Cavity & Gingiva - Pathology

()Map ALIMENTARY SYSTEM (Map)

Introduction

• Stomatitis - generalised inflammation throughout mouth.

• Glossitis - inflammation of tongue.

• Pharyngitis - pharynx inflammation.

Functional Anatomy

See anatomy and physiology of the oral cavity

Developmental Pathology

A congenital cleft palate defect (Courtesy of Alun Williams (RVC))

Cleft Palate

• The commonest structural defect is probably the various forms of cleft palate due to:
  • failure of fusion and the ingrowths of the palatine shelves or
  • frontonasal and maxillary processes.

Erosive & Ulcerative Pathology

• "True ulcer" occurs when connective tissue under epithelium is exposed i.e. stratum germinativum is breached and then lesion takes much longer to heal.

Bovine Virus Diarrhoea Virus

• Mucosal Disease: erosive condition produces small multiple, cleanly punched out lesion in mouth
• Neutrophils invade the ulcer and if bacterial colonisation occurs, further excavation follows. Either:

1. This lesion develops a granular base and becomes diphtheritic.
2. If bacterial colonisation does not take place, healing occurs within fourteen days.

• Seen in most parts of mouth (or maybe on muzzle) e.g. dental pad, cheeks, sides of tongue
• Lesions extend throughout gut with particularly big ulcers in small intestine over Peyers patches. Necrosis occurs in lymph nodes and spleen

Histology

• No vesicular stage, prickle cells die off from surface resulting in layer of necrotic debris over epithelial layer
• Infection penetrates inward through stratum germinativum.
• Epithelium does not recover as animal does not recover

Vesicular Pathology

Pathology

• Damage to prickle cells (stratum spinosum).
• Appears as accumulation of fluid within epithelium, quickly erodes leaving hyperaemic stratum germinativum.
• Heals by proliferation of new cells, so long as infection does not continue.

Pathogenesis

May be caused by:

1. Ingestion of hot food (corrosive liquids)
2. Systemic viral diseases. e.g:
   1. Foot and Mouth disease - ruminants and pigs
   2. Vesicular stomatitis - horse, pigs, cattle
   3. Vesicular exanthema - pigs

N.B. All are indistinguishable from FMD clinically.

Foot and Mouth Disease (FMDV)

Pathology

Gross

1. Initially - hyperaemia of mucosa (e.g. catarrhal inflammation) then within 12 hours produces fluid filled vesicles on dorsum of tongue, may be other places
2. Small vesicle coalesce to produce big ones -i.e. Bullae
3. Very quickly rupture; epithelium appears dirty grey in colour because of necrosis - sloughed skin, very good for diagnosis
4. Leave painful, hyperaemic epithelium
5. Looks like "ulcer "with ragged edge but not a true ulcer as stratum germinativum retained and will rapidly heal completely in about 2 weeks unless becomes secondarily infected

Microscopic lesions

• Degeneration of prickle cells
• Cells "balloon" as fill with fluid and then die to produce vesicle containing straw coloured or clear fluid

Swine Vesicular Disease

• May produce vesicles in mouth that are indistinguishable from foot and mouth disease
• Swine vesicular disease produces sporadic large outbreaks
  • Approximately 5% have lesions in mouth, foot lesions much more common

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).

Catarrhal Stomatitis

• Non-specific, general stomatitis

Pathology

• Starts as hyperaemia and oedema of tongue or pharynx with mucoid exudate on surface.
• Lymphoid follicles on soft palate may enlarge and proliferate.
• Often see white spots due to epithelial hyperplasia and increased mucous secretion.
  • (can be scraped off to leave ordinary mucosa underneath).
• May produce bad smell.
• Resolves normally if not secondarily infected.

Pathogenesis

• May be caused by:
  • Low grade streptococcal infection
  • Ingestion of toxins
  • Result of other more systemic diseases

Eosinophilic Inflammation

Eosinophilic granuloma

This is a complex of diseases affecting skin and oral cavity mainly of cat, which include:

1. Oral eosinophilic granuloma
2. Linear granuloma of skin
3. Eosinophilic plaque of skin

Clinical

• Any age, but usually young adults.
• Mainly affects lips, may also occasionally affect frenulum of tongue.
• Sometimes called "rodent ulcer "
• Not neoplastic - it is an inflammatory disease but is progressive and destructive.

• May see small plaque or becomes very infiltrative.
• In worst cases may erode away whole nose.

Pathogenesis

• Histologically lots of eosinophils, polymorphs.
• Exaggerated eosinophilic response.

Immune Mediated Pathology

Autoimmune

• Occasionally see vesicles on the oral mucosa. associated with autoimmune diseases such as pemphigus vulgaris.

Proliferative Pathology

Hyperplastic

Polychlorinated Napthalene Poisoning

• Polychlorinated biphenyl's (PCB's).
• Used in all sorts of things.
• Do not break down in environment and very toxic.
• Poisoning was classically seen as proliferative stomatitis when PCB used to lubricate feed pellet making machine.
• Vitamin A antagonist produces hyperkeratosis of mouth (like Vitamin A deficiency).

Papular

Orf

• Pox infection
• Quite a common zoonotic disease

Clinical

• In sheep produces a proliferative nodule/papular mass on lips
• In flocks in which it is endemic it is seen in lamb
• If flock is non-immune seen in ewes too but much worse in lambs (may spread to inside of mouth)
• Can spread to udder of ewe

Pathology

• Poxvirus infections produce local infection of prickle cells in epithelium with proliferation of cells and formation of papule followed by ulceration / necrosis and covered by necrotic epithelium
• Eventually scabs form and crust drops off
• Scabs - very infectious ( N.B.if touch -> catch it)

Bovine Papular stomatitis

Ring Zone Lesions of BPS - Calf (Courtesy of Alun Williams (RVC))

• Parapox virus
• Very similar disease to orf but seen in cattle and generally milder condition.
• Must be differentiated from Foot and Mouth Disease and Mucosal Disease.
• Sporadic, in cattle, less than 1 year old.
• Develop papules on the muzzle, external nares and in the oral cavity; the oesophagus and forestomachs may also be affected.
• Usually heals spontaneously.

Pathogenesis

• The early lesions are round areas of intense congestion up to 1.5 cm in diameter.
• The centre becomes necrotic and slightly depressed.
• Slow peripheral extension of this lesion gives a classical ring zone formation with concentric rings of
  • yellow (necrosis),
  • grey (epithelial hyperplasia)
  • red (congestion).

Histology

• There are focal areas of hydropic degeneration in the stratum spinosum
• Large eosinophilic intracytoplasmic inclusion
• Epidermis is markedly thickened.
• The superficial layers of the epithelium become necrotic and slough.
• Vesicle formation is not a feature of this disease.

Neoplastic

Squamous cell carcinoma

Oral squamous cell carcinoma. Courtesy of T. Scase

Metabolic Pathology

Uraemia

Lesions due to uraemia associated with pyelonephritis/chronic renal failure (Courtesy of Alun Williams (RVC))

• In terminal renal failure animal may present with painful ulcers in mouth, which become secondarily infected with Fusiformis.
  • High concentrations of toxic materials in the blood results in degeneration of small arterioles.
• In the mouth, this damage to the blood supply can cause epithelial necrosis.
• Usually seen as erosions along the ventrolateral borders of the tongue and on the cheeks, especially opposite the teeth.
• In some cases there may be more extensive necrosis which may involve subepithelial tissue
  • for example, the tip of the tongue may slough.
• Most commonly seen in dog sometimes in cat.

Nutritional Pathology

Nicotinic Acid Deficiency

• May also cause epithelial necrosis and sloughing.

Traumatic Pathology

Ulcers Following Trauma

• 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.

• Deep ulcers may occur as a result of trauma in any species.
• These readily become secondarily infected by Fusiformis.
• Produces a fibrin-covered ulcer.
• Responds to antibiotics, but may leave a defect or scar in mucosa.

Learning Tools

Cavity and Gingiva Flashcards