Pathology of the oral cavity Flashcards
Developmental abnormalities of the oral cavity
Palatoschisis (cleft palate)
Cheiloschisis (cleft lip or hare lip)
Prognathia
Brachynathia (micromandible or hypognathia)
Agnathia
Palatoschisis and cheiloschisis
Cleft palate and clept lip
Among most common developmental abnormalities
Genetic or toxin in origin
Can mean an inability to create a negative pressure in the oral cavity
Many die due to starvation or aspiration pneumonia
Treatment of Palatoschisis (cleft palate) and cheiloschisis (cleft lip or hare lip)
If small defect: may be corrected surgically
If large defect: surgery will be costly and difficult, may not be compatible with life
Prognathia
refers to the characteristic of having projecting jaws, in some dog breeds is part of their phenotype (Brachycephalics).
Brachynathia (micromandible or hypognathia)
An abnormal shortness of the mandible, rarely seen
Can cause abnormal wearing of the teat
Agnathia
A congenital abscence of all or a major proportion of the jaw
Anatomy of the tooth
Crown - above gum
Root
3 parts:
- enamel
- dentine
- pulp cavity
Abnormalities of the teeth
Malocclusions
Discolouration of teeth
Discolouration of the oral cavity
Odontodystrophy
Infection of teeth
Malocclusions of the teeth
failure of the upper and lower incisors to interdigitate properly leading to uneven wear and in some species e.g. rodents - difficulty in prehension and mastication.
Can be caused by polydontia/oligodontia.
Discolouration of teeth - Congenital porphyria, congenital pink tooth or erythropoietic porphyria
Teeth are pink due to congenital inability to metabolise haemoglobin pigments. Porphyrins are incorporated into dentin and fluoresce, easily demonstrated under ultraviolet light.
These pigments also produce photosensitivity in skin. This results in severe sunburn if animal exposed to normal levels of sunlight, especially in light skin or hypopigmented areas.
Discolouration of teeth by drugs
Some drugs are also photosensitising agents e.g. phenothiazine which was used as an anthelmintic and tetracycline antibiotics. If you inject bitches with tetracycline when pregnant, produces puppies with brown teeth, which fluoresce under UV light.
Discolouration of teeth by haemosiderin
Haemosiderin may also produce pinky / brown colour to teeth usually due to damage and haemorrhage into tooth.
Discolouration of teeth by pus
-Pus in tooth results in discolouring of tooth (N.B. single tooth rather than all teeth as in porphyria).
Anaemia of the oral cavity
Very pale, confirm with blood sample
Jaundice of oral cavity
yellow, icterus.
Main 3 pathogenesis of jaundice in an animal are:
- pre-hepatic (haemolysis),
- hepatic (hepatitis - viral, bacterial, parasitic, immune mediated, toxic etc.),
-post-hepatic/obstructive (obstructions or compressions of the biliary system - neoplasia (e.g. of duodenum))
Cyanosis of oral cavity
Cardiac insufficiency or toxic
Discolouration of the oral cavity
Anaemia
Jaundice
Cyanosis
Congestion
Petechial haemorrhages
Odontodystrophy
Caused by toxic, nutritional, and metabolic insults.
Damage to ameloblasts (which form enamel) in utero upsets permanent incisor formation.
Enamel is marked by pits, lines, etc.
In canines:
* Segmental enamel hypoplasia occurs as a result of hyperthermia and viral infections (distemper virus).
* Infection of ameloblasts must occur before 6 months of age or in utero.
Infection of teeth
- direct infeciton of pulp cavity
- Gingival crevice inflammation
Direct infection of pulp cavity
e.g. in a dog whose canine tooth has been snapped off while biting stones etc. to expose pulp.
May have infection in pulp cavity from circulating pyaemia producing pulpitis.
Gingival crevice inflammation
mostly in carnivores (dogs and cats), may occur in horses.
Gingival inflammation starts because of dental calculus (tartar – subgingival plaque).
Formation of dental calculus
Dental plaque becomes calcified and whole crown may become covered in brown chalky material.
Dental calculus forms more common from diets high in minerals and diets consisting of soft rather than hard crunchy food.
Calculus gives brittle dirty brown covering to tooth. May not affect enamel at all but may produce mild gingivitis round edge and gum starts to recede. This exposes more of crown, may reach level of dentine and infection may enter the alveolus and loosen ligaments holding tooth in. Tooth will become loose and fall out.
A more virulent infection into the alveolus produces alveolar periostitis. Infection spreads from pulp or from gingivitis to produce alveolar periostitis. May break out of alveolus into bone causing osteomyelitis.w
Stomatitis
Generalised inflammation throughout the mouth
common in animals and can be related with infectious and non-infectious (physical trauma, chemicals, uraemia, autoimmune diseases) causes.
Erosions, ulcerations and necrosis are commonly seen as the final result of mild stomatitis as ingested substances move around the oral cavity leading to more damage to mucosa.
Cheilitis
Inflammation of the lips
Glossitis
Inflammation of the tongue
Palatitis
Inflammation of the palate
Gingivitis
Inflammation of the gingiva
Tonsilitis
Inflammation of the tonsils
Pharyngitis
Inflammation of the pharynx
Classification of types of inflammation of mucosa: (any mucosal surface) From mildest to most severe
Catarrhal
Vesicular / erosive
Ulcerative
Diptheritic / fibrinous
Haemorrhagic
Catarrhal stomatitis
Non-specific, general stomatitis. May produce bad smell
Pathogenesis of catarrhal stomatitis
low grade streptococcal infection
ingestion of toxins
result of other more systemic diseases
Pathology of catarrhal stomatitis
Starts as hyperaemia and oedema of tongue or pharynx with mucoid exudate on surface.
Lymphoid follicles on soft palate may enlarge and proliferate (hyperplasia), often seen as white spots.
There is an increased mucous secretion (can be scraped off to leave ordinary mucosa underneath).
Resolves normally if not secondarily infected.
Vesicular / Erosive stomatitis
Damage to prickle cells (stratum spinosum) with hydropic degeneration leads to vesiculation (fluid within epithelium).
Lesion quickly erodes leaving hyperaemic stratum germinativum, which heals by proliferation of new cells, so long as infection does not continue.
Pathogenesis of vesicular/erosive stomatitis
Ingestion of hot food (corrosive liquids)
autoimmune disease (pemphigus vulgaris, bullous pemphigoid, mucous membrane phemphigoid)
Vesicular stomatitis pathology
The macroscopic lesions in vesicular stomatitides are epitheliotrophic, mostly in the mouth and are associated with viruses.
Vesiculation or blistering is present early in the course of diseases in this type of stomatitis.
Erosions, ulceration, necrosis, and secondary bacterial or fungal infection occurs later.
Vesicles in dogs
Vesicles in mouth are often caused by hot food - especially in dogs.
Can produce quite big vesicles, but will heal.
No major problems associated with vesicles on tongue in dogs (except if due to drinking battery acid, but this also produces vomiting).
Occasionally see vesicles with autoimmune disease (pemphigus) in mouth or on lips of dog.
“True ulcer” occurs when connective tissue under epithelium is exposed i.e. stratum germinativum is breached and then lesion takes much longer to heal.
Secondary bacterial invaders of these lesions may result in more severe stomatitis.
Erosive and ulcerative stomatitis
Erosions are loss of part of the surface epithelium, whereas ulcers are full epithelium loss exposing the basement membrane or tissues beneath the basement membrane.
These lesions can be related to infectious and non-infectious causes.
Feline calicivirus.
Foreign bodies, uraemia, feline eosinophilic granuloma complex, autoimmune diseases.
Aetiology of ulcerative glossitis in cats
Calicivurs (7-80%), picornavirus and feline immunodeficiency virus (FIV)
Animals affected by Ulcerative glossitis in cats
Youngish to middle age
Clinical and pathology of Ulcerative glossitis in cats
Whole back of mouth with ulcerative granulation tissue
Aetiolofy of Eosinophilic granuloma complex
Not known
Autoimmune?
Animals affected by Eosinophilic granuloma complex
Any age, usually young adult cats
Clinical and pathology of Eosinophilic granuloma complex
Skin and oral cavity affected
Stomatitis and infiltrative eosinophilic stomatitis
Ulcerative glossitis (cat)
Unable to eat although wants to.
Hurts to open mouth.
Chronic, tends to start at angle of jaw (bilateral), progression quite slow but over weeks affects whole of back of mouth.
May also affect tongue.
Pathology of ulcerative glossitis in cats
Epithelium lost over whole of mucosa, lots of macrophages, lymphocytes, and proliferating fibrous response at base.
Pathogenesis of ulcerative glossitis (cat)
Probably viral.
Calicivirus found in 7-80%, also often find picornavirus and feline immunodeficiency virus (FIV). Probably calicivirus that starts it.
Feline calicivirus causes mainly a respiratory infection. The infection may be followed by autoimmune / exaggerated immune response which produces lesions.
Also owners often claim develops after ‘having cold’ prior to it.
Will heal eventually, but takes time and cat loses lots of condition.
Eosinophilic ulcer
Or eosinophilic granuloma, lick granuloma, labial ulcer, rodent ulcer. In cats of all ages.
Mainly affects mucocutaneous junctions of the lips, may also occasionally affect frenulum of tongue and skin.
Inflammatory disease but is progressive and destructive. In worst cases may erode away whole nose.
Pathogenesis of eosinophilic ulcers
Histologically lots of eosinophils, neutrophils.
Exaggerated eosinophilic response.
Treatment of eosinophilic ulcers
corticosteroids if confirmed
Uraemia
In terminal renal failure (chronic renal disease) animal may present with fetid ulcerative stomatitis, painful ulcers in mouth, which become secondarily infected with bacteria.
Most commonly seen in dog sometimes in cat.
Ulcers on lateral elements on tongue.
Vasculitis.
Physical causes of ulcerative stomatitis
any animal that is exposed to coarse feed or sharp things in food can suffer from ulcers in mouth.
They often become secondarily infected with production of metastatic infection that may result in large abscess on point of jaw. i.e. trauma on tongue may lead to secondary infection that may lead to abscess in drainage lymph node.
Fibrinous/diphtheric stomatitis
Severe damage to epithelium produces exudation of fibrin -with formation of dry white fibrinous deposit - diphtheritic membrane.
Deep ulcers may occur due to trauma and produce a fibrin-covered ulcer.
Usually associated with organism Fusobacterium necrophorum found everywhere in environment (but N.B.- strict anaerobe).
Produces lesions that damage epithelium due to toxin that damages vessels.
Often a secondary invader but can be a primary pathogen.
Haemorrhagic inflammation
Complete loss of integrity of epithelium leading to haemorrhage.
Uncommon.
Epithelium lost and haemorrhage produces blue / black discoloration of the tongue, hence the name.
Proliferative stomatitis
Stick injuries in dog
Sticks may damage to pharynx with oedema and swelling in pharynx and secondary infection.
Can kill dog.
Pieces of wood may remain embedded in back of throat resulting in chronic inflammation.
