DEFINITION/OVERVIEW
- Any change from the norm: the normal color varies and depends on the shade, translucency, and thickness of enamel
- Translucent enamel is bluish-white; opaque enamel is grey-white
- Extrinsic: from surface accumulation of exogenous pigment
- Intrinsic: secondary to endogenous factors discoloring the underlying dentin
ETIOLOGY/PATHOPHYSIOLOGY
- Extrinsic discoloration
- Bacterial stains: chromogenic bacteria give a green to black-brown to orange color that is usually 1 mm above the gingival margin on the tooth
- Plaque-related: a black-brown stain; usually secondary to the formation of ferric sulfide from the interaction of bacterial ferric sulfide and iron in the saliva; plaque on the dentition is usually white
- Foods: charcoal biscuits and similar products penetrate the pits and fissures of the enamel; foods that contain abundant chlorophyll can produce a green discoloration
- Gingival hemorrhage: gives a green staining; results from the breakdown of hemoglobin into green biliverdin
- Dental restorative materials: amalgam gives a black-gray discoloration
- Medications
- Products containing iron or iodine give a black discoloration
- Those containing sulfides, silver nitrate, or manganese give a gray-to-yellow to brown-to-black discoloration
- Those containing copper or nickel give a green discoloration
- Products containing cadmium give a yellow-to-golden brown discoloration (e.g., 8% stannous fluoride combines with bacterial sulfides, giving a black stain; chlorhexidine gives a yellowish-brown discoloration)
- Products containing iron or iodine give a black discoloration
- Metal
- Wear from chewing on cages or food dishes (Fig. 31-1)
- From removed orthodontic brackets or bands
- Wear from chewing on cages or food dishes (Fig. 31-1)
- Crown fragments: less translucency due to dehydration of fragment
- Discolored restorations
- Tooth wear with dentin exposure: tertiary dentin, reparative dentin, secondary dentin
- A calculus-covered crown ranges in color from a dark yellow to a dark brown
- Bacterial stains: chromogenic bacteria give a green to black-brown to orange color that is usually 1 mm above the gingival margin on the tooth
- Intrinsic discoloration
- Hyperbilirubinemia: affects all teeth
- Occurs during the developmental stages of the dentition (during dentin formation) as bilirubin accumulation in the dentin occurs from excess red blood cell breakdown
- Extent of tooth discoloration depends on the length of hyperbilirubinemia (one can see lines of resolution on the teeth once the condition has been resolved); gives a green discoloration
- Occurs during the developmental stages of the dentition (during dentin formation) as bilirubin accumulation in the dentin occurs from excess red blood cell breakdown
- Localized red blood cell destruction, usually one tooth
- Usually follows a traumatic injury to the tooth
- Discoloration comes from hemoglobin breakdown within the pulp from a pulpitis and secondary release into adjacent dentinal tubules (Fig. 31-2)
- Discoloration goes from pink (pulpitis) to gray (pulpal necrosis or resolution) to black (liquefactive necrosis)
- Blood factors that cause tooth discoloration are hemoglobin, methemoglobin, hematoidin, hemosiderin, hematin, hemin, and sulfmethemoglobin
- Discoloration comes from hemoglobin breakdown within the pulp from a pulpitis and secondary release into adjacent dentinal tubules (Fig. 31-2)
- Usually follows a traumatic injury to the tooth
- Amelogenesis imperfecta: developmental alteration in the structure of enamel affecting all teeth
- Teeth have a chalky appearance and a pinkish hue
- Can be a problem in the formation of the organic matrix, mineralization of the matrix, or the maturation of the matrix
- Teeth have a chalky appearance and a pinkish hue
- Dentinogenesis imperfecta: developmental alteration in the dentin formation; enamel separates easily from the dentin, resulting in grayish discoloration
- Both amelogenesis imperfecta and dentinogenesis imperfecta in humans are inherited conditions that have many modes of inheritance: X-linked dominant, X-linked recessive, autosomal dominant, autosomal recessive
- The mode of inheritance in animals has not been studied
- Both amelogenesis imperfecta and dentinogenesis imperfecta in humans are inherited conditions that have many modes of inheritance: X-linked dominant, X-linked recessive, autosomal dominant, autosomal recessive
- Infectious agents (systemic): parvovirus, distemper virus, or any infectious agent that causes a sustained body temperature rise; affects the formation of enamel
- A distinct line of resolution is visible on the teeth; affects all teeth if extended insult; results in enamel hypoplasia/hypocalcification where the pitted areas have black edges and the dentin is brownish
- Dental fluorosis: affects all teeth; excess fluoride consumption affects the maturation of enamel, resulting in pits (enamel hypoplasia) with black edges; the enamel is a lusterless, opaque white, with yellow-brown zones of discoloration
- Tooth erosion from the exposure to acids from constant vomiting results in enamel pitting and darkened staining
- Attrition: tooth-to-tooth wear results in crown loss and reparative dentin formation (yellow-brown color)
- Abrasion: tooth wear against another surface—chewing on tennis balls or due to chronic allergies (chewing the hair/skin)—results in reparative dentin formation (yellow-brown)
- Aging: older animals’ dentition is more yellow and less translucent
- Malnutrition (generalized, vitamin D deficiency, vitamin A deficiency): if severe, this can result in demarcated opacities on the enamel
- Hyperbilirubinemia: affects all teeth
- Internal/external resorption
- Internal resorption: follows pulpal injury (trauma) causing vascular changes with increased oxygen tension and a decreased pH, resulting in destruction (resorption) of the tooth from within the pulp from dentinoclasts; tooth has pinkish hue; usually one tooth affected
- External resorption: many factors cause this, such as trauma, orthodontic treatment, excessive occlusal forces, periodontal disease (as well as treatment), tumors, and periapical inflammation; reabsorption can occur anywhere along the periodontal ligament and can extend to the pulp; osteoclasts resorb the tooth structure
- Often the area is repaired by deposition of osteodentin
- Internal resorption: follows pulpal injury (trauma) causing vascular changes with increased oxygen tension and a decreased pH, resulting in destruction (resorption) of the tooth from within the pulp from dentinoclasts; tooth has pinkish hue; usually one tooth affected
- Medications and discoloration
- Tetracycline: binds to calcium, forming a calcium orthophosphate complex that is laid down into the collagen matrix of enamel; occurs on all teeth; occurs only when the enamel is being formed; results in a yellow-brown discoloration
- With long-term use of tetracycline drugs in mature animals, discoloration of the tooth occurs secondarily to the involvement of the underlying secondary dentin formation
- Amalgam (as with extrinsic stains)
- Iodine/essential oils
- Macrolide antibiotic (reported in humans)
- Due to increased number of karyopcynosis of the ameloblast at the transitional stage of development resulting in vacuolar degeneration of the ameloblast and cystic change at maturation resulting in hypocalcification giving a white discolored lesion with horizontal stripes on the enamel
- From endodontically treated teeth with the medicaments penetrating the dentinal tubules
- Bacterial “creeping” (leakage) occurs around the margins of a restoration and are usually blackish in color
- Tetracycline: binds to calcium, forming a calcium orthophosphate complex that is laid down into the collagen matrix of enamel; occurs on all teeth; occurs only when the enamel is being formed; results in a yellow-brown discoloration