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Case report

Blackwell Science, Ltd

Dermal arteritis of the nasal philtrum in a Giant Schnauzer and

three Saint Bernard dogs

Arteritis of the nasal philtrum

SHEILA M. F. TORRES,* TIMOTHY O. BRIEN and DANNY W. SCOTT

*Department of Small Animal Clinical Sciences, Department of Veterinary Diagnostic Medicine, College of
Veterinary Medicine, University of Minnesota, Saint Paul, MN 55108, USA Departments of Clinical Sciences
and Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
(Received 3 December 2001; accepted 9 July 2002)

Abstract Arteritis of the nasal philtrum is described in four dogs. Two of the Saint Bernards were related. The
lesions were solitary, well-circumscribed, linear ulcers that were neither pruritic nor painful. The age of the dogs
at the time the owners first noticed the lesion ranged from 3 to 6 years. The ulcers had been present for 0.55 years
before diagnosis was pursued. Three of the dogs experienced repeated, mild episodes of arterial bleeding from
the ulcers. Two dogs also experienced a severe episode of bleeding that required surgical intervention. Histopathological findings included a V-shaped ulcer, neutrophilic dermal inflammation subjacent to the ulcer and lymphoplasmacytic dermatitis bordering the ulcer. The most remarkable pathological findings were present in the deep
dermal arteries and arterioles subjacent to the ulcer. The changes were characterized by subendothelial spindle
cell proliferation with marked extracellular matrix deposition that stained blue with Alcian Blue (mucin) and
Massons trichrome (collagen) and resulted in intimal thickening, and stenosis of dermal arteries and arterioles.
Immunohistochemical studies suggested that the proliferating spindle cells were of either myofibroblast or
smooth muscle origin (actin and vimentin positive). Anti-inflammatory therapy (glucocorticoids; tetracycline
and niacinamide; fish oil) may be beneficial for long-term control of this condition, however, long-term maintenance treatment appears to be necessary.
Keywords: arteritis, dermis, dogs, Giant Schnauzer, nasal philtrum, Saint Bernard, skin

INTRODUCTION

MATERIALS AND METHODS

Disorders affecting the nasal plane (planum nasale) of

dogs are uncommon but well recognized, and include:
discoid and systemic lupus erythematosus, pemphigus
foliaceous/erythematosus, pemphigus vulgaris, contact hypersensitivity, uveodermatologic syndrome, nasal
hyperkeratosis of Labrador Retrievers, idiopathic
nasodigital hyperkeratosis, sterile pyogranuloma
syndrome, vitiligo, nasal hypopigmentation, mycotic
infections, leishmaniasis, distemper, vasculopathies and
neoplasia.117 However, to our knowledge, none of
these disorders is reported to exclusively affect the
nasal philtrum (philtrum of the nasal plane).
The purpose of this study is to present the clinical,
histopathological, histochemical, and immunohistochemical findings of a previously unreported skin
condition affecting the nasal philtrum of three Saint
Bernards and a Giant Schnauzer.

Skin biopsy specimens were obtained with a 6-mm

punch biopsy instrument under general anaesthesia
(cases 1, 2, and 4) or at necropsy (case 3), fixed in
10% neutral formalin solution, paraffin-embedded,
sectioned at 5 m, and stained with haematoxylin and
eosin (H&E), Congo Red, Alcian Blue and Massons
trichrome. Immunohistochemical staining for desmin,
smooth muscle actin and factor VIII-related antigen
was performed on a Dako Autostainer (Dako, Carpinteria, CA, USA) briefly described as follows. Sections
were deparaffinized through four changes of citrisol
solvent (3 min each), rehydrated through a graded
ethanol and distilled water series and pretreated by
microwaving (desmin and smooth muscle actin) in 0.1
citrate buffer or pretreated with protease (factor
VIII, Proteinase K, cat. #S300402, Dako) solution and
rinsed [all rinses except where otherwise specified are
0.05 Tris-buffered saline (TBS), pH 7.2, with 0.05%
Tween 20]. Endogenous peroxidase was quenched with
3% hydrogen peroxide for 15 min and sections rinsed.
Nonspecific binding was blocked with normal goat
serum (1:10 in TBS) for 15 min followed by incubation
with primary antibody (incubation time and dilution

Correspondence and reprints to, Sheila M. F. Torres, Department of

Small Animal Clinical Sciences, College of Veterinary Medicine,
University of Minnesota, C339 Veterinary Hospitals, 1352 Boyd
Avenue, Saint Paul, MN 55108, USA. Tel.: +1-612-625-3715; E-mail:
torre009@tc.umn.edu
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S. M. F. Torres et al.

optimized for each antiserum). Primary antisera

(Dako) were mouse monoclonal antibodies directed
against human -smooth muscle actin (clone 1A4,
1:400), or human desmin (clone D33, 1:100), and a
rabbit polyclonal antiserum against human factor VIII
(1:600). Following a rinse, sections were incubated
with biotinylated goat antirabbit and mouse IgG (cat.
# LSAB2 Kit, Dako) for 15 min. Sections were again
rinsed and incubated with streptavidinhorseradish
peroxidase label (LSAB2 kit, Dako) for 15 min, rinsed
and incubated with 3-amino-9-ethylcarbazole (AEC
ready-to-use kit, Dako) with hydrogen peroxide for
10 min. Sections were then rinsed for 5 min in distilled
water followed by running tap water rinse for 5 min
and counterstained with Mayers hematoxylin (Sigma,
St. Louis, MO, USA) for 25 min. Slides were then
rinsed in running tap water and coverslipped with
aqueous mounting medium. Negative staining control
consisted of the above procedure with the primary
antibody omitted. Positive control staining for all three
primary antisera above was performed on sections of
dog tongue in which desmin antiserum labels skeletal
muscle fibres and some vascular smooth muscle cells;
smooth muscle actin antiserum labels vascular smooth
muscle cells; and factor VIII antiserum labels vascular
endothelial cells. Biopsy specimens were also taken
from the nasal philtrum of a normal Saint Bernard and
processed in an identical fashion.

Case 1
A 5-year-old, male castrated Saint Bernard was presented to the Veterinary Teaching Hospital, University
of Minnesota (VTHUMN) with an 18-month history
of a gradually enlarging fissure localized to the nasal
philtrum. The affected area had multiple episodes of
mild arterial bleeding during the past 4 months. Three

weeks prior to presentation at the VTHUMN, the

dog experienced a severe arterial bleeding episode and
had the lesion sutured at an emergency clinic to obtain
haemostasis. Since the problem started the owner
had applied many topical products such as petrolatum,
glycerin, shark liver oil, phenylephrine HCL, cetyl and
stearyl alcohols, EDTA, parabens, lanolin and tocopherol (Preparation H, Whitehall-Robins Healthcare,
Madison, NJ, USA) petrolatum, anhydrous lanolin,
mineral oil, vitamin A and vitamin D (Vitamin A &
D ointment, Clay-Park Laboratories, Inc., Bronx,
NY, USA) and antibiotic/glucocorticoid ointments.
There was only minor improvement with these
treatments. On presentation, the dog had a solitary,
well-circumscribed, linear ulcer involving the nasal
philtrum (Figs 1 and 2). The lesion was 5 cm in
length, 21.5 cm in width and 25 mm in depth. The
ulcer was widest at its dorsal margin, nearest the
external nares. A haemopurulent crust was covering
the lesion. There was no pain or pruritus, and the
dog was otherwise healthy. Cytologic examination of
impression smears taken from the moist exudate
present underneath the crust revealed large numbers
of cocci, rods, degenerated neutrophils, keratinocytes,
and red blood cells. Bacterial culture and susceptibility
testing yielded Staphylococcus aureus; haemolytic
Streptococcus sp.; and Pseudomonas aeruginosa which
showed susceptibility to amikacin, gentamicin and
ticarcillin. The disorders considered as differential
diagnoses included discoid lupus erythematosus,
vasculopathy, trauma, fixed drug eruption and fungal
infection. Haemogram and chemistry profile obtained
before general anaesthesia and biopsy were unremarkable.
Histological examination of skin biopsy specimens
revealed a V-shaped ulcer bordered by pseudocarcinomatous epidermal hyperplasia and moderate-tomarked dense parakeratotic hyperkeratosis. Epidermis
bordering the ulcer also contained spongiosis, intracellular oedema, apoptotic keratinocytes (stratum basale and

Figure 1. Nasal philtrum, lateral view of case 1; Saint Bernard

dog with a well-circumscribed ulcer of the nasal philtrum. A
haemopurulent crust is covering the lesion.

Figure 2. Nasal philtrum, frontal view of case 1; Saint Bernard dog

with ulcer of the nasal philtrum. The ulcer extends to approximately
three-quarters of the nasal philtrum and it is covered with a
haemopurulent crust. A fissure is present on the planum nasale.

CASE REPORTS

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Arteritis of the nasal philtrum

Figure 3. Skin of nasal philtrum; normal Saint Bernard. Small

artery in nasal philtrum. LU = lumen and arrowhead indicates
position of internal elastic membrane. The space between the
endothelial cells and the internal elastic membrane (tunica intima)
is barely visible in a normal small dermal artery. H&E.
Bar = 100 m.

Figure 4. Skin of nasal philtrum; case 1. Small artery in nasal

philtrum with markedly thickened tunica intima as a result of subendothelial spindle cell proliferation and prominent extracellular
deposition of a homogeneous to fibrillar eosinophilic material.
LU = lumen and arrowhead marks the internal elastic membrane.
H&E. Bar = 50 m.

stratum spinosum), lymphocytic and/or neutrophilic

exocytosis, foci of hydropic degeneration of basal cells
and superficial necrosis. One small intracorneal
accumulation of degenerate neutrophils and cocci was
present. The dermis bordering the ulcer contained foci
of subepidermal bandlike fibrosis, oedema, pigmentary
incontinence, and variable numbers of lymphocytes
and plasma cells. The dermal ulcer was associated
with necrosis, haemorrhage and neutrophilic infiltration,
and peripheral areas of perivascular-to-interstitial
lymphoplasmacytic dermatitis.
The most remarkable pathological changes were
present in the deep dermal arteries and arterioles subjacent to the ulcer. Findings included subendothelial
spindle cell proliferation with prominent extracellular

277

Figure 5. Skin of nasal philtrum; case 1. Mucin deposition (dark

blue stain) in the expanded tunica intima of a small artery in the
dermis adjacent to the cutaneous ulcer. LU = lumen and arrowhead
marks the internal elastic membrane. Alcian Blue. Bar = 50 m.

Figure 6. Skin of nasal philtrum; case 1. Collagen deposition (blue

stain) in the expanded tunica intima of a small artery in the dermis
adjacent to the cutaneous ulcer. LU = lumen and arrowhead marks
the internal elastic membrane. Massons trichrome. Bar = 25 m.

matrix deposition that stained blue with Alcian Blue

(not metachromatic) and blue with Massons trichrome (collagen). The presence of these extracellular
substances resulted in intimal thickening and stenosis
of the deep dermal arteries and arterioles (Figs 3 6).
Homogeneous eosinophilic acellular (hyaline) deposits
were present in some areas of the thickened vessels.
This material stained blue with Massons trichrome
(collagen) and did not stain with Congo Red (not
amyloid). Spindle cells proliferating in the thickened
areas of vascular intima were positive for smooth
muscle actin (Fig. 7) and vimentin, occasionally positive
for desmin, and were negative for factor VIII-related
antigen (data not shown). These findings are consistent with either myofibroblast or smooth muscle-like
differentiation of the proliferating intimal cells. Some
affected arterioles and arteries had focal areas of
intramural oedema and haemorrhage, and small-tomoderate numbers of karyorrhectic nuclei, neutrophils,
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S. M. F. Torres et al.

Figure 9. Skin of nasal philtrum; case 1. Deep dermal artery. Note

intramural haemorrhage, neutrophils (arrow) and karyorrhectic
nuclei (leukocytoclasis). H&E. Bar = 57 m.
Figure 7. Skin of nasal philtrum; case 1. Spindle cells in the
thickened tunica intima of this small artery are immunohistochemically positive (redbrown stain) for smooth muscle actin.
The staining is consistent with differentiation to myofibroblast
or smooth muscle cells. LU = lumen and arrowhead marks the
internal elastic membrane. Avidinbiotin immunohistochemistry,
smooth muscle actin-specific mouse monoclonal antibody (clone
1A4), AEC chromogen Mayers haematoxylin counterstain.
Bar = 100 m.

Figure 10. Nasal philtrum, frontal view of case 2; Saint Bernard

dog with ulcer of the nasal philtrum. Linear ulcer spanning the
nasal philtrum. A haemopurulent crust covers the ulcer.

Figure 8. Skin of nasal philtrum; case 1. Stenotic dermal arteriole.

Note intramural mucin, haemorrhage and pyknotic nuclei, as well
as perivascular accumulations of lymphocytes and plasma cells.
H&E. Bar = 57 m.

and lymphocytes (Figs 8 and 9). Affected vessels also

had mild-to-moderate perivascular accumulations of
lymphocytes and plasma cells, and focal perivascular accumulations of haemosiderin and haemosiderophages. Occasional perivascular lymphoid nodules
were present.
The final clinicopathological diagnosis was idiopathic
proliferative arteritis. The dog was managed with twice
daily topical applications of gentamicin sulfate and
betamethasone valerate (Gentocin Otic, ScheringPlough, Kenilworth, NJ, USA) to treat the secondary
bacterial infection until recheck appointment 2 weeks
later. He was also started on 1.1 mg kg1 per day of oral
prednisone (Prednisone, Roxane Laboratories, Inc.
Columbus, OH, USA) to manage the deep dermal
inflammation and vasculitis. At 2-week recheck
appointment a moderate improvement was noticed.
2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 275 281

No signs of infection were present and impression

smears of the lesion revealed no organisms. The ulcer
appeared shallower compared with the time of presentation and the owner reported no bleeding episodes.
Because of concerning signs of polyuria, polydipsia
and polyphagia the dose of prednisone was reduced to
the lowest maintenance dose that prevented bleeding
episodes. The dog has been maintained under control
for 6 months on 0.25 mg kg1 of prednisone every
other day. The ulcer is shallower, smaller, nonexudative, but still present.
Cases 2 4
Cases 2 and 3 were seen at the VTHUMN, and case 4
was seen at the Cornell University Companion Animal
Hospital. Clinical information for these cases is
presented in Table 1. The clinical, histopathological,
histochemical, and immunohistochemical features of
the nasal philtrum ulcers in these dogs (Fig. 10) were as
described for case 1. The ulcers varied from 3 to 5 cm
in length, 215 mm in width, and 25 mm in depth.
The ulcers were widest at their dorsal margin, nearest
the external nares. Results of haemogram, serum
chemistry panel, and urinalysis were normal in case 4.

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Arteritis of the nasal philtrum

279

Table 1. Clinical information for four dogs with arteritis of the nasal philtrum*
Lesion
duration
(years)

Case

Breed

Sex

Age
(years)

St. Bernard

MC

1.5

2
3

St. Bernard
St. Bernard

FS
M

9
6

5.0
0.1

Giant Schnauzer

FS

0.5

Haemorrhage
Multiple episodes of mild bleeding from lesion during past 4 months.
Severe haemorrhage 3 weeks prior to examination
Multiple episodes of mild bleeding from lesion for past 12 months
Mild bleeding from lesion for past 1 month.
Severe haemorrhage 2 days prior to examination
None observed

*Case 1 is son of dog in Addendum. Case 2 is sibling of dog in Addendum. MC = castrated male; FS = spayed; M = male.

Table 2. Therapies used in four dogs with arteritis of the nasal philtrum
Case

Initial treatment

Maintenance treatment

1
2

1.1 mg kg1 prednisone orally every 24 h for 2 weeks

1.1 mg kg1 prednisone every 24 h, 500 mg tetracycline
every 8 h, 500 mg niacinamide
every 8 h, and 1 capsule/
4.5 kg fish oil* orally every 24 h for 8 weeks
1.1 mg kg1 prednisone every 24 h for 10 days

0.25 mgkg1 prednisone orally every 48 h for 6 months

Tetracycline, niacinamide, and fish oil for 9 months
Mild, intermittent recurrences of ulcer

Topical flucinolone in dimethyl sulfoxide

every 12 h for 3 weeks

Euthanized due to bleeding from nasal lesion, melena,

haematemesis, respiratory distress, and seizures.
Necropsy findings included gastric ulcer, gastric foreign body
(piece of towel), pulmonary thromboses consistent with
disseminated intravascular coagulation, and steroid hepatopathy
Topical flucinolone in dimethyl sulfoxide twice weekly for 1.5 years.
All attempts to discontinue treatment result in recurrence of ulcer

*EPA, Puritans Pride, Inc., Oakdale, NY, USA (contains 180 mg eicosapentaenoic acid and 120 mg docosahexaenoic acid per capsule).
Synotic, Fort Dodge, Fort Dodge, IA, USA.

Medications used in these cases are presented in

Table 2. When presented to the VTHUMN, one Saint
Bernard (case 3) was lethargic and depressed, the
mucous membranes were pale, and the nasal philtrum
ulcer was bleeding moderately. The dog was kept in the
intensive care unit for 7 days to control the bleeding
and treat the anaemia.

DISCUSSION
Although a variety of diseases can affect the nasal
planum of dogs,117 none is known to selectively affect
the nasal philtrum. The arteritis and ulcer of dogs
described herein, which affects exclusively the nasal
philtrum, has not, to our knowledge, been reported
previously in the veterinary or human literature.
Clinically, the condition had a tardive onset in all four
dogs, with the age at the time the owners first noticed
the lesion ranging from about 3 to 6 years. Lesions
occurred exclusively in the skin of the nasal philtrum
and were characterized by solitary linear ulcers. The
ulcers varied from 3 to 5 cm in length, 215 mm in
width (widest dorsally near the external nares), and 2
5 mm in depth. Affected dogs were neither pruritic nor
painful, and were otherwise healthy. Three of the four
dogs experienced repeated episodes of bleeding from
their lesion, and two dogs experienced episodes of
severe arterial bleeding which in one case required
emergency treatment for blood loss.

The nasal philtrum arteritis reported herein occurs

predominantly in Saint Bernard dogs. This observation
and the close familial relation between two of the dogs
suggest that this may be an inherited disorder. However, the occurrence in adult animals suggests that
other factors must play a role. Trauma was not known
to be an initiating factor in any of the dogs. Neither was
there a consistent history of drug or vaccine administration preceding the onset of lesions. We suspect that
the primary lesion is inflammation of the arterioles
and arteries of the nasal philtrum which results in
the progressive spindle cell proliferation, extracellular
matrix deposition and thickening of the vascular walls.
However, vascular inflammation was not the dominant
feature of these cases and no evidence of systemic vasculitis or other systemic vasculopathy was found in the
one dog in which a necropsy was performed. This may
be a factor of chronicity. It must be remembered that,
in humans, the chronic phase of several inflammatory
disorders of large- and medium-sized vessels can be
characterized by little or no inflammation, fraying of
the lamina elastica, thickening of the intima, myofibroblastic proliferation and intramural and perivascular fibroblastic proliferation.18
As the disease process progresses in these dogs,
vascular walls become progressively thickened causing
partial occlusion of the vessels, which then may lead to
local ischaemia, necrosis, and ulceration of the skin of
the nasal philtrum. The vasculopathy may also cause
weakness of the vascular walls with subsequent rupture,
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S. M. F. Torres et al.
mild bleeding episodes from a nasal philtrum ulcer.
The dog was the sibling of case 2 and the sire of case 1.
Clinical features of the nasal philtrum ulcer were as
described for cases 14, but no skin biopsy was performed (Fig. 11). A 2-month course of therapy with
tetracycline and niacinamide was ineffective. The lesion
was controlled with the administration of 1.1 mgkg1
prednisone orally every 24 h for 2 weeks. The dog was
successfully managed with 0.25 mg kg1 prednisone
orally every 24 h for the subsequent year.

REFERENCES

Figure 11. Nasal philtrum, frontal view of case referred in

addendum; Saint Bernard dog with ulcer of the nasal philtrum.
Linear ulcer spanning the nasal philtrum. A bed of granulation
tissue is present underneath the ulcer.

resulting in the haemorrhage which was quite marked

in two of the dogs.
A fascinating aspect of this disorder is the targeting
of the large vessels of the nasal philtrum. The wellrecognized large-to-medium-sized vessel diseases of
humans can be localized (temporal arteritis, Mondors
disease) or multifocal (polyarteritis nodosa, Kawasaki
disease), but are clinically very different from the
arteritis described in these dogs.18 From an anatomical
standpoint, the most likely explanation for the peculiar
localization of this canine arteritis is a targeting of the
lateral nasal branches of the infraorbital arteries, the
lateral nasal branches of the maxillary arteries, the rostral
septal branches of the palatine arteries or some combination of these. These are the vessels that supply the
canine nasal philtrum.19 Further angiographic and dissection studies should address these possibilities.
Anti-inflammatory therapy appeared to be beneficial in this condition. One dog was well controlled
(complete healing) for 1.5 years with the topical application of flucinolone in dimethyl sulfoxide. Another
dog was satisfactorily controlled (smaller ulcer, no
bleeding) with alternate-morning prednisone for
6 months. One dog was well controlled (complete healing) with tetracycline, niacinamide, and fish oil for
9 months. However, long-term maintenance treatment
appears to be necessary. From a therapeutic standpoint, it seems more likely that the benefits of antiinflammatory agents (glucocorticoids; tetracycline and
niacinamide; omega 3 fatty acids) are due to suppressing vascular inflammation rather than suppressing
fibroblastic and myofibroblastic proliferation.

ADDENDUM
A 3-year-old-intact male Saint Bernard was presented
to the VTHUMN with a 2-month duration of multiple
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1. Angarano, D.W. Dermatoses of the nose and the footpads in dogs and cats. In: Kirk, R.W., ed. Current Veterinary Therapy, 10th edn. Philadelphia: W.B. Saunders,
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Rsum Une artrite de la truffe est dcrite chez quatre chiens. Deux des Saint Bernard avaient un lien de
parent. Les lsions consistaient en des ulcres isols, bien dlimits et linaires, sans douleur ou prurit. Lge
lapparition des symptmes variait entre 3 et 6 ans. Les lsions taient prsentes 0.5 5 ans avant le diagnostic.
Des pisodes de saignement rpts ont t rapports pour trois des chiens. Une intervention chirurgicale lie
des saignements importants a t ncessaire dans deux cas. Lexamen histopathologique a montr la presence
dun ulcre en forme de V, surmontant une inflammation dermique neutrophilique et dlimit par une dermatite
lymphoplasmocytaire. Les modifications les plus remarquables atteignaient les artres et les artrioles autour de
lulcre. Il sagissait dune proliferation des cellules sous-endothliales avec un dpt dans la matrice extracellulaire prenant la coloration par le bleu Alcian (mucine) et le trichrome de Masson (collagne), qui provoquait un
paississement de lintima et une stnose des artres et des artrioles. Ltude immunohistochimique a indiqu
que ces cellules taient soit des myofibroblastes soit dorigine musculaire (marquage positif pour lactine et la
vimentine). Lutilisation de traitements anti-inflammatoires (glucocorticodes, tetracycline et niacinamide, huiles
de poisson) peut tre bnfique pour le traitement de cette maladie, cependant une thrapeutique au long cours
semble ncessaire.
Resumen Se describe una arteritis del philtrum nasal en cuatro perros. Dos de los San Bernardos estaban
emparentados. Las lesiones consistan en lceras solitarias, bien delimitadas y lineares, no prurticas ni dolorosas.
La edad de los animales cuando los dueos detectaron por primera vez la lesin era de entre 3 y 6 aos. Las
lceras haban aparecido entre 0.5 y 5 aos antes del diagnstico. Tres de los perros manifestaron episodios leves
y repetidos de sangrado arterial en las lceras. Dos perros tambin experimentaron un episodio grave de sangrado
que requiri una intervencin quirrgica. Los hallazgos histopatolgicos incluyeron una lcera en forma de V,
inflamacin drmica neutroflica subyacente a la lcera y una dermatitis linfoplasmactica alrededor de la lcera.
Los hallazgos patolgicos ms destacables se encontraban en las arterias drmicas profundas y arteriolas subyacentes a la lcera. Las alteraciones se caracterizaban por una proliferacin subendotelial de clulas fusiformes
con abundante depsito de matriz extracelular que mostraba una coloracin azul con azul Alciano (mucina) y
con tricrmica de Masson (colgeno), resultando en un engrosamiento de la ntima, y estenosis de las arterias y
arteriolas drmicas. Los estudios inmunohistoqumicos sugirieron que la proliferacin de clulas fusiformes
consista en miofibroblastos o en clulas de origen muscular liso (positivas a actina y vimentina). La terapia
anti-inflamatoria (glucocorticoides; tetraciclina y niacinamida; aceite de pescado) puede ser beneficiosa para el
control a largo plazo de esta presentacin, sin embargo, el mantenimiento del tratamiento a largo plazo parece
necesario.
Zusammenfassung Arteritis des Nasenphiltrums wird bei vier Hunden beschrieben. Zwei der Bernhardiner
waren verwandt. Die Lsionen waren solitre, gut umschriebene, lineare Geschwre, die weder Juckreiz
zeigten noch schmerzhaft waren. Das Alter der Hunde zum Zeitpunkt, als Besitzer die Lsion zum ersten Mal
bemerkten, schwankte zwischen 3 und 6 Jahren. Die Geschwre waren 6 Monate bis 5 Jahre vorhanden, bevor
eine diagnostische Aufarbeitung erfolgte. Drei der Hunde zeigten wiederholte, milde Episoden von arteriellen
Blutungen in den Geschwren. Zwei der Hunde zeigten eine schwere Blutungsepisode, die chirurgische
Intervention erforderte. Histopathologische Befunde beinhalteten ein V-frmiges Geschwr, neutrophile
dermale Entzndung unter und lymphoplasmazytische Dermatitis angrenzend an das Geschwr. Die
bemerkenswertesten Vernderungen waren in den tiefen dermalen Arterien und Arteriolen unter dem Geschwr
vorhanden. Die Vernderungen waren durch subendotheliale Spindelzellproliferation mit ausgeprgter extrazellulrer Matrixdeposition gekennzeichnet, die sich mit Alcianblau (Muzin) und Masson Trichromfrbung
(Kollagen) anfrbte und in Verdickung der Intima und Stenose der dermalen Arterien und Arteriolen resultierte.
Immunhistochemische Studien deuteten auf einen Ursprung von Myofibroblasten oder glatten Muskelzellen
hin (positiv mit Aktin und Vimentin). Entzndungshemmende Therapie (Glukokortikoide, Tetrazyklin und
Niacinamid, Fischl) sind fr die langfristige Kontrolle dieser Erkrankung mglicherweise von Nutzen,
Langzeittherapie scheint allerdings ntig zu sein.

2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 275281