Difference between revisions of "Cavity & Gingiva - Pathology"

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#REDIRECT[[:Category: Oral Cavity and Gingiva - Pathology]]
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{{review}}
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 +
 
 +
==Introduction==
 +
*Stomatitis - generalised inflammation throughout mouth.
 +
 
 +
*Glossitis - inflammation of [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]].
 +
 
 +
*Pharyngitis - pharynx inflammation.
 +
 
 +
==[[:Category:Oral Cavity - Developmental Pathology]]==
 +
 
 +
===[[Cleft Palate]]===
 +
 
 +
==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 - WikiBlood|Neutrophils]] invade the ulcer and if bacterial colonisation occurs, further excavation follows. Either:
 +
::#This lesion develops a granular base and becomes diphtheritic.
 +
::#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 - Anatomy & Physiology|cheeks]], sides of [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]]
 +
*Lesions extend throughout gut with particularly big ulcers in small intestine over [[Peyer's Patches - Anatomy & Physiology|Peyers patches]]. Necrosis occurs in lymph nodes and [[Spleen - Anatomy & Physiology|spleen]]
 +
 
 +
====<span id="BVDHistology">Histology</span>====
 +
*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
 +
 
 +
===[[Malignant Catarrhal Fever Virus]]===
 +
 
 +
==Vesicular Pathology==
 +
===Pathology===
 +
*Damage to [[prickle cell]]s ([[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:
 +
#Ingestion of hot food (corrosive liquids)
 +
#Systemic viral diseases. e.g:
 +
##[[picornaviridae#Foot and Mouth Disease Virus|Foot and Mouth disease]] - ruminants and pigs
 +
##[[Vesicular stomatitis]] - horse, pigs, cattle
 +
##[[Vesicular exanthema]] - pigs
 +
 +
N.B. All are indistinguishable from FMD clinically.
 +
 
 +
===[[Foot and Mouth Disease (FMDV)]]===
 +
 
 +
====Pathology====
 +
=====Gross=====
 +
#Initially - hyperaemia of mucosa (e.g. catarrhal inflammation) then within 12 hours produces fluid filled vesicles on dorsum of [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]], may be other places
 +
#Small vesicle coalesce to produce big ones -i.e. Bullae
 +
#Very quickly rupture; epithelium appears dirty grey in colour because of necrosis - sloughed skin, very good for diagnosis
 +
#Leave painful, hyperaemic epithelium
 +
#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 [[Oral Cavity - Tongue - Anatomy & Physiology|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 [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] or pharynx with mucoid exudate on surface.
 +
*Lymphoid follicles on [[Soft Palate - Anatomy & Physiology|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 [[:Category:Streptococcus species|streptococcal]] infection
 +
**Ingestion of toxins
 +
**Result of other more systemic diseases
 +
 
 +
==Granulomatous and pyogranulomatous Inflammation==
 +
==Eosinophilic Inflammation==
 +
===Eosinophilic granuloma===
 +
This is a complex of diseases affecting skin and [[Oral Cavity Overview - Anatomy & Physiology|oral cavity]] mainly of cat, which include:
 +
#Oral eosinophilic granuloma
 +
#[[Linear granuloma]] of skin
 +
#[[Eosinophilic plaque]] of skin
 +
 
 +
====Clinical====
 +
*Any age, but usually young adults. 
 +
*Mainly affects [[Lips - Anatomy & Physiology|lips]], may also occasionally affect '''frenulum of [[Oral Cavity - Tongue - Anatomy & Physiology|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.
 +
 
 +
==Necrotizing Inflammation==
 +
==Lymphocytic and plasmacytic Inflammation==
 +
==Immune Mediated Pathology==
 +
===Autoimmune===
 +
*Occasionally see vesicles on the oral mucosa. associated with autoimmune diseases such as [[pemphigus]] vulgaris.
 +
 
 +
===Hypersensitivity===
 +
==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====
 +
*[[Poxviridae|Pox]] infection
 +
*Quite a common '''zoonotic''' disease
 +
 
 +
=====Clinical=====
 +
*In sheep produces a proliferative nodule/papular mass on [[Lips - Anatomy & Physiology|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====
 +
[[Image:BPS.gif|right|thumb|125px|<small><center>Ring Zone Lesions of BPS - Calf (Courtesy of Alun Williams (RVC))</center></small>]]
 +
*Parapox virus
 +
*Very similar disease to orf but seen in cattle and generally milder condition. 
 +
*'''Must be differentiated from [[#Foot and Mouth disease|Foot and Mouth Disease]] and [[#Bovine Viral Diarrhoea / Mucosal disease|Mucosal Disease.]]'''
 +
*Sporadic, in cattle, less than 1 year old.
 +
*Develop papules on the muzzle, external nares and in the [[Oral Cavity Overview - Anatomy & Physiology|oral cavity]]; the [[Oesophagus - Anatomy & Physiology|oesophagus]] and [[Stomach and Abomasum - Anatomy & Physiology|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.''
 +
 
 +
====Papilloma====
 +
 
 +
===Neoplastic===
 +
====Squamous cell carcinoma====
 +
[[Image:oral squamous cell carcinoma.jpg|right|thumb|125px|<small><center>'''Oral squamous cell carcinoma'''. Courtesy of T. Scase</center></small>]]
 +
 
 +
==Degenerative Pathology==
 +
==Metabolic Pathology==
 +
===Uraemia===
 +
[[Image:uraemia.gif|right|thumb|125px|<small><center>Lesions due to uraemia associated with pyelonephritis/chronic renal failure (Courtesy of Alun Williams (RVC))</center></small>]]
 +
*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 [[Oral Cavity - Tongue - Anatomy & Physiology|tongue]] and on the [[Cheeks - Anatomy & Physiology|cheeks]], especially opposite the [[Oral Cavity - Teeth & Gingiva - Anatomy & Physiology|teeth]].
 +
*In some cases there may be more extensive necrosis which may involve subepithelial tissue
 +
**for example, the tip of the [[Oral Cavity - Tongue - Anatomy & Physiology|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 [[Oral Cavity - Tongue - Anatomy & Physiology|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.
 +
 
 +
==Vascular Pathology==
 +
==Learning Tools==
 +
::[[Alimentary Flashcards - Pathology#Cavity and Gingiva Flashcards|Cavity and Gingiva Flashcards]]

Revision as of 13:46, 24 May 2010



Introduction

  • Stomatitis - generalised inflammation throughout mouth.
  • Glossitis - inflammation of tongue.
  • Pharyngitis - pharynx inflammation.

Category:Oral Cavity - Developmental Pathology

Cleft Palate

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

Malignant Catarrhal Fever Virus

Vesicular Pathology

Pathology

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

Granulomatous and pyogranulomatous Inflammation

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.

Necrotizing Inflammation

Lymphocytic and plasmacytic Inflammation

Immune Mediated Pathology

Autoimmune

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

Hypersensitivity

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.

Papilloma

Neoplastic

Squamous cell carcinoma

Oral squamous cell carcinoma. Courtesy of T. Scase

Degenerative Pathology

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.

Vascular Pathology

Learning Tools

Cavity and Gingiva Flashcards