Oral Pathology 1 Lecture 6 PDF

 Abnormalities Of Teeth I Environmental alterations of teeth Environmental effects on tooth structure development Post-developmental structure loss Environmental discolorations of teeth Localized disturbances...

 Abnormalities Of Teeth I Environmental alterations of teeth Environmental effects on tooth structure development Post-developmental structure loss Environmental discolorations of teeth Localized disturbances in eruption Developmental alterations of teeth  Developmental alterations in the number of teeth  Developmental alterations in the size of teeth  Developmental alterations in the shape of teeth  Developmental alterations in the structure of teeth 1. Environmental effects on tooth structure development  The ameloblasts are extremely sensitive to external stimuli, and many factors can result in abnormalities in the enamel.  When multiple factors are active simultaneously, the severity of the enamel defects is worse.  The primary hereditary abnormalities of the enamel that are unrelated to other disorders are termed amelogenesis imperfecta.  Dental enamel is unique in that remodeling does not occur after initial formation.  Therefore, abnormalities in enamel formation are permanent.  The enamel develops in three major stages: 1) Matrix formation: enamel proteins laid down. 2) Mineralization: minerals deposited, and majority of original proteins removed. 3) Maturation: final mineralization and remnants of original proteins removed.  The timing of the ameloblastic damage has a great effect on the location and appearance of the defect in the enamel.  The cause of the damage does not appear to be of major importance, because many different local and systemic stimuli can result in defects that have similar clinical appearances.  The final enamel represents a record of all significant insults received during tooth development. Clinical and radiographic Features  Almost all visible environmental enamel defects can be classified into one of three patterns: 1. Hypoplasia 2. Diffuse opacities 3. Demarcated opacities  The altered enamel may be localized or present on numerous teeth, and all or part of the surfaces of each affected tooth may be involved. Enamel hypoplasia: o A quantitative defect. o Occurs in the form of pits, grooves, or larger areas of missing enamel. Enamel opacities: o Qualitative defects. o May be diffuse or demarcated. o Appear as variations in the translucency of enamel. o Affected enamel is of normal thickness. A. Diffuse opacities: o Affected teeth demonstrate an increased white opacity with no clear boundary with the adjacent normal enamel. B. Demarcated opacities: o Show areas of decreased translucence, increased opacity, and a sharp boundary with the adjacent enamel. o The opacity may be white, cream, yellow, or brown. o Yellow or brown opacities are more porous than white opacities, and more strongly associated with post-eruptive loss of enamel.  Environmental enamel abnormalities are extremely common.  A common pattern is seen as a result of systemic influences, such as exanthematous fevers, that occur during first 2 years of life.  Horizontal rows of pits or diminished enamel are present on anterior teeth and first molars.  Enamel loss is bilaterally symmetric, and location of defects correlates well with Extensive Hypoplasia of Permanent Dentition Due developmental stage of affected teeth. to Childhood Illness and Antibiotic Use  A similar pattern of enamel defects can be seen in the cuspids, bicuspids, and second molars when the inciting event occurs around the age of 4 to 5 years. (1) Turner Hypoplasia  Another frequent pattern of enamel defects seen in permanent teeth is caused by periapical inflammatory disease or traumatic injury of the overlying deciduous tooth.  The altered tooth is called a Turner tooth.  The appearance of the affected area varies according to the timing and severity of the insult.  The enamel defects vary from focal areas of white, yellow, or brown discoloration to extensive hypoplasia, which can involve the entire crown.  The process is noted most frequently in the permanent bicuspids because of their relationship to the overlying deciduous molars.  Anterior teeth are involved less frequently.  In addition to classic Turner teeth, an increased prevalence of demarcated opacities has been reported in the permanent successors of carious primary teeth. (2) Molar-Incisor Hypomineralization (MIH):  A pattern of hypomineralization that predominantly affects the permanent first molars.  The process is defined as a hypomineralization of 1-4 permanent first molars, although the incisors also are affected frequently.  Prevalence varies widely from one country to another.  Affected enamel may be white, yellow, or brown, with a sharp demarcation between the defective and surrounding normal enamel.  Yellow or brown opacities appear to be more porous and are often associated with post-eruptive enamel loss.  With loss of enamel, the teeth become more sensitive leading to avoidance of proper oral hygiene with rapid caries development.  During attempts at dental therapy, these teeth often are highly sensitive and very difficult to anesthetize.  There appears to be spectrum of the disease in which only the molars may be affected, or the incisors also may be involved.  The extent of incisor involvement appears to correlate with the number of affected molars.  Affected incisors demonstrate only white opacities that primarily create esthetic problems.  The etiology of MIH remains unclear and may be multifactorial.  Suggested influences include: o Nutritional status. o Birth and neonatal factors. o Previous childhood illnesses. o High fever. o Antibiotics such as tetracycline or amoxicillin. o Environmental toxins. o Long duration of breast feeding (thought to transmit pollutants such as dioxin). o Fluoride. (3) Hypoplasia Caused by Antineoplastic Therapy  Dental developmental alterations can arise secondary to use of therapeutic radiation or chemotherapy.  Degree and severity of alterations related to patient’s age at treatment, form of therapy, and dose and field of radiation, if used.  The most severe alterations are associated with radiation; even low doses Stunting of the mandibular are associated with mild developmental defects in both enamel and dentin. incisor roots.  Frequently noted alterations include: o Hypodontia. o Microdontia. o Radicular hypoplasia. o Enamel hypoplasia. 26-year-old female who received chemotherapy and radiotherapy at age of 5 years. V-shaping and shortening in the roots and alveolar bone loss in the mandible.  Radiotherapy can also cause mandibular hypoplasia and a reduction of the vertical development of the lower third of the face.  Mandibular hypoplasia may be: o a direct effect of radiation, or o growth failure related to altered pituitary function caused by cranial radiation.  Chemotherapy alone results in much less dramatic alterations including: enamel hypoplasias and discolorations, slightly smaller tooth size, and occasional radicular hypoplasia.  6-year-old patient at diagnosis who received chemotherapy and radiotherapy. Notice 2-year-old patient at diagnosis who received tapering of mandibular first and chemotherapy and radiotherapy. Notice second premolars (dark microdontia of maxillary and mandibular second asterisks) and blunted canine premolars and second molars (asterisks). (light asterisks). (4) Dental Fluorosis  Ingestion of excess amounts of fluoride can result in significant enamel defects known as dental fluorosis.  Fluoride appears to create enamel defects through retention of the amelogenin proteins in the enamel structure.  This leads to the formation of hypomineralized enamel that alters light reflection and creates the appearance of white, chalky areas.  Most of the problems associated with dental fluorosis are aesthetic, particularly when the anterior teeth are affected.  The severity of dental fluorosis is dose and time-dependent.  Affected teeth are usually caries resistant, and the altered tooth structure appears as areas of white opaque enamel that may have zones of yellow to dark-brown discoloration.  In the past, areas of moderate-to-severe enamel fluorosis were termed mottled enamel.  True enamel hypoplasia is uncommon but can occur as deep, irregular, and brownish pits.  Because other factors can result in a similar pattern of enamel damage, a definitive diagnosis requires: o bilaterally symmetric distribution of defects. o evidence of prior excessive fluoride intake, or elevated levels of fluoride in enamel or other tissues.  Initially, fluoride’s ability to reduce caries was thought to be mainly due to fluorapatite crystal formation.  It is now agreed that the post-eruptive effects of fluoride are predominant and control caries by altering the demineralization and remineralization process that occurs at the tooth/bacterial biofilm interface.  Consumption of optimally fluoridated water has been associated with a low frequency of mildly altered enamel.  Close monitoring of all sources of fluoride intake during the first 3 years of life is recommended strongly.  A significant reduction in dental fluorosis can be seen if brushing with fluoride toothpaste does not start until after 12 months of age.  In addition, reconstitution of infant formula with fluoridated water should be avoided. (5) Syphilitic Hypoplasia  Congenital syphilis results in a pattern of enamel hypoplasia that is well known but currently so rare.  Anterior teeth altered by syphilis are termed Hutchinson incisors: o Crowns shaped like straight-edge screwdrivers, with greatest circumference present in middle third and a constricted incisal edge. o Middle portion of incisal edge often demonstrates a central hypoplastic notch.  Altered posterior teeth are termed mulberry molars: o Constricted occlusal tables. o Disorganized surface anatomy that resembles the surface of a mulberry. Treatment and Prognosis (To all Environmental effects on tooth structure development)  Most defects in the enamel are cosmetic rather than functional dental problems.  Those affected by dental fluorosis often benefit from surface microabrasion and restorative dentistry.  Other types of environmental enamel hypoplasia are associated with an increased prevalence of caries secondary to focal loss of enamel or because of imperfect enamel.  Aesthetically or functionally defective teeth can be restored through a variety of techniques, such as: o Composite resin restorations. o Labial veneers. o Full crowns. 2. Post-developmental structure loss  Tooth structure can be lost after its formation by a variety of influences beyond caries or traumatic fractures.  Destruction can begin on the enamel surface of the crown through abrasion, attrition, erosion, or abfraction.  In addition, loss of tooth structure can begin on the dentin or cemental surfaces of the teeth by external or internal resorption. TOOTH WEAR  Tooth wear, also termed tooth surface loss, is a normal physiologic process that occurs with aging.  It must be considered pathologic when the degree of destruction creates functional, aesthetic, or dental sensitivity problems.  Although the four causes of tooth wear (i.e., attrition, abrasion, erosion, and abfraction), are often discussed as independent pathoses, most of these types of tooth loss are the result of a combination of influences.  Many cases of attrition are accelerated by the presence of abrasive materials in the mouth.  Erosion or abrasion often further damages areas of dentin exposed by attrition or abfraction.  Areas softened by erosion are more susceptible to attrition, abrasion, and abfraction.  The clinician should appreciate that acquired environmental loss of tooth structure is often multifactorial. (1) Attrition  The loss of tooth structure caused by tooth-to-tooth contact during occlusion and mastication.  Some degree of attrition is physiologic, and the process becomes more noticeable with age.  When the amount of tooth loss is extensive and begins to affect aesthetic appearance and function, the process must be considered pathologic.  The following factors can accelerate tooth destruction by attrition: o Poor-quality or absent enamel (e.g., fluorosis, environmental or hereditary enamel hypoplasia, or dentinogenesis imperfecta). o Premature contacts (edge-to-edge occlusion). o Intraoral abrasives, erosion, and grinding habits. Clinical Features  Occurs in both deciduous and permanent dentitions.  Most frequently, the incisal and occlusal surfaces are involved.  Large, flat, smooth, and shiny wear facets are found in a relationship that corresponds to the pattern of occlusion.  Thus, the lingual surfaces of anterior maxillary teeth and the labial surfaces of the anterior mandibular teeth are affected.  The interproximal contact points also are affected from the vertical movement of the teeth during function.  Over time, this interproximal loss can result in a shortening of the arch length.  Pulp exposure and dentin sensitivity are rare because of the slow loss of tooth structure and the deposition of reparative tertiary dentin within the pulp chamber. (2) Abrasion  The pathologic wearing away of tooth structure or restoration secondary to the mechanical action of an external agent.  The most common cause of abrasion is toothbrushing that combines abrasive toothpaste with heavy pressure and a horizontal brushing stroke.  Other items frequently associated with dental abrasion include pencils, toothpicks, pipe stems, and bobby pins.  Chewing tobacco, cracking nuts and seeds, biting fingernails or thread, and using dental floss inappropriately also can cause clinically significant abrasion. Clinical Features  Abrasion has a variety of patterns, depending on the cause.  Toothbrush abrasion appears as horizontal cervical notches on the buccal surface of exposed radicular cementum and dentin.  The defects usually have sharply defined margins and a hard, smooth surface.  If acid also is present, then the lesions are more rounded and shallower.  The degree of loss is greatest on prominent teeth (i.e., cuspids, bicuspids, and teeth adjacent to edentulous areas) and occasionally is more advanced on the side of the arch opposite the dominant hand.  Thread biting, cracking nuts and seeds, or the use of pipes or bobby pins usually produces rounded or V-shaped notches in the incisal edges of anterior teeth.  The inappropriate use of dental floss or toothpicks results in the loss of interproximal radicular cementum and dentin. (3) Erosion  The loss of tooth structure caused by a nonbacterial chemical process.  Due to exposure to acids or chelating agents (anions which can bind or complex calcium).  Saliva aids remineralization and contains bicarbonate with a significant buffering ability.  Salivary buffering capability is reduced in situations with low flow rates such as therapeutic radiation, certain medications, and Sjögren syndrome (dry mouth).  Because saliva has the ability to remineralize tooth surfaces exposed to acid, it appears that areas of erosive damage must have some abrasive component that removes the softened enamel before remineralization.  Sources of acid in the mouth: o Often foods or drinks. o Some medications (e.g., chewable vitamin C and aspirin tablets). o Swimming pools with poorly monitored pH. o Chronic involuntary regurgitation (e.g., hiatal hernia, esophagitis, chronic alcoholism, and pregnancy). o Voluntary regurgitation (e.g., psychologic problems, bulimia, and occupations that require low body weight). o Industrial environmental exposure. Clinical Features  The tooth loss does not correlate with functional wear patterns or with those typically associated with known abrasives.  The predominant sites of tooth loss are those not protected by the serous secretions of the parotid and submandibular glands.  Facial and palatal surfaces of maxillary anterior teeth and facial and occlusal surfaces of mandibular posterior teeth are affected most frequently.  The classic pattern is a cupped lesion in which a central depression of dentin is surrounded by elevated enamel.  Cupped areas are seen on the occlusal cusp tips, incisal edges, and marginal ridges.  Commonly affects facial surfaces of maxillary anteriors and appears as shallow spoon-shaped depressions in the cervical portion of the crown.  Posterior teeth frequently exhibit extensive loss of occlusal surfaces, and the edges of metallic restorations may be become above the level of tooth structure.  After a portion of cuspal enamel is lost, dentin is destroyed more rapidly than the remaining enamel, resulting in a concave depression of dentin surrounded by an elevated rim of enamel.  The more rapid dissolution of dentin can lead to undermined enamel that often is lost easily by chipping.  Occasionally, entire buccal cusps are lost.  When palatal surfaces are affected, the exposed dentin has a concave surface and shows a peripheral white line of enamel.  Active erosion typically reveals a clean, unstained surface, whereas inactive sites become stained and discolored.  Erosion limited to the facial surfaces of the maxillary anterior teeth is often associated with dietary sources of acid.  When the tooth loss is confined to incisal portions of anterior teeth of both arches, an external environmental source is suggested.  When erosion is located on palatal surfaces of maxillary anterior teeth and occlusal surfaces of posterior teeth of both arches, regurgitation of gastric secretions is a probable cause.  The location of the tooth structure loss may suggest the cause of the damage but is not completely reliable. (4) Abfraction  Loss of tooth structure from occlusal stresses that create repeated tooth flexure with failure of enamel and dentin at a location away from the point of loading.  When occlusal forces are applied eccentrically to a tooth, the tensile stress is concentrated at the cervical fulcrum, leading to flexure that may produce disruption in the chemical bonds of the enamel crystals in the cervical areas.  Once damaged, the cracked enamel can be lost or more easily removed by erosion or abrasion.  While some propose that abfraction causes most cervical tooth loss; others believe that little evidence exists to indicate that this sequence of events actually occurs in the mouth.  Abfraction is considered by others to be a theoretical concept that has never been proven to apply to human teeth in normal function.  They suggest that the engineering models used to justify abfraction have not taken into consideration the cushioning provided by the surrounding bone and periodontium, which may dissipate occlusal forces acting on a tooth.  They also maintain that dentin can withstand greater tensile stress than enamel, thus it is difficult to see how such a mechanism could contribute to abrasion of the more elastic dentin.  Due to the uncertain causes for this pattern of enamel loss, investigators have warned against destructive, irreversible treatment such as extensive occlusal adjustments. Clinical Features  Wedge-shaped defects limited to the cervical area of the teeth and may closely resemble cervical abrasion or erosion.  Clues to the diagnosis include defects that are deep, narrow, and V-shaped and often affect a single tooth with adjacent unaffected teeth.  In addition, occasional lesions are subgingival, a site typically protected from abrasion and erosion.  The lesions predominantly affect the facial surfaces of the bicuspids and molars. TOOTH WEAR: CLINICAL FEATURES  In all forms of tooth wear, the process typically proceeds at a slow rate that allows deposition of tertiary dentin and prevents pulp exposure, even when extensive loss of tooth structure is present.  In some cases, especially in the deciduous dentition, the tooth loss can proceed at a more accelerated rate, which results in a near or frank exposure of the pulp. TOOTH WEAR: TREATMENT AND PROGNOSIS  Normal levels of attrition require no therapy.  Intervention is reserved for cases that create a pathologic degree of tooth loss.  The clinician must remember that tooth wear has a multifactorial cause.  Immediate therapy directed toward resolution of tooth sensitivity and pain, if any.  Identifying the causes and protecting the remaining dentition are important goals.  Treatment varies with the cause and may include restorative dentistry, occlusal guards, desensitizing agents and fluoride application.  Patient education about the possible causes is important. 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