Category:Teeth - Pathology

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Introduction

See anatomy and physiology of the teeth

Functional Anatomy

• The gingival crevice is an important site for disease processes in mouth to begin.

• In ruminants and rodents teeth may fail to oppose properly or to allow side to side movement of jaws. This produces uneven wear (especially in horse). Sharp edges are produced on the outside of the teeth in the upper jaw and inside of the teeth in the lower jaw, which causes painful feeding and inanition (not eating).
  • Approximately 75% of wasting horses have dental abnormalities.

• This is not a problem in carnivores as do they not use teeth for mastication.

• If a teeth is lost the opposing teeth may become very long and stop mouth closing properly.
  • Seen mostly in rodents - teeth may even penetrate through lip.

Defence Mechanisms

Developmental Pathology

Erythropoietic Porphyria.

• "Congenital Pink Tooth"
• Occurs in cattle, cats and sometimes pigs
• Teeth are pink due to congenital inability to metabolise haemoglobin pigments. These pigments also produce photosensitivity in skin.
• This results in severe sunburn if animal exposed to normal levels of sunlight.

Discoloration of a single tooth is more likely to be caused by pus in the tooth.

Photosensitising agents

• Phenothiazine which was used as an anthelmintic
• Tetracycline - if one injects bitches with tetracycline when pregnant, puppies are born with brown teeth, which fluoresce under UV light.
• Haemosiderin may also produce pinky / brown colour to teeth usually due to damage and haemorrhage into tooth.

Abnormal Wear of Teeth

• Abnormal wear of teeth in herbivores may result from irregular grinding of molars as well as from periodontal disease.
• Sharp edges usually form on the lingual aspect of the mandibular teeth and the buccal aspects of the maxillary molars and may cause quite severe oral lacerations.
  • The condition is sometimes known as “shear mouth”.

• Malocclusion of teeth may be acquired as a result of trauma and loss or displacement of teeth.
• It is particularly important in those teeth which continue to grow excessive growth, interference with prehension of food or even growth of the tooth into adjacent structures.
• Malocclusions in dogs and cats may arise from retention of deciduous teeth in the young animal.

• Malocclusion of teeth may also occur as a result of malformations of the jaws. The terminology used for these is rather confusing and the following should assist:
  • Prognathism is an abnormally long lower jaw.
  • A similar effect is produced by brachygnathia superior (ie short maxilla). Both conditions may be referred to as undershot jaw.
    • A typical breed affected is the Boxer.
  • Retrognathism is an unusually short lower jaw. This may also be called brachygnathia inferior (i.e. short mandible). The condition is referred to as overshot jaw or parrot mouth.
    • Typical breeds affected are the Borzoi or Rough Collie.

Abnormal Numbers of Teeth

• Abnormal numbers of teeth can vary from total lack (anodontia), to too few (oligodontia), to increased numbers (polyodontia).

Infection of teeth

Dental caries

• Only really seen in primates, but may be seen in horse caused by bacterial decalcification of enamel.
• Acid producing organisms enter dentine and underun enamel.
• Infection may spread to pulp cavity.

Infundibular Impaction

• Seen in the ruminant and horse.
• Food material impacted in infundibulum undergoes bacterial fermentation and results in enzymic damage to enamel and dentine.

Direct infection of pulp cavity

• For example, a dog whose canine has been snapped off while biting stones etc. exposes pulp.
• Also possible that infection in pulp cavity originates from a circulating pyaemia producing pulpitis.

Gingival crevice inflammation

• Mostly in carnivores (also cats), may occur in horses.
• Gingival inflammation starts because of dental calculus (tartar) from diets high in minerals and diets consisting of soft rather than hard crunchy food.
• Dental plaque becomes calcified and whole crown may become covered in brown chalky material.
• Calculus gives brittle dirty brown covering to tooth.
• This may not affect enamel at all but may produce mild gingivitis round edge and the gum may start to recede.
• This exposes more of crown, may reach level of dentine and infection may enter the alveolus and loosen ligaments holding tooth in and ultimately the tooth will become loose and fall out.

• Pyorrhoea is unusual in sheep but, nonetheless, periodontal disease with “broken mouth” is a major cause of culling of ageing ewes.

Alveolar Periostitis

• A more virulent infection into the alveolus produces alveolar periostitis.
• Infection spreads from pulp or from gingivitis to produce the periostitis.
• This may then break out of the alveolus into the bone causing osteomyelitis.
  • Seen in infection of carnassial teeth in dogs as chronic sinus discharging below eye. So called 'malar' abscess.
• Only treated by removal of tooth.
• Abscess may break through into maxillary sinus. If drained will get recovery.
  • Other maxillary cheek teeth can be involved in pyaemic infection with sinus formation.
• Hard to evaluate on mandible, may produce fistula that also needs tooth removal.

Granulomatous and pyogranulomatous Inflammation

Mandibular Osteomyelitis

• "Lumpy jaw"

Clinical

• Seen mainly in cattle and exotics caused by Actinomyces bovis producing osteomyelitis of mandible.
• Mostly young animals.
• Will not heal without treatment and jaw enlarges until animal cannot eat.

Pathogenesis

• Starts as alveolar periostitis of lower cheek teeth, due to ingestion of poor coarse roughage e.g. straw or hay with lots of thistles.
• Slowly enlarging mandible (occasionally maxilla) due to granulomatous inflammation producing much fibrous tissue.
• No real pus formation but "sulphur granules" in middle of lesion.
• Organism causes "pyogenic granuloma."

• Can grow to enormous size (e.g. size of grapefruit) and whole of mandible is blown apart by multiple foci of infection.

Also see:Actinobacillosis - "Wooden Tongue" (Courtesy of Alun Williams (RVC))

Pathology

3 major features:

1. Inflammatory removal of bone. As cortex of bone is pushed out by central inflammation produces thinning of bone cortex with proliferation of new periosteal bone. The centre of the mandible is eroded forming a honeycomb-like bone. Eventually will erode through bone producing granulomatous lesion on bottom of mandible and eventually eroding through skin.
2. Granuloma with micro abscess's in centre with greenish / yellow granules in middle of pus. These granules known as "sulphur bodies". Sulphur body is a colony of tangled mass of Actinomyces filaments. This is surrounded by neutrophils and macrophages forming a pyogenic granuloma.
3. Masses of fibrous tissue surround the granuloma and fill the spaces where bone has been destroyed.

Odontoclastic resorptive lesions

• Cats
  • Odontoclasts attack external and internal to the tooth.
  • Initially start at the neck/cervical region and extend into tooth root and also enter the root via the apical foramen (stage 3 lesions)
  • 20%+ of cats have them
  • Different from caries – demineralization by bacteria fermenting CHO on the enamel.
  • ORLs – only occur when odontoclasts resorb the tooth/bone
    • continues with remodeling of alveolar bone until ankylosis
    • fixation of periodontal ligament and lamina dura so that the tooth is permanently fixed to the bone.
• Odontoclasts normally only active in young animals to resorb the deciduous teeth to make way for the permanent teeth – so represents abnormal activation in adults.
• Can have inflammatory infiltrates into the resportive lesions

Eosinophilic Inflammation

Necrotizing Inflammation

Lymphocytic and plasmacytic Inflammation

Proliferative Pathology

Hyperplastic

Focal fibrous hyperplasia^[1]

• 44% of cases.
• Dense collagenous tissue, with ulceration/superficial inflammation
• Dystrophic calcificaition within the fibrous connective tissue stroma (often highly cellular, with 'young stellate fibroblasts'
• No odontogenic epithelium seen.
• Occasional strands of surface epithelium growing down into the stroma.
• Most of these were previously diagnosed as fibromatous or ossifying epulides.

Neoplastic

Peripheral odontogenic fibroma^[1]

• aka: Fibromatous epulis of periodontal ligament origin
• 17% of cases.
• Proliferation of fibrous tissue with variety of osteoid, cementum or dentine-like material.
• Isolated strands or islands of odontogenic epithelium always present (ie: suggesting induction of connective tissue by the epithelial cells).
• The stroma contains neoplastic fibroblasts, with varying cellularity.
• The overlying epitheluim is normal.

Peripheral ameloblastoma^[1]

• aka: basal cell carcinoma, acanthomatous ameloblastoma, acanthomatous epulis
• 18% of cases.
• Islands and sheets of mature odontogenic epithelium within a collagenous fibrous connective tissue stroma of low/moderate cellularity.
• Each of the islands bounded by a row of tall columnnar cells.
• These palisading cells exhibit polarisation away from the basement membrane and had cytoplasmic vacuolation.
• Central cells had a basaloid appearance.
• Often infiiltrating into the underlying bone.
• Synonymous with basal cell carcinoma.

Central ameloblastoma^[1]

• Different from peripheral ameloblastoma - cystic changes and follicular arrangement of ameloblasts and stellate reticulum cells, resembling the basic structure of the enamel organ.

Degenerative Pathology

Odontodystrophy

• Damage to ameloblasts (which form enamel) in utero upsets permanent incisor formation.
• Enamel is marked by pits, lines etc.

In ruminants:

• Damage to enamel formation most often caused by fluoride poisoning.
• Seen in cattle grazing on pasture contaminated by cement works effluent.
• Chalky mottling and yellow brown pitting of tooth.

In canines:

Very severe systemic disease early in life / or in utero may result in severe discoloration or pitting of teeth due to effect on enamel formation. (e.g. distemper in dog)

Metabolic Pathology

Nutritiona Pathology

Traumatic Pathology

Vascular Pathology

References

With thanks to Andrew Jefferies (Cambridge) and Alun Williams (RVC) for providing access to their lecture materials

1. ↑ ^{1.0 1.1 1.2 1.3} J Comp. Path. 1992 (106), 169-182 The Histological Nature of Epulides in Dogs F. J. M. Verstraete*, A. J. Ligthelmf and A. WeberT. ... review of 154 oral 'epulis' from dogs reviewed with the current (at the time) human literature.

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