Professional Documents
Culture Documents
Oral Manifestations of Systemic Disorders in Dogs
Oral Manifestations of Systemic Disorders in Dogs
net/publication/237253088
Article
CITATIONS READS
9 4,977
3 authors, including:
Some of the authors of this publication are also working on these related projects:
All content following this page was uploaded by Boaz Arzi on 09 March 2015.
An animal with oral lesions presents the veterinarian with a diagnostic challenge. Many systemic
disorders have oral manifestations, and therefore the oral cavity might be considered a window for
making a diagnosis. These oral manifestations must be recognized for the patient to receive ap-
propriate diagnosis and treatment. The literature and clinical cases with disorders involving one or
more organs or tissues and pathological manifestations in the oral cavity were reviewed.
Key Words: systemic, disorders, oral, lesions, dogs, cats
Hypothyroidism
2a Structural or functional abnormalities
of the thyroid gland can lead to deficient
production of thyroid hormone. Primary
hypothyroidism is the most common form
in dogs. It usually results from destruction
of the thyroid gland due to lymphocytic
thyroiditis (immune-mediated) and idi-
opathic atrophy of the thyroid gland.6 The
pathogenesis for oral lesions in hypothyro-
id animals includes a potential underlying
immune-mediated process and bleeding
tendency.
In breeds prone to hypothyroidism
(e.g., golden retriever, Labrador retriever)
extensive periodontal disease and mucosal
2b bleeding can be seen.
Figure 2a and 2b — A dog with primary hyperpara-
thyroidism. Note the bone loss on the computerized
Diabetes Mellitus (DM)
tomography 3D reconstructive image. DM is a chronic metabolic disorder
characterized by hyperglycemia, asso-
Hypoadrenocorticism (Addison’s Dis- ciated with irregularities in the metabolism
ease) of carbohydrates, lipids, proteins; and sus-
Hypoadrenocorticism is classified as ceptibility to the development of specific
primary or secondary adrenocortical insuf- forms of renal, ocular, neurological and
ficiency. Primary adrenocortical insuffi- cardiovascular diseases.10 DM increases
ciency is the most common form and in- the susceptibility to erosion and ulceration
volves a deficiency of both mineralocorti- of the mucosa.10
coid and glucocorticoid secretions.6 The Oral manifestations may include ke-
etiology is usually immune-mediated, or totic malodor, high frequency of periodon-
iatrogenic associated with acute withdraw- tal disease, xerostomia, bone resorption,
JVCS, Vol. 1, No. 4, October 2008 115
Arzi et al
nature. Most inflammatory oral lesions in The oral lesions are similar in cause
cats are associated primarily or secondarily and presentation to those in FIV infection.
with bacteria,21 but viruses may also play a
role in oral tissue. A number of viruses in Feline Herpesvirus Type-1 (FHV-1)
cats are carried in oral tissue and shed in Rhinotracheitis
saliva including feline immunedeficiency Feline herpesvirus type-1 (FHV-1) is
virus (FIV), feline leukemia virus (FeLV), a pathogen that infects only cats.24 The in-
feline herpesvirus type-1 (FHV-1), feline fection has a high prevalence within the
calicivirus (FCV), and feline syncytium- worldwide population of cats and causes
forming virus (FeSFV). Although these vi- significant morbidity. Although cats are
ruses replicate in the oral cavity, it is un- typically infected at a young age, the virus
certain whether or not they actually cause can cause lifelong problems due to latency
disease in oral tissue; and if they do, and reactivation. FHV-1 is transmitted via
whether their role is causal or indirect.22 close contact and exchange of bodily flu-
ids, particularly respiratory and ocular se-
Feline Immunodeficiency Virus (FIV) cretions. Over-crowded conditions and
Feline immunodeficiency virus (FIV) close housing such as a catteries and shel-
is an exogenous single stranded RNA virus ters greatly increase the likelihood of viral
in the family Retroviridae, subfamily Len- transmission.24 Kittens are most suscepti-
tivirinae.23 FIV produces reverse transcrip- ble to primary infections, especially as ma-
tase enzyme to catalyze the insertion of ternal antibodies wane.
viral RNA into the host genome. FIV in- Clinical manifestations of rhino-
fection of cats has a worldwide distribu- tracheitis are seen with varying degrees of
tion. Aggressive biting behavior is thought gingivitis, and oral ulceration on the rostral
to be the primary route of transmission of part of the tongue (Figure 5).
FIV. Male, outdoor cats older than six
years of age are most commonly infected.
Postnatal transmission from FIV-infected
queen to kittens in milk has been docu-
mented.23
The oral lesions are believed to occur
due to the systemic immune-suppressive
effect of the virus and include various de-
grees of gingivitis, gingival proliferation,
gingival and mucosal ulcerations, exuda-
tion and periodontitis.
Feline Leukemia Virus (FeLV)
Feline leukemia virus (FeLV) is a
single-strand RNA virus in the family Ret-
roviridae, subfamily Oncovirinae. The vi-
rus produces reverse transcriptase which
catalyzes formation of provirus of FeLV
and its insertion into the host cell ge-
nome.23 The principal route of infection by
FeLV is prolonged contact with infected
cat saliva or nasal secretions; grooming or
sharing of common water or food sources
effectively result in infection. FeLV infec-
tion has a worldwide distribution. Infec- Figure 5 — Ulcerative glossitis caused by herpesvi-
tion is most common in outdoor male cats rus in a cat.
between one and six years of age.
118 JVCS, Vol. 1, No. 4, October 2008
Oral manifestation of systemic disorders
Feline Calicivirus (FCV) sion of the virus. Contact with infected sa-
Feline calicivirus (FCV) is a single- liva with mucous membranes and open
strand RNA virus and is a major cause of wounds rarely cause disease. 29 The two
acute oral and upper respiratory tract dis- classical clinical presentations have been
ease in domestic cats.25 Calicivirus is high- divided into “furious or psychotic” and
ly contagious and moderately environmen- “dumb or paralytic”.
tally persistent. It is spread by direct con- Oral manifestations include excessive
tact, by fomites over significant time and salivation, diminished facial sensation,
distance. dropped jaw and lingual lacerations.
Varying degrees of gingivitis, oral ul-
cerations and exudation, glossitis and oral Fungal Cryptococcosis in Cats
vesicles may be seen. Cryptococcus neoformans causes a
common systemic fungal disease in cats.30
Canine Distempervirus (CDV) The most common route of infection is
Canine distempervirus (CDV) is through inhalation.31 Cutaneous and sub-
usually seen as a multi-systemic disease cutaneous routes of infection may also oc-
with multifocal progressive involvement cur. In addition to the upper and lower res-
of the central nervous system (CNS).26 piratory tract and cutaneous and subcuta-
Clinical signs may vary, depending on the neous involvements, oral lesions may oc-
virulence of the virus strain, environmental casionally be noted.30 The oral lesions may
conditions, and host age and immune sta- include diffuse ulcerations of the oral mu-
tus.26 Young, unvaccinated dogs are most cosa, tongue, gingival, and palate. In addi-
commonly affected by severe generalized tion, gingival proliferation may be noted.30
distemper. In infected dogs, non-neurologic
signs (ocular and nasal discharge, cough- Leptospirosis
ing, vomiting, diarrhea) are seen first; then Leptospires are 0.1-0.2 µm wide by
neurologic signs begin one to three weeks 6-12 µm long motile, filamentous spiro-
after the dogs start to recover from system- chetes that infect animals and humans.23
ic illness.26 Infection by leptospires occurs in both ru-
Multiple dental developmental ab- ral and suburban environments. Clinical
normalities may be noted in the permanent cases are most commonly diagnosed in the
dentition such as unerupted teeth, partial summer and early fall. Leptospires are
eruption, oligodontia, enamel hypoplasia passed in urine and enter the body through
and root hypoplasia, which can be loca- abraded skin or intact mucous membranes.
lized but in most cases is generalized. Transmission also occurs by bite wounds,
Enamel and dentin hypoplasia result from veneral contact, transplacental and inges-
damage by the virus to the ameloblasts tion. Leptospirosis is a multisystemic dis-
while the teeth are developing. ease caused by various species such as
Leptospira canicola, L. icterohaemorrha-
Rabies (RABV) giae, and L. pomona.1
Rabies (RABV) is a Lyssavirus in the The oral lesions depend on the spe-
family Rhabdoviridae. Foxes, coyotes and cies. L. canicola causes severe congestion
wolves are among the most susceptible to of oral mucus membranes, potential ure-
RABV infection. Skunks, raccoons, bats, mia-related oral ulcerations, hemorrhage,
cows, and cats are considered highly sus- glossitis and necrosis especially at the tip
ceptible while domestic canines, sheep, of the tongue.1 L. icterohaemorrhagiae
goats and horses are only moderately sus- causes severe oral mucus membrane con-
ceptible.27 Young of every species are gestion and thrombocytopenia-related pe-
more susceptible than mature animal.28 A techiation and hemorhage.
bite by an animal shedding virus in saliva
is the most common method of transmis-
JVCS, Vol. 1, No. 4, October 2008 119
Arzi et al
References
1. Anderson JG. Approach to diagnosis of canine oral riology of periodontal disease in the cat. Arch Oral
lesions. Compend Cont Educ Pract Vet 1991; Biol 1988; 33: 677-683.
13: 1215-1226. 22. Tenorio AP, Franti CE, Madewell BR, et al. Chron-
2. Hutt FB, De Lahunta A. A lethal glossopharyngeal ic oral infections of cats and their relationship to
defect in the dog. J Hered 1971; 62: 291-293. persistent oral carriage of feline calici-, immunode-
3. Nelson WR, Couto CG. Hematology and immunol- ficiency, or leukemia viruses. Vet Immunol Immu-
ogy. In: Nelson WR, Couto CG, 2nd ed. Small ani- nopathol 1991; 29: 1-14.
mal internal medicine. St. Louis: Mosby, 1998; 23. Nelson WR, Couto CG. Infectious diseases. In: Nel-
1159-1238. son WR, Couto CG, 2nd ed. Small animal internal
4. Callan MB, Bennett J, Phillips D, et al. Inherited medicine. St. Louis: Mosby, 1998; 1273-1301.
platelet delta-storage pool disease in dogs causing 24. Stiles J. Feline herpesvirus. Clin Tech Small Anim
severe bleeding: an animal model for a specific Pract 2003; 18: 178-185.
ADP deficiency. Thromb Haemost 1995; 74: 949- 25. Gaskell R, Dawson S. Feline respiratory disease. In:
953. Greene CE, ed. Infectious diseases of the dog and
5. Giger U, Callan M, Phillips D, et al. Inherited plate- cat. 2nd ed. Philadelphia: WB Saunders Co, 1998;
let gamma storage pool disease in dogs causing se- 97-106.
vere bleeding: an animal model. Proceedings, 26. Nelson WR, Couto CG. Neuromuscular disorders.
American Society of Hematology Annual Meeting, In: Nelson WR, Couto CG, 2nd ed. Small animal in-
1993. ternal medicine. St. Louis: Mosby, 1998; 1013-1016.
6. Nelson WR, Couto CG. Endocrine disorders. In: 27. Greene CE, Rupprecht CE. Rabies and other lyssa-
Nelson WR, Couto CG, 2nd ed. Small animal inter- virus infections. In: Greene CE, ed. Infectious dis-
nal medicine. St. Louis: Mosby, 1998; 671-798. eases of the dog and cat. 2nd ed. Philadelphia: WB
7. Thrall MA. Regenerative anemia. In: Veterinary Saunders Co, 2006; 167-183.
hematology and clinical chemistry. Philadelphia: 28. Blancou J, Aubert MFA, Artois M. Fox rabies. In
Lippincot Williams& Wilkins, 2004; 115. Baer GM, ed. The natural history of rabies. 2nd ed.
8. Fossum TW. Small animal surgery. 2nd ed. St. Boca Raton: CRC press, 1991; 258-285.
Louis: Mosby, 2002; 285-286. 29. Jackson AC. Rabies pathogenesis. J Neurovirol
9. Nelson AW. Upper respiratory diseases. In: Slatter 2002; 8: 267-269.
DH, ed. Textbook of small animal surgery. 3rd ed. 30. Odom T, Anderson JG. Proliferative gingival lesion
Philadelphia: WB Saunders Co, 2003; 815-818. in a cat with disseminated cryptococcosis. J Vet
10. Regezi JA, Sciubba JJ, Jordan RC. Oral pathology - Dent 2000; 17: 177-181.
clinical pathologic correlations. 4th ed. Philadel- 31. Gerds-Grogan S, Dayrell-Hart B. Feline cryptococ-
phia: WB Saunders Co, 2003. cosis: a retrospective evaluation. J Am Anim Hosp
11. Nelson WR, Couto CG. Oncology. In: Nelson WR, Assoc 1997; 33: 118-122.
Couto CG, 2ed. Small animal internal medicine. St. 32. Scully C, Challacombe SJ. Pemphigus vulgaris: up-
Louis: Mosby, 1998; 1123-1143. date on etiopathogenesis, oral manifestations, and
12. Mellor PJ, Haugland S, Murphy S, et al. Myeloma- management. Crit Rev Oral Biol Med 2002; 13:
related disorders in cats commonly present as 397-408.
extramedullary neoplasms in contrast to myeloma in 33. Edwards IR, Aronson JK. Adverse drug reactions:
human patients: 24 cases with clinical follow-up. J definitions, diagnosis, and management. Lancet
Vet Intern Med 2006; 20: 1376-1383. 2000; 356: 1255-1259.
13. Carpenter JL, Andrews LK, Holzworth J. Tumours 34. Femiano F, Lanza A, Buonaiuto C, et al. Oral ma-
and tumour-like lesions. In: Holzworth J. Diseases nifestations of adverse drug reactions: guidelines. J
of the cat: medicine and surgery. Philadelphia: WB Eur Acad Dermatol Venereol 2008; 22: 681-691.
Saunders Co, 1987; 406-596. 35. Scully C. Drug effects on salivary glands: dry
14. Engle GC, Brody RS. A retrospective study of 395 mouth. Oral Dis 2003; 9: 165-176.
feline neoplasms. J Am Anim Hosp Assoc 1969; 5: 36. Scully C, Azul AM, Crighton A, et al. Nicorandil
21-31. can induce severe oral ulceration. Oral Surg Oral
15. Priester WA, McKay FW. The occurrence of tumors Med Oral Pathol Oral Radiol Endod 2001; 91: 189-
in domestic animals. Natl Cancer Inst Monogr 1980; 193.
(54): 1-210. 37. Scully C, Bagan JV. Adverse drug reactions in the
16. Cutright DE, Bauer H. Cell renewal in the oral mu- orofacial region. Crit Rev Oral Biol Med 2004; 15:
cosa and skin of the rat. I. Turnover time. Oral Surg 221-239.
Oral Med Oral Pathol 1967; 23: 249-259. 38. Vescovi P, Meleti M, Manfredi M, et al. [Pathoge-
17. Sheffy BE, Williams AJ. Nutrition and the immune nesis of cyclosporine induced gingival overgrowth].
response. J Am Vet Med Assoc 1982; 180: 1073- Minerva Stomatol 2003; 52: 219-229.
1076. 39. Majcherczyk J, Szymanska-Jachimczak EI. Verfar-
18. Jemmolt J, Barysenko J, Barysenko M, et al. Aca- bung der Zahne und Knochen bei jungen Tieren
demic stress, power motivation, and decrease in se- durch Tetracycline [Discoloration of the teeth and
cretion rate of salivary secretory immunoglobulin A. bones in young animals caused by tetracycline].
Lancet 1983; 1: 1400-1402. Zahnarztl Prax 1965; 16: 61-3.
19. Hupp JR, Williams TP, Firriolo FJ. Dental clinical 40. Bennett IC, Law DB. Incorporation of tetracycline
advisor. St. Louis: Mosby, 2006; 335-337. in developing enamel and dentin in dogs. J Dent
20. Frost P, Williams CA. Feline dental disease . In: Vet Child 1967; 34: 93-5.
Clin North Am 1986; 16: 851-873. 41. Yoneda T, Hashimoto N, Hiraga T. Bisphosphonate
21. Mallonee DH, Harvey CE, Venner M, et al. Bacte- actions on cancer. Calcif Tissue Int 2003; 73: 315-
JVCS, Vol. 1, No. 4, October 2008 123
Arzi et al