![]() Background, Pathophysiology, Causes of Extrinsic Discoloration. Numerous causes for intrinsic tooth discoloration exist. Stain distribution varies from localized (eg, 1 or 2 teeth) to a regional or generalized involvement of primary and secondary teeth. Localized discoloration may be a result of either preeruptive or posteruptive processes, whereas widespread involvement indicates a deviation in normal tooth formation. An understanding of the timing of tooth formation (particularly calcification and eruption sequences) can help explain the causes of intrinsic discoloration (see Causes). Dental materials. Dental restorations most commonly cause intrinsic discoloration. Although clinical laboratories generally measure the total serum calcium level, it is occasionally valuable to measure the serum level of ionized calcium.![]() Amalgam restorations can generate corrosion products (eg, silver sulfide), leaving a gray- black color in the tooth, especially in large cavity preparations with undermined enamel. Pins, composites, and glass ionomer and acrylic restorations gradually can leave a gray hue in the tooth adjacent to the material. ![]() Other dental materials that cause intrinsic discoloration include eugenol, formocresol, root canal sealers, and polyantimicrobial pastes. In the absence of extrinsic staining, this age- related phenomenon is due to a progressive loss in enamel from attrition or tooth wear that reveals the natural yellow color of underlying dentin. Note the image below. Areas of complete enamel loss are most commonly found on the incisal (chewing) surfaces of anterior teeth. This loss frequently occurs in older adults, whose teeth show a contrast in colors between enamel and dentin. Tooth abrasion manifests as yellow areas in which the enamel surface is lost (eg, buccal cervical regions) as a result of overzealous toothbrushing with a hard- bristled or medium- bristled toothbrush. Note the image below. The erosion of enamel caused by frequent ingestion of acidic foods and beverages and from the regurgitation of acid from the stomach (eg, anorexia or bulimia nervosa) can lead to a yellow tooth discoloration. In patients with anorexia or bulimia, a yellow discoloration develops on lingual tooth surfaces where the acid reflux material makes contact with the teeth. Certain tooth surfaces are at greater risk for dental caries. These surfaces include the occlusal grooves and pits of posterior teeth (class I caries), the smooth surfaces between teeth (class II caries for posterior teeth, class III caries for anterior teeth), and the smooth surfaces at the enamel- cementum interface at the free gingival margin (cervical, root surface, or class V caries Caries also may involve the incisal edge of anterior teeth (class IV or VI). Note the image below. The pathogenesis of dental caries begins with an incipient lesion confined to the enamel layer. Once the enamel layer is breached, caries tends to rapidly progress in the dentin, undermining the superficial enamel layer. Incipient carious lesions are associated with plaque accumulation and manifest as chalky white areas of discoloration secondary to hypocalcification. Patients with orthodontic brackets are at great risk for caries because of suboptimal plaque removal. As caries progresses into the dentin, the overlying translucent enamel reveals the color of the underlying caries and appears yellowish brown. ![]() Extrinsic dental stains are caused by predisposing factors and. Background A high dietary calcium intake is strongly suspected of increasing the risk of kidney stones. However, a high intake of calcium can reduce the urinary. Displaying Powerpoint Presentation on Slide 1 available to view or download. Download Slide 1 PPT for free. Slide 1 Powerpoint Presentation. Nama Generik MDC Kategori Indikasi Dos; Abacavir Sulphate 600 mg and Lamivudine 300 mg Tablet: J05AR02964T1001XX: A*: Antiretroviral combination therapy of HIV. ScienceDirect is the world's leading source for scientific, technical, and medical research. Explore journals, books and articles. Extensive caries that involve destruction of both enamel and dentin produce a color that ranges from light brown, to dark brown or almost black as seen in the images below. The brown color is attributed to the formation of Maillard pigments (reaction between proteins and small aldehydes produced by cariogenic bacteria), melanins, lipofuscins, and uptake of various food colors and bacterial pigments. Such teeth commonly are referred to as Turner teeth as seen in the image below. Unerupted permanent incisors commonly are affected after intrusion injuries to primary incisors in young children who fall on their faces. Trauma that occurs to erupted teeth also causes discoloration as seen in the images below. This discoloration frequently occurs in teeth that have fully formed roots and have sustained irreversible pulpal injury caused by avulsions, intrusions, luxations and subluxations, or fractures involving the pulp chamber. ![]() Trauma can cause intrapulpal hemorrhage and iron sulfide deposition along the dentinal tubules, producing a bluish black cast. Some occlusal trauma occurs over a protracted period of time (eg, excessive orthodontic forces). Rarely, this trauma leads to pulpal hemorrhage; however, it can produce a subtle grayish brown cast. Infections. Periapical odontogenic infections of the primary teeth can disrupt normal amelogenesis of the underlying secondary (permanent) successors and involve a potential for localized enamel hypoplasia. PHYSIOLOGY OF ADULT HOMO SAPIENS - BLOOD (HAEMATOLOGY : PLASMA, BLOOD CELLS, AND COAGULATION) AND LYMPH (see also circulation, diseases affecting blood and. Altmetric: 1; Views: 1,916; More detail. Systematical Evaluation of Mechanically Strong 3D Printed Diluted magnesium Doping Wollastonite Scaffolds on. The above policy is based on the following references: Bone Graft Substitutes: U.S. Food and Drug Administration (FDA), Center for Devices and Radiological Health. Crown formation begins in utero; therefore, the potential for extensive intrinsic discoloration of the primary dentition may be present throughout pregnancy. Although rare, maternal rubella or cytomegalovirus infection and toxemia of pregnancy can lead to tooth discoloration, which generally manifests as a focal opaque band of enamel hypoplasia that is confined to the primary teeth forming enamel at the time of maternal infection as seen in the image below. Crown formation of the secondary dentition occurs until the child is aged approximately 8 years. Systemic postnatal infections (eg, measles, chicken pox, streptococcal infections, scarlet fever) can also cause enamel hypoplasia. The bandlike discolorations on the tooth are visualized where the enamel layer has variable thickness and becomes extrinsically stained after tooth eruption. Medications. Since the 1. Once in the bloodstream, tetracycline can be incorporated into the calcification process of developing teeth, in which it affects either primary or secondary dentition after maternal or childhood ingestion, respectively. Tetracyclines diffuse through dentin to the enamel interface, chelating calcium ions and incorporating into hydroxyapatite as a stable orthophosphate complex. The amount of drug incorporation is ultimately determined by the distribution of tooth discoloration and is equivalent to serum blood levels and the duration of exposure. When the affected teeth first erupt, they have a bright- yellow bandlike appearance that fluoresces under ultraviolet light, although upon exposure to sunlight, the color gradually changes to gray or red- brown. Note the image below. Minocycline is a second- generation derivative of tetracycline. The ingestion of minocycline can lead to a green- gray or blue- gray intrinsic staining of teeth. Unlike with other tetracyclines, staining occurs during and after the complete formation and eruption of teeth. This binding causes the formation of insoluble salts that are either exuded from gingival crevicular fluid to extrinsically stain the enamel or intrinsically incorporated into the secondary dentin. ![]() In its mildest form, fluorosis appears as faint white lines or streaks on the enamel. Moderate fluorosis has more obvious opaque regions referred to as enamel mottling, whereas severe fluorosis appears with extensive mottling that readily chips and stains and leads to pitting and brown discoloration. Note the image below. An increase in the prevalence of mild- to- moderate fluorosis has been observed in the United States over the last decade, even in areas with nonfluoridated public water supplies. Clinicians can help in preventing fluorosis by teaching parents about fluoride use and good toothbrushing habits for children. Fluoride sources are numerous and include naturally or artificially fluoridated drinking water, commercially available beverages, foods prepared in fluoridated water, chewable vitamins, oral healthcare products (eg, toothpastes, mouthrinses, oral fluoride supplements), and professional fluoride products prescribed by dentists. The fluoride concentration of naturally fluoridated water varies depending on geographic location. For example, in some areas of Africa, the concentration may be as high as 1. Artificially fluoridated water supplies usually have a fluoride concentration of 1 ppm. Several clinical indices have been developed to measure fluorosis. Deficiencies can result in dose- related or exposure- related enamel hypoplasia. Diseases that can cause hyperbilirubinemia and intrinsic tooth discoloration include sickle cell anemia; thalassemia; hemolytic disease of the newborn (HDN) due to either Rhesus factor, ABO, or other erythrocyte antigen incompatibility; biliary atresia . These diseases have the potential to cause hyperbilirubinemia and the subsequent dose- dependent incorporation of biliverdin (a by- product pigment of bilirubin) into developing teeth, producing a jaundicelike yellow- green tint on the tooth surfaces. These diseases have the potential to cause hemolysis and the subsequent dose- dependent incorporation of biliverdin (by- product pigment of bilirubin) into developing teeth, producing a jaundicelike yellow- green tint on the tooth surfaces. These are hereditary diseases with a propensity for intrinsic tooth discoloration. AI affects both primary and secondary dentitions and demonstrates numerous clinical manifestations that are classified into the following 4 types . Hypoplastic teeth with rough or pitted enamel surfaces are at a greater risk for extrinsic staining. The teeth typically have an abnormally thin enamel layer that reveals the yellow color of dentin beneath the enamel. Teeth with hypomaturation have soft enamel with a mottled opaque white, yellow, or brown discoloration. The enamel in the hypocalcified type is yellow to orange, soft, and lost soon after eruption. Therefore, hypocalcified teeth develop dark stains and are at high risk for dental caries. One type is associated with osteogenesis imperfecta, and the other type affects the teeth alone. The primary and secondary teeth are affected, and they have a brown or blue appearance with a distinctive translucent quality. The enamel chips off easily, and the teeth are prone to occlusal wear and caries. DD occurs in 2 types. This notice is based on the. Dental Plaque Subcommittee of the. Nonprescription Drugs Advisory Committee (NDAC) and is part of FDA's. OTC drug products. Submit. reply comments by October 2. Submit electronic comments to http: //www. Sherman, Center for Drug. Evaluation and Research (HFD- 5. Food and Drug Administration, 5. Fishers Lane, Rockville, MD 2. The report has been prepared. FDA, and the agency has not yet fully evaluated the. The Subcommittee's findings appear in this document to obtain. Subcommittee's recommendations. This document represents the best. Subcommittee, but does not necessarily. The Subcommittee. An antigingivitis/antiplaque active ingredient combined. Therefore, the agency is. Data are needed to. The agency invites supporting data and information. OTC use. The agency is seeking specific. While an ingredient may also be. Subcommittee stated that the. II. C of. this document). The Subcommittee agreed, however, that the exact. However, the Subcommittee's proposed indication for this. Because the. Subcommittee believed that none of the submitted active ingredients. More importantly, because of the safety concern. Under the OTC drug review procedures. TFM, which. has the status of a proposed rule. Final agency action occurs in the. All submitted. information will be put on public display in the Dockets Management. Branch (see ADDRESSES) after June 3. U. S. C. 5. 52(b), or. Federal Food, Drug, and Cosmetic Act (the act). U. S. C. Requests for confidentiality should be submitted to. Robert L. Sherman, Center for Drug Evaluation and Research (see FOR. FURTHER INFORMATION CONTACT). On or after that date. OTC drug products that are subject to the monograph and that contain. NDA) or abbreviated new drug application (ANDA). The final regulations. OTC drug review under Sec. In accordance with these regulations, a request for data and. OTC drug products bearing. Federal. Register of September 1. FR 3. 85. 60). These claims included the. Vincent's disease, periodontal disease, and tooth- . Robertson, Chairperson. Charles N. Bertolami (resigned March 2. William H. Bowen (term ended October 3. Carlos E. Norman. Burton Rosan. Christine D. Wu. The Subcommittee, comprised of two members from the Panel plus five. Panel, was subsequently formed to evaluate. Each of the following was a voting member of the. William H. Bowen, Chairperson (term ended April 1. Robert J. Genco, Chairperson (from April 1. December 3, 1. 99. Ralph D'Agostino. Max A. Listgarten. Shelia M. Mc. Guire. Eugene D. Savitt. Stanley R. Saxe. Jorgen Slots (resigned April 1. Christine D. Wu. Several nonvoting liaison representatives served on the. Subcommittee. Jean Frazier, served as the consumer liaison until. June 6, 1. 99. 6, followed by Susan Cohen, until May 1. Donald S. Curro, served as industry liaison. October 3. 1, 1. 99. Lewis P. Chapman served as CDER Executive. Secretary to the Subcommittee until December 1. Andrea Neal until May 9, 1. Rhonda Stover (interim). May 1. 99. 8, followed by Kathleen Reedy. Rippere served as. CDER liaison to the Subcommittee until June 7, 1. Robert. L. Mason served as special assistant to the. Subcommittee until June 7, 1. Working meetings of the. Subcommittee were held on December 1. June 2. 8 and 2. 9. October 1. 1, and December 5, 6, and 7, 1. April 1. 0, 1. 1, and 1. August 1. 4 and 1. December 4 and 5, 1. June 6 and 7, and. December 1. 6 and 1. October 2. 9 and 3. May 2. 7, 2. 8, and 2. October 2. 2, and December 2 and 3, 1. Joint meetings of the Panel and. Subcommittee were held on August 2 and 3, 1. December 6. 1. 99. Minutes of most Subcommittee meetings are on public display in. Dockets Management Branch (see ADDRESSES). Bartizek, Kenneth Baumgartner. William J. Cheever, Philip Cole, W. Crisanti. Catherine C. Davis, Phillip Derfler, John M. Gary Flamm, William. E. Graham, Robert Heller, Jane. E. Hyman, Eugene Kamper, Linda M. Marshall, Stephanie A. Mc. Clanahan, Stephen H. Merski, David. Morrisson, Kevin P. Lee. Peeler, Julie H. Serafino, Samuel Shapiro, Robert L. Sherman, Chakwan. Siew, Gregory Singleton, James Skiles, Thomas J. William. Soller, Steven D. Stookey, Howard Strassler. Stanley Tarka, Jr., John M. Treacy, Jack Vincent, Frank A. Volpe. Michael Weintraub, Clifford W. White, Robert. White, Charles Wiggins, David Williams, Gary M. Williams, Deborah Winn. Roy Witkin, and Patrice Wright. No person who so requested was denied. Panel or Subcommittee. The ADA also provided its ``Guidelines. Acceptance of Chemotherapeutic Products for the Control of. Supragingival Plaque and Gingivitis'' to the Subcommittee for. OTC antigingivitis/antiplaque ingredients. Submission of Data and Information. Under the notices published in the Federal Register of September. FR 3. 86. 50), and March 8, 1. FR 9. 91. 5), the following. OTC drug products that the Panel/. Subcommittee determined contained active ingredients or labeling. Submissions by Firms. Table 1.- -Firms and Submitted Products. Firm Submitted Products. American Xyrofin (Morgan, Lewis & Xylitol All Natural Toothpaste. Bockius) Washington, DC 2. Xytol 3. 2 Dental Cream. Merck, Frankfurter, Germany Thera- Med, Cholordont M. Michaels Research Associates, Therasol Brush & Rinse Antiplaque. Inc., Milford, CT 0. Oral Hygiene Solution, Therasol. Brush & Rinse Liquid Dentifrice. Oral Irrigant. FDA has defined ``active ingredient'' in its current good. Sec. The term includes. Active Ingredients Submitted For Review. Labeled Ingredients Contained in Marketed Products Submitted to the. Alkyl dimethyl amine oxide. Alkyl dimethyl glycine. Bromchlorophene. Carbamide peroxide. Cetylpyridinium chloride. Chlorhexidine digluconate. Dicalcium phosphate dihydrate. Hydrogen peroxide. Methyl salicylate. Peppermint oil. Polydimethylsiloxane. Povidone iodine. Sanguinaria extract. Sodium bicarbonate. Sodium citrate. Sodium lauryl sulfate. Soluble pyrophosphate. Stannous fluoride. Stannous pyrophosphate. Unsaponifiable fraction of corn oil. Zinc chloride. Zinc citrate. Some of these ingredients (bromchlorophene, chlorhexidine. United States. 3. Although the Subcommittee. OTC drug review. as part of this advance notice of proposed rulemaking and, therefore. In addition, although xylitol was. Subcommittee, the two firms that submitted data. Subcommittee. Referenced OTC Volumes. All ``OTC Volumes'' cited throughout this document refer to. Federal Register of September 1. March 8. 1. 99. 1. The information included in these volumes, except for those. Sec. General Statements and Recommendations. The Subcommittee adopted the following definitions as its intended. OTC drug. products for the reduction or prevention of dental plaque and. The Subcommittee was aware that some degree of variation. The hard concretions (i. Calculus on. teeth is clinically classified into supragingival calculus, which is. Organized coherent gel- like or mucoid masses. Plaque also contains other cells (e. It adheres to the teeth and other surfaces of the oral. It occurs at the orifice of the gingival crevices and in the. Plaques may differ markedly in biochemical or. The shallow groove between the tooth and. An inflammatory lesion of the gingiva that is. Gingivitis is characterized by. The gingiva also may bleed upon gentle provocation such as. Gingivitis is usually not. Self- administered processes aimed at. A thin, colorless, translucent film derived from. A few hours after deposition. These processes. represent the earliest stages of plaque formation. A disease condition of the periodontium. A synonymous term for calculus. Background and General Discussion of Terms. The Subcommittee was charged with the evaluation of the safety and. OTC drug products in light of present- day knowledge and. Manufacturers included some of these scientific articles in. FDA to provide a scientific basis for claims made. Data supplied by. Subcommittee in making judgments. Plaque. Plaque, also known as dental plaque and/or microbial plaque, has. Plaque has a critical etiological role. It is now clear that dental plaque is a variable biologic. Plaque from. sites of similar clinical health within individual subjects tends to be. Even though there is considerable variation within dental. Dental plaques are subdivided into supragingival plaque. The distinction resides in the location of. The microbial populations may. Because the matrix provides plaque. The tenacity of plaque to adhere to the surfaces of. For example, microorganisms found in dental. Actinomyces species, Streptococcus sanguis, S. This difference in. Some dental plaques are not. However, the two types of. The pathogenic potential is. It may be prudent to treat all plaques as having pathogenic. Calculus. Calculus is a hard concretion that forms on the teeth or dental. Human. calculus is essentially mineralized dental plaque, which is almost. There may also be loosely held materials. In germ- free animals. Ref. However, in humans, virtually all calculus seen clinically. Calculus formation occurs in an orderly fashion. The process occurs more. Calculus. may also form supragingivally, coronal (toward the crown) to the. Supragingival calculus is found in greater amounts on. Both subgingival and supragingival calculus are often. Although. subgingival calculus is a contributing factor in the development of. Subgingival calculus interferes with the regeneration of. The. formation of supragingival calculus can be limited through mechanical. Preventing subgingival calculus formation, if. Present methods do. Gingivitis. Gingivitis, an inflammation of the gingiva, affects most of the. The signs of gingivitis are tissue. The gingiva may also bleed upon gentle provocation. Some signs of. gingivitis, such as bleeding, can be identified by lay persons. While most cases of periodontitis are believed to start. Histologically, gingivitis is characterized by. Sometimes the epithelium lining the sulcus (crevice. In. gingivitis, the junctional epithelium usually is at or near the. In the early stages of gingivitis when. Under these conditions, self- treatment of gingivitis is. When OTC drug products for the prevention and control of. It is limited to the. However, people are seldom.
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