Disorders of Tooth Eruption and Shedding

Disorders of Tooth Eruption and Shedding

• Predeciduous Dentition: Infants may be born with teeth-like structures.
• Types:
  • Natal teeth: Deciduous teeth present at birth.
  • Neonatal teeth: Deciduous teeth erupting within the first 30 days of life.
• Postpermanent Dentition: Several teeth erupt after all permanent teeth have been lost, particularly after a full denture is inserted. The mandibular central incisors are often involved.

Premature Eruption, Natal, and Neonatal Teeth

• Coronal enamel and dentine formation is normal for the tooth's chronological age.
• Premature eruption sometimes results in hypoplastic enamel; root formation is missing or irregular.

Premature Eruption

• Infrequent in deciduous and permanent teeth.
• Possibly related to local factors (superficial location of tooth germ, early shedding of deciduous teeth).
• May be seen in children with endocrine abnormalities (excess growth hormone, hyperthyroidism).

Retarded Eruption

• Several conditions can cause delayed eruption, including endocrinopathies (e.g., hypothyroidism), prematurity, nutritional deficiencies, chromosome abnormalities (e.g., Down syndrome).
• Also associated with migration problems, traumatic tooth germ displacement or large crowns.
• Often accompanied by impacted supernumerary teeth (e.g., cleidocranial dysplasia).

Premature Loss

• Usually a result of dental caries, sequelae, chronic periodontal disease
• Sometimes associated with hypophosphatasia, hereditary palmar-plantar hyperkeratosis, and other systemic periodontitis.

Persistence of Deciduous Teeth

• Deciduous teeth fail to shed at the expected time.
• Often associated with a missing or displaced permanent successor.
• May stem from systemic conditions (e.g., cleidocranial dysplasia).

Impacted Teeth

• Teeth prevented from erupting due to physical barriers or lack of space.
• Causes: micrognathia, retained deciduous teeth, supernumerary teeth, odontogenic cysts, or tumors, or cleft palate.
• Completely impacted teeth are entirely surrounded by bone; partially impacted teeth are only partially surrounded by bone. Commonly impacted are mandibular third molars, maxillary canines, premolars and less commonly second molars.

Submerged Teeth

• Deciduous teeth are ankylosed (fused to bone).
• Often deciduous molars; occlusal table is below the occlusal plane of other teeth.
• The underlying permanent tooth may be impacted or erupt buccally or lingually.

Discoloration of Teeth

• Extrinsic: Surface accumulation of exogenous pigments. Examples of causes are bacterial stains, iron, tobacco, foods and beverages, gingival hemorrhage, restorative materials and medications.
• Intrinsic: Endogenous factors discoloring underlying dentin. Examples of causes are amelogenesis imperfecta, dentinogenesis imperfecta, dental fluorosis, erythropoietic porphyria, hyperbilirubinemia, trauma, localized red blood cell breakdown and medications.

Chromogenic Bacteria

• Vary in color (green, black-brown, orange).
• Common in children.
• Initially discolor the labial surfaces of anterior teeth and gingiva.

Plaque-Related Stains

• Mostly black-brown.
• Usually not bacterial in origin but ferric sulfide formation from interaction of bacterial hydrogen sulfide and iron in saliva or gingival fluid.

Tobacco, Tea, or Coffee-Related Stains

• Creates brown discoloration.
• Tar components dissolve in saliva, easily penetrate enamel fissures.
• Amalgam can cause black-gray discoloration, particularly seen in younger patients with open dentinal tubules.
• Medications (e.g., iron or iodine-containing products) in the past were associated with tooth discoloration.
• Current culprits are stannous fluoride and chlorhexidine.

Stannous Fluoride

• May discolor labial anterior and occlusal posterior teeth.

Chlorhexidine

• Associated with yellowish-brown interproximal staining near gingival margins.

Congenital Porphyrias (e.g., Gunther Disease)

• Autosomal recessive disorder of porphyrin metabolism.
• Increased porphyrin synthesis and excretion.
• Marked reddish-brown coloration of teeth (UV light fluorescence), mainly deciduous teeth.

Congenital Hyperbilirubinemia (Neonatal Jaundice)

• Mild, transient jaundice common in newborns (especially rhesus incompatibility).
• Bile pigments may be deposited in enamel and dentin, often confined to dentin, causing green to yellowish-brown discoloration particularly along the neonatal incremental line.

Pulp Necrosis

• Lysis of necrotic tissue and red blood cells due to hemorrhage leads to pigmented products diffused into dentin - results in tooth discoloration.

Tetracycline Staining

• Tetracycline taken during pregnancy or childhood can cause yellowish-grey bands, turning brown over time.
• Permanent incorporation of the antibiotic in the calcified tissues results in a bright yellow fluorescence under UV light.

Age Changes

• Enamel: Becomes more brittle, less permeable and sometimes darker.
• Dentin: Continued formation of secondary dentin, reducing pulp chamber, transparent dentin.
• Roots: Become brittle.
• Cementum: Increased thickness.
• Pulp: Gradual decrease in volume, decreased vascularity, increase in collagen fiber content and reduce healing potential.

Loss of Tooth Structure: Attrition

• Wearing of tooth surfaces from tooth-to-tooth contact due to mastication.
• Types:
  • Physiological attrition: Normal aging process
  • Pathological attrition: Abnormalities in occlusion, chewing pattern or structural defects - this is a clinical concern.
• Normal occlusal attrition is 30 µm/year for molars.

Etiological Factors for Pathological Attrition

• Abnormal occlusions: Malocclusion and crowning of teeth leading to traumatic contacts during chewing that may cause tooth wear.
• Acquired: Tooth extractions that can change the chewing forces and lead to altered wear patterns.
• Premature contact: Edge-to-edge contact leading to exaggerated pathological attrition.
• Abnormal chewing habits: Parafunctional habits (e.g., bruxism) and habitual chewing of coarse or abrasive food.

Structural Defects

• Conditions like amelogenesis imperfecta or dentinogenesis imperfecta that reduce enamel and dentin hardness cause teeth to be more susceptible to attrition.
• Men tend to show more severe attrition than women.
• Attrition may be seen in both deciduous and permanent dentition.

Abrasion

• Pathological wearing away of tooth substance from external agents like abrasive dentifrices, habits, occupational hazards (e.g., floss, toothpicks), or injuries.
• Usually occurs on exposed root surfaces, more commonly on the left side in right-handed individuals.

Erosion

• Chemical loss of tooth substance without bacterial action.
• Types:
  • Intrinsic (e.g:, gastroesophageal reflux, vomiting)
  • Extrinsic (e.g., acidic beverages, citrus fruits).
• Usually affects labial and buccal surfaces of teeth; appears as a smooth, shallow, highly polished depression on enamel adjacent to the cementoenamel junction.

Abfraction

• Tooth structure loss from stress on the tooth caused by occlusal stresses or abnormal occlusal forces (e.g., eccentric forces).
• Especially affects buccal or labial cervical areas of teeth.

Resorption of Teeth

• Physiologic resorption: Deciduous teeth resorption prior to shedding. Transient microscopic areas of superficial resorption in permanent teeth that are repaired by cementum or bone-like tissue formation.
• Pathologic resorption: More common; External (root surface) or internal (pulpal surface) in origin. Caused by osteoclast/odontoclasts on dentin surface of the pulp.

External Resorption Causes

• Cysts
• Dental trauma
• Excessive mechanical/occlusal forces
• Grafting of alveolar clefts
• Hormonal imbalances
• Periodontal treatment/inflammation
• Pressure from impacted teeth
• Reimplantation of teeth
• Tumors

Internal Resorption

• Mostly anterior incisors affected.
• Secondary to pulpitis or often idiopathic.
• Characterized by a pink spot (pink tooth of mummery) as the resorptive process approaches the surface.
• Continues as long as the vital pulp remains and extensive loss of tooth structure can occur, predisposing to fractures.

Radiographic Appearance of Root Resorption

• Radiographic finding includes fusiform enlargement of pulp chambers within the crown or root.
• Microscopy shows loose connective tissue with increased vascularity and potentially few inflammatory cells.