carious lesions and severity of cavitation are illustrated in Figs. 1-6. Progression of dental caries through the calcified parts of the tooth into the inner (pulpal) part of the tooth follows rather regular patterns. Pit and fissure caries starts as a point in the enamel. At the depth of a pit or fissure it spreads along the dentino-enamel junction, forming a triangle-shaped radiolucent area in the enamel with the base toward the dentino-enamel junction and the apex toward the tooth surface. A radiolucent triangle may appear in the dentin with the apex disposed toward the pulp of the tooth as the caries spreads at the dentino-enamel junction (Fig. 3).
WILLIAM F. VIA, JR., D.D.S., MS.: Professor and Chairman, nosis, Uniuersity of North Carolina School of Dentistry, Chapel
370
SEMINARS
IN ROENTGENOLOGY,
Department of Oral Hill, N. C. 27514.
Diag-
VOL. 6, No. 4 (OCTOBER), 1971
371
DISEASESINVOLVINCTHETEETH
Smooth surface caries seen in profile appears as two triangles. The enamel triangle base is at the tooth surface and its apex at the dentino-enamel junction, The dentin triangle has its base on the dentino-enamel junction and the apex toward the pulp ( Fig. 1) . Cemental caries resembles a semicircular radiolucency with the widest part at the root surface (Fig. 6). Progression of the lesion proceeds along the same patterns with enlargement of the radiolucency in all planes. It must be remembered that the bacteria progress in the dentin at a rate more rapid than the appearance of the radiolucency. The pulpal tissue of the tooth will exhibit histologic signs of inflammation long before the caries-caused radiolucency reaches the pulpal tissue. Bacterial invasion may result in death of the pulpal tissue and infection of the periapical tissues. PULPAL
CHAMBER
CHANGES
The dental pulp is the mature form of the organ which forms the dentin of the tooth. It serves as the nutritional and nerve supply for the dentin. As a matter of fact, the dentin may be considered a part of the pulpal tissue because the protoplasmic processes of the odontoblast penetrate the dentin to the dentino-enamel junction. The pulpal tissue contains the odontoblasts which form secondary dentin as a response to stimulation of the odontoblast processes. The pulp further contains fibroblasts, undifferentiated mesenchymal cells which may differentiate into osteoblasts, odontoblasts, or osteoclasts. In addition, pulpal tissue contains a circulatory system, including lymphatics, and the appropriate elements of nervous tissue. The pulpal tissue reacts to stress in a manner quite similar to periosteum or endosteum of bone, This is characterized by resorption of damaged calcified tissue followed by repair. There is a buildup of calcified areas in the pulpal tissue in response to external stimuli to the dento-enamel junction from caries, occlusal wear, or minor trauma to the tooth. Calcification may take the form of pulp stones or may be laid down on the walls of the pulp chamber by the odontoblast in response to a small carious lesion, a dental restoration, or a fracture of enamel and dentin, as in the breaking off of a corner of an incisor tooth (Figs. 7, 8, and 9). Resorption of the pulp chamber wall may take place as a response to an overwhelming bacterial invasion which may cause metaplasia of the pulpal tissue to granulation tissue. Trauma to the tooth can cause interference with the blood supply of the pulp. The odontoblastic layer of the pulpal tissue may be lost. This cellular breakdown may stimulate the undifferentiated mesenchymal cells of the pulp to form osteoclasts (odontoclasts) and result in resorption of the dentin wall of the pulp chamber (Fig. 10 and 11). PERIRADICULAR
CHANGES
When the defense mechanisms in the pulpal tissues are unable to contain the bacterial invasion or have been sufficiently damaged by trauma, periapical inflammation may result. There are one or more openings in the apex of the tooth through which blood vessels, lymphatics, and nerves enter or leave the
372
WILLIAM
F. VIA,
JR.
pulpal tissue. Through these openings, a noxious agent that has overwhelmed the pulp or breakdown products of pulpal degeneration may escape the pulpal cavity and enter the periradicular tissues. The tissue immediately surrounding the apex of the tooth is the periodontal ligament or membrane. This ligament contains all of the elements of periosteum, in addition to some specialized cementum cells. Cementum is similar to cortical bone in many respects, but lacks a haversian system. Cementum is the tissue that connects the fiber bundles of the periodontal ligament to the tooth root surface. It responds to stress in essentially the same manner as periosteal bone. An inflammatory process starting in the periradicular tissue causes resorption of the lamina dura, or tooth socket, surrounding the apex of the root. The first change of periradicular inflammation seen radiographically is thickening of the periapical portion of the periodontal ligament caused by resorption of the lamina dura (Figs. 12 and 13). As the lesion progresses, it tends to become spherical and surround the apex of the tooth (Fig. 14). Numerous studies have shown that one cannot determine the character of a periapical lesion by its radiographic appearance. Granuloma, cyst, and abscess exhibit See figures on facing page. Fig. L-Smooth surface caries. Small enamel and dentin carious lesion (white arrow). The black arrow showsa large smooth surface lesion involving enamel and penetrating deep into the dentin. Fig. 2.-Smooth
surface caries. The arrow indicates enamellesions.
Fig. 3.-Pit and fissure caries. The pit and fissurecaries triangles have a common base upon the dentino-enamel junction. The enamel triangle of caries has its apex in the central pit of the rotated bicuspid (top arrow). The apex of the dentin extension of the cariesis indicated by the bottom arrow. Fig. 4.-Extensive smooth surface and pit and fissure caries. The pit and fissure lesion is in the mandibular secondmolar. The lesions in the distal portions of the first molar and second premolar (arrow) are smooth surface type caries. The latter involves the pulpal tissue. Fig. 5.-Medium sized carious lesion (A) is seenin the distal portion of the mandibular secondmolar. Note also the normal appearing pulp chamber in the mandibular first molar. B. Eighteen months later. Note the exposure of the pulp tissue in the mand!bular secondmolar by caries (right arrow) and internal resorption in the pulp chamber walls in the first molar (left arrow). Internal resorption results from loss of the odontoblastic layer of cells in the pulp chamber and their replacement in part by osteoclasts,as a responseto inflammation. Fig. 6.-Cemental caries. The carious lesion (arrow) is confined to the cementum and dentin of the root and doesnot affect the enamel. Fig. ‘I.-Severely abraded teeth. They have been worn down almost to the neck of the tooth. The pulp chambers (arrow) have become smaller by apposition of secondary dentin in responseto the mechanical stimulation of the abrasion. Fig. 8.-Pulp stone, probably the result of irritation to the pulpal tissue from the restorationsplaced in the tooth.
DISEASES
INVOLVING
THE TEETH
373
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WILLIAM
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I1ISI:ASE.S ISVoL\:ISC,THETEETH
the same radiographic characteristics .7 Histologic examination of the tissue removed from a periapical lesion is the only sure way of differentiating them. Figures 15 and 16 illustrate other simulators of periapical infection. In addition to radiolucencies, chronic inflammation of the periradicular tissues
or complete healing after a minor pulpal infection may cause periapical response in the form of certain patterns of calcification. The usual reaction is one of calcification in the marrow spaces surrounding the apex of the root. This may take the form of an enostosis (Fig. 17). These calcifications often indicate healing of the periradicular tissues, If, however, a thickened periodontal ligament space about the apex of the tooth is in evidence, the health of the tooth is still open to question ( Fig. 18). PERIODONTAL
DISEASE
Periodontal disease may be defined as a bacterial process resulting from accumulation of baclerial plaques about the teeth that cause loss of the supporting structures with loosening and exfoliation of the teeth as the end result in severe cases.There is a great body of evidence presented by Keyes to support the hypothesis that periodontal disease is the result of bacterial invasion into the gingival crevices surrounding the teeth. 3-s The disease starts with the See figures on facing page. Fig. 9.-Secondary dentin and sclerotic dentin. The white arrows indicate areas of sclerotic dentin. The black arrow shows filling in of the pulp chamber with secondary dentin. Both are normal and desirable reactions. Fig. I&-Internal resorption pulpal blood supply.
resulting
from trauma
Fig. Il.-Internal resorption in a primary pulp chamber of this tooth in response to B. The opposite side, same patient. The (arrow) and root canals is a result of trauma absence of the permanent successor should
causing
interference
with
the
tooth. A. Note the diminutive size of the irritation from the caries and restoration. internal resorption in the pulp chamber or bacterial invasion. Bilateral congenital be noted.
Fig. le.-Early periapical changes of periradicular inflammation. Thickening of the periodontal ligament space due to resorption of cementurn of root and lamina dura indicates chronic inflammation of these tissues from bacterial invasion from the infected pulpal tissue. Fig. IX-Chronic periapical infection resulting in thickened periodontal ligament and thickened lamina dura as evidence of enostosis of the marrow spaces surrounding both roots (white arrow). This is a response to chronic inflammation of the pulpal tissue which followed pulp exposure and capping (black arrow). Fig. 14.-P&apical infection. The distofacial root shows a large area of periapical radiolucency (arrow) which may be a granuloma, cyst, or abscess. Such lesions are indistinguishable from each other on the radiograph. Fig. IS.-Incomplete root formation (arrowheads) simulating periapical This normal stage of root development must be distinguished from periapical
infection. infection
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F. VU,
JR.
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See figures on facing page. Fig. 16.-Postoperative defect simulating periapical infection. An apicectomy has been recently performed on this endodontically treated tooth. This can be differentiated from periapical infection by history. Fig. 17.-Root resorption and development of enostosis (arrows), pulpal inflammat’o I n. Note also the pulpal calcification.
a result of chronic
Fig. 18.-Periapical radiolucency and root resorption of long-standing. Compare the puIp chamber sizes. The right incisor (right arrow) has a large pulp chamber, the left incisor (left arrow) has a normal thin pulp chamber as seen in the elderly, This indicates that the pulp in the right incisor was devitalized, probably many years prior to the time of this radiograph. Periapical radiolucency and root resorption (bottom arrow) are also a result of the long-standing chronic irritation caused by necrosis of the pulpal elements. Fig. 19.-Periapical arrows). The lesion (lower white arrow). Fig. 20.4ocalized
infection as an extension of a periodontal pocket (upper is complicated by cemental caries exposing the pulpal The black arrow indicates dental calculus. periodontal
disease. The arrow
indicates
an infrabony
white tissue
pocket.
Fig. 21.-Severe generalized periodontal disease and calculus accumulation (horizontal arrow). Note loss of alveolar bone to apical third of roots (vertical arrows). Fig. 22.~Severe localized periodontal disease causing loss of alveolar bone down to the apex of the root of the second molar (arrows) and extending horizontally to the middle third and interradicular area of the first molar. Fig, 23.~Early cates periodontal
periodontal disease. A moderate loss of alveolar bone height indi.. disease (upper arrow). Note also the large accumulation of calculus about the necks of the teeth (lower arrow).
Fig. 24.-Periodontal disease.A. Infrabony pockets in an interproximal view (black arrows). B. Normal side. White arrow shows narmal alveolar bone contour. Note that the bone crest in the interproximal area is parallel to a line connecting the enamel edges of the approximating teeth (parallel lines).
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F. VIA,
JR.
attachment of bacteria to the surface of a tooth. They propagate and form gelatinous plaques which invade the gingival crevice and initiate the periodontal disease. This results in inflammation and subsequent loss of the crevicular epithelium and invasion of the soft tissue of the gingiva and periodontal ligament by the advancing bacterial colonies. The bacteria attach themselves to the cementum of the root and may cause root caries in addition to the periodontal disease (Fig. 19). The organisms which are most frequently implicated are diphtheroids which have been shown to develop filamentous branching forms in some in vitro and in vivo studies.4 Calculus, the calcified material seen on radiographs as spurs or convex concretions on the root and crown surfaces of teeth, has also been considered a cause of periodontal disease. Calculus occurs at two sites, above the gingiva or below, that is, within the gingival crevice. It is composed of organic matter, water, and inorganic salts. The inorganic component is mainly calcium phosphate with small amounts of magnesium and carbonate. There is no logical basis for postulating different etiologies for the two types of calculi. They have a common origin, saliva. Rather than causative, calculus may be a protective reaction of the host to the onslaught of periodontal disease. Bacteria are not essential in the formation of calculus8 (Figs. 19, 21 and 23). Periodontal disease may be localized or generalized; that is, it may affect the entire dentition equally or it may affect only a single or a group of teeth. The loss of alveolar bone may be general about the crown of the tooth, or a pocket may extend down the wall of the tooth interproximally (Figs. 20-23). The outer wall of this pocket may be bony, the inner wall of course being the
Fig. 25.-Root
resorption.
Blunting of the roots is an occasionalfinding following
orthodontic treatment. Fig. 26.-Retained primary canine tooth with root resorption. There is no permanent successorto the primary tooth to cause the type of resorption one seesduring the normal shedding process.The resorption (arrow) here is a result of occlusal trauma becausethe root surface area in a primary root is much smallerthan in a permanent tooth. The periodontal ligament is stressedto the point of blood supply interference, resulting in resorption of the root and repair with alveolar bone.
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DISEASESINVOLVlNGTHETEETH
Fig. 27.-Damage to unerupted permanent tooth, resulting from trauma to a primary tooth. A. Age 2. An accident had intruded his primary incisor (arrow) causing interruption of blood supply to the developing permanent central incisor. B. The location of the lesion datesthe time of the incident, Note the hypoplastic lateral incisor (arrow) and compare it to the normal lateral incisor of the opposite side (C).
cementum of the root, hence the term infrabony pocket. It is necessary to differentiate infrabony pockets from difference in height of alveolar bone caused by tooth tipping or resulting from developmental stages in young individauls. The crest of the alveolar bone generally parallels a line drawn between the cemento-enamel junction of adjacent teeth ( Fig. 24). MINOR TOOTH TRAUMA
Throughout the course of an individual’s life, his maxillary and mandibular incisor teeth may be subject to frequent trauma. The incident may be minor, involving only slight loosening of a tooth due to stretching of the periodontal ligament, or may result in complete exfoliation of the tooth. With respect to the damage to the pulpal tissue following trauma, both primary and permanent teeth react much the same way. If the blood or nerve suppIy to the pulpal at the apical foramen, the amount of damage may be tissue is interrupted severe. Slight injury generally results in stimulation of the pulpal tissue to lay down calcified material and eventually the entire pulp chamber is filled with this calcified “‘scar tissue.” If the blood supply is interrupted completely, the tissue within the pulpal chamber may degenerate and the normal maturation of the pulp chamber, i.e., diminution in size over the years, may not take place (Fig. 18). Injury to a tooth may also produce root resorption. Even the minor trauma caused by orthodontic tooth movement may sometimes do this (Fig. 25). Root resorption can also result from overstressing the periodontal ligament ( Fig. 26). Trauma to primary teeth during the developmental stages of the permanent
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WILLIAMF.VLA,JR.
teeth poses certain special problems. When an injury involves, for instance, a maxillary primary central incisor at age 2, there is a good chance that the developing permanent tooth, whose crown is only half formed, will be damaged. If in the movement of the primary tooth root there is interference with the blood supply of the cells forming enamel on the permanent tooth, or if there is contact between the moving tooth root and the developing permanent tooth, an area of enamel hypoplasia will result on the crown of the permanent tooth, This may take many forms (Fig. 27). It may be a single pit in the enamel surface or it may be a ring of enamel hypoplasia about the crown of the developing tooth.rr One can predict the time at which the traumatic incident took place by the position of the defect on the permanent tooth if he consults any of the growth and development charts that are available.9, 11 When a permanent tooth is damaged to the extent that the pulp degenerates completely, an acute inflammatory response seldom follows; rather, there is a chronic inflammatory response at the apex and, of course, the narmal laying down of secondary dentin, with narrowing of the pulp chamber does not take place (Fig. 18). REFERENCES 1. Fitzgerald, R. J., Jordan, H. V., and Archard, H. 0.: Dental caries in gnotobiotic rats infected with a variety of Lactobacillus acidophilus. Arch. Oral Biol. 11:473, 1966. 2. Frostell, G., Keyes, P. H., and Larson, R. H.: Effect of various sugars and sugar substitutes on dental caries in hamsters and rats. J. Nutr. 93:65, 1967. 3. Keyes, P. H.: Research in dental caries. J. Amer. Dent. Ass. 76:1357, 1968. 4. --: Are periodontal pathoses caused by bacterial infections on cervicoradicular surfaces of teeth? J. Dent. Res. 49:223, 1970. 5. -, and Jordan, H. V.: Periodontal lesions in the Syrian hamster. III. Findings related to an infectious and transmissible component. Arch. Oral Biol. 9:377, 1964. 6. Larson, R. H., and Fitzgerald, R. J.:
Caries development in rats of different ages with controlled flora. Arch. Oral Biol. 9:705, 1964. 7. Mehta, F. S., and Shroff, B. C.: Aspects of dental diseases in the Indian aborigines, Int. Dent. J. 15:182, 1965. 8. Review article: The inhibitions of calculus. Dent. Abstr. 12:539, 1967. 9. &hour, I., and Massler, M.: Studies in tooth development: growth pattern of human teeth. J. Amer. Dent. Ass. 27: 1178, 1940. 10. Via, W. F., Jr.: Enamel defects induced by trauma during tooth formation. Oral Surg. 25:49, 1968. 11. Wuehrmann, A. H., and MansonHing, L. R.: Dental Radiology. fed. 2). St. Louis, Mosby, 1969, p. 279.