Veterinary Dermatology 2003, 14, 159166

Blackwell Publishing Ltd.

Concurrent follicular dysplasia and interface dermatitis

in Boxer dogs
MILENE A. RACHID*, CHRISTOPHER D. DEMAULA*, DANNY W. SCOTT*,,
WILLIAM H. MILLER*,, DAVID A. SENTER and SHERRY MYERS
Departments of *Biomedical Sciences and
Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
Prairie Diagnostic Services, 52 Campus Drive, Saskatoon, SK, Canada S7N 5B4
(Received 19 August 2002; accepted 23 December 2002)

Abstract Recurrent or persistent follicular dysplasia and interface dermatitis are described in nine Boxers. Data
on age, sex, seasonality of alopecia and histopathological features of the follicular dysplasia in these nine Boxers
are comparable with those described in previous reports. The interface dermatitis was characterized by multifocal
annular crusted lesions confined to the areas of follicular dysplasia. The inflammatory lesions were neither pruritic nor painful and affected dogs were otherwise healthy. Histopathologically the clinically inflammatory lesions
were characterized as an interface dermatitis. Immunohistochemical studies failed to demonstrate immunoglobulins or complement at the basement membrane zone or within blood vessel walls. In dogs with recurrent or persistent disease, the follicular dysplasia and interface dermatitis ran identical, concurrent courses of spontaneous
remission and recurrence, or persistence, respectively. One dog with persistent disease was treated successfully
with tetracycline and niacinamide for the interface dermatitis, and melatonin for the follicular dysplasia.
Although the aetiopathogenesis of this newly described condition and the relationship between the two histological reaction patterns are not known, photoperiod and genetic predisposition appear to play a role.
Keywords: Boxer, dog, follicular dysplasia, interface dermatitis.

INTRODUCTION
Follicular dysplasia is well-recognized in the Boxer.16
A more-or-less bilaterally symmetric, well-circumscribed
alopecia and hyperpigmentation are seen, especially
over the flank region. In most cases, the condition is
seasonal and recurrent.
We recently recognized an interface dermatitis
occurring within the areas of follicular dysplasia in
nine Boxers. The purpose of this study is to report the
clinical, histopathological and immunopathological
features of this newly recognized interface dermatitis in
Boxers with recurrent (seasonal) and persistent (nonseasonal) follicular dysplasia.

owners and /or referring veterinarians of the latter three

dogs were contacted to acquire further historical, clinical,
laboratory and therapeutic information.
In order to determine if this apparently novel interface
dermatitis was something new, or had been overlooked
in the past, a retrospective study was performed. Case
records for all Boxers with a history of flank alopecia
and for which skin biopsy specimens had been submitted to the Surgical Pathology Service at the CUHA
between 1988 and 2001 were re-examined. Dogs were
included in our study only if they had appropriate
clinical and histopathological criteria for recurrent or
persistent follicular dysplasia.46 The owner and/or
referring veterinarian of each dog was contacted to
acquire further historical, clinical, laboratory and therapeutic information.

MATERIALS AND METHODS

Case selection
We first examined a Boxer with concurrent follicular
dysplasia and interface dermatitis at the Cornell University Hospital for Animals (CUHA) in January 2001.
By the end of 2001, we had examined two more
affected Boxers at the CUHA, and received skin biopsy
specimens from three additional affected Boxers. The
Correspondence: Danny W. Scott, Departments of Biomedical
Sciences, Clinical Sciences, College of Veterinary Medicine, Cornell
University, Ithaca, NY 14853, USA. E-mail: shb3@cornell.edu
2003 European Society of Veterinary Dermatology

Histopathological studies
All skin biopsy specimens had been taken with a 6-mm
punch biopsy instrument, fixed in 10% buffered formalin, routinely processed and embedded in paraffin.
Four-micrometre sections had been cut and stained
with haematoxylin and eosin (H&E) and acidorcein
Giemsa (AOG). All biopsy specimens (the original
slides) were systematically reviewed using a standardized histopathological evaluation form (Fig. 1).
A grading system was used to evaluate the severity
of the hair follicle dysplasia.3 Dysplastic hair follicles
were identified as primary hair follicles wherein the
159

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M. A. Rachid et al.

Figure 1. The histopathological evaluation form used for this study.

infundibular region was dilated and filled with usually

concentrically arranged orthokeratotic hyperkeratosis.
One or more secondary hair follicles and/or sebaceous
gland ducts (toes, tentacles) were also filled with
orthokeratotic keratin and extended into the subjacent
dermis. Dysplastic hair follicles were graded as mild
(toes were less than one-half the length of the dilated
infundibular portion of the hair follicle), moderate
(toes were approximately one-half to equal to the
length of the infundibulum), and severe (toes were
greater in length than the dilated infundibulum).
The number of dysplastic hair follicles per pilosebaceous unit (PSU) was recorded as follows:3 small
25% of the PSU examined; moderate > 25% but
< 75% affected; and large 75% affected.
Immunological studies
The histopathological features of the interface dermatitis prompted us to perform immunopathological
studies. Additional 4-m sections of skin biopsies were
prepared as above, and immunohistochemical staining
for immunoglobulins and complement was performed
essentially as described previously.7 Briefly, the sections were placed on Probe-On-Plus microscope slides
(Fisher Scientific, Houston, TX, USA), deparaffinized
in xylene, and rehydrated in graded ethanolwater
solutions. Endogenous peroxidase activity was blocked

with 0.5% hydrogen peroxide in methanol. The sections were then rinsed with 70% ethanol followed by
Brij detergent in phosphate-buffered saline (BrijPBS).
Antigenic sites were recovered by digestion with pepsin
for 30 min at 37 C. The sections were then rinsed in
BrijPBS, and blocked with 10% normal goat serum
in PBS. Sections were incubated with rabbit antibody (0.55.0 g mL1; Zymed Laboratories, Inc., San
Francisco, CA, USA) specific for canine immunoglobulin A (IgA), IgG, IgM or complement (C3) for 1 h at
37 C and rinsed with BrijPBS. Negative control sections were treated with nonimmune rabbit serum (1:50
dilution) in similar fashion. Biotinylated antirabbit
secondary antibody (Zymed Laboratories, Inc.) was
applied for 15 min at room temperature, rinsed with
BrijPBS, and followed by streptavidinhorseradish
peroxidase conjugate (Zymed Laboratories, Inc.)
according to the manufacturers instructions. Diaminobenzadine (DAB) chromagen was diluted 1:50 in
0.1 TrisHCl containing 0.01% hydrogen peroxide,
immediately applied to the sections for 15 s, and
rinsed off with distilled water. Sections were then
counter-stained with Azure B, dehydrated and coverslipped with Permount mounting medium. The locations of positively staining cells and skin structures
in sections from nine cases meeting the selection
criteria and from three randomly chosen dogs with

2003 European Society of Veterinary Dermatology, Veterinary Dermatology, 14, 159166

Table 1. Clinical, laboratory tests, and therapeutic information on nine Boxers with concurrent follicular dysplasia and interface dermatitis

Seasonality

Laboratory tests

Previous therapy

4.5

FS

Unknown

9.5

MC

October to April

Omega-6/omega-3 fatty acids

and cephalexin orally; topical
glucocorticoid-antimicrobial
Orbifloxacin and cephalexin orally

FS

2.5

January to May

Haemogram, urinalysis,
serum total thyroxine,
skin scrapings
Serum total thyroxine, serum
thyrotropin, antinuclear antibody
Woods light, skin
scrapings, fungal culture

MC

2.5

January to May

Woods light, skin

scrapings, fungal culture

MC

Persistent

Hemogram, serum chemistry

panel, urinalysis, thyroid
panel, antinuclear antibody

MC

December to April

February to June

Skin scrapings, fungal

culture, serum total thyroxine
None

None

March to August

None

None

FS

November to April

None

Cephalexin orally

Case*
1

Sulfadimethoxine-ormetoprim,
cephalexin, and methylprednisolone
orally; benzoyl peroxide shampoo
Sulfadimethoxine-ormetoprim,
cephalexin, and methylprednisolone
orally; benzoyl peroxide shampoo
Cephalexin orally; novel
protein diet

Cephalexin orally

Subsequent therapy
and follow-up
None; owners
moved to
Puerto Rico
None; spontaneous
remission
None; spontaneous
remission
None; spontaneous
remission
Tetracycline and
niacinamide orally
resolved dermatitis;**
melatonin orally
resolved alopecia
None; spontaneous
remission
None; spontaneous
remission
None; spontaneous
remission
None; spontaneous
remission

Follicular dysplasia and interface dermatitis in Boxers

*Cases 3 and 4 were siblings.

FS = spayed female; MC = castrated male; M = intact male.
Cases 3, 4 and 8 were followed for two years. They developed the identical dermatoses at the same time of year, and spontaneously resolved a second time.
All tests negative or within normal limits.
Cases 2, 6 and 7 were lost to follow-up after their initial episode of alopecia and dermatitis.
**The tetracycline and niacinamide were stopped twice, and the dermatitis relapsed both times.

161

2003 European Society of Veterinary Dermatology, Veterinary Dermatology, 14, 159166

Sex

Duration of disease
(months) prior
to biopsy

Age
(years)

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M. A. Rachid et al.

Table 2. Immunohistochemical findings in skin biopsy specimens from nine Boxers with interface dermatitis and three dogs with inflammatory
skin disease
Cell staining in the epidermis

Cell staining in the dermis*

ECM staining

Vessel staining

Case No.
IgA
IgG
IgM
C
IgA IgG IgM
C
IgA
IgG
IgM
C
IgA IgG IgM C
Boxers
1

W+ W+

+
W+
WP+
+
W+ +

+
+

+
W+
W+

W+ +
+
W+
3

W+ +

+
4

ND
W+ +

ND W+
W+

ND W+ +
+
ND
5

W+ W+ W+

WP+ +
WP+
+
+
+
W+
6

W+ +
W+

+
+
+

+
+
+
+
7

W+ +
W+

WP+

+
W+
8

W+

+
+
+

+
+
W+

+
+

+
+
W+
Inflamed dog skin
Atopy
+
+
W+
ND
+
+
W+
ND +
+
W+
ND +
+
+
ND
Bacterial pyoderma
+
+
+
Atopy
+
+
W+
+
*Lymphocytes and plasma cells.
ECM, extracellular matrix; ND, not done; W+, weak positive defined as < 20 cells/section, or light staining of the ECM or vessels; WP+, weak/
patchy staining of the ECM.
The uniformly negative epidermal staining does not include stratum corneum where anti-Ig antibodies reacted nonspecifically in every case.
ECM staining was in the interstitium of the superficial dermis, but not the basement membrane zone. Interpreted as leakage from vessels in
inflamed areas.
Vessel staining was in the lumen and on the endothelium, but not the vessel wall.

inflammatory skin disease (positive controls) were

recorded (Table 2).

RESULTS
Nine Boxers with concurrent follicular dysplasia and
interface dermatitis were identified. Three of these nine
dogs were identified in the retrospective histopathological study and had biopsies performed in 2000 (case 6),
1998 (case 7) and 1991 (case 9). Clinical information on
the dogs is presented in Table 1.
Typically, the owners recognized the simultaneous
onset of the noninflammatory alopecia and hyperpigmentation and the multifocal inflammatory lesions.
The earliest inflammatory lesions were variously
described as resembling bumps (papules), bites
(papules), pustules or blisters (vesicles). The inflammatory lesions occurred only within the areas of typical follicular dysplasia (Figs 2 and 3). When the dogs
were examined by veterinarians, papules, pustules and
vesicles were no longer present. Veterinarians observed
inflammatory lesions that were multiple, more-or-less
bilaterally symmetric, well-circumscribed, annular, 2
15 mm in diameter, raised, crusted, scaly, alopecic and
hyperpigmented. They were neither pruritic nor painful, and the dogs were otherwise healthy.
There was no consistent relationship between the
onset of the dermatitis and previous vaccination, drug
therapy or heartworm preventives. Routine laboratory
tests were performed on many of the dogs (Table 1),
and were negative or within normal limits. Five of the
patients had been acquired from shelters within the last
one to three years, and previous medical history was
not available. Only two of the dogs (siblings) were
known to be related. These two dogs lived in the same

Figure 2. Case 2. Note the annular crusts within the area of wellcircumscribed alopecia and hyperpigmentation on the right lateral
trunk of the dog.

Figure 3. Case 2. Annular crusts and well-circumscribed alopecia

and hyperpigmentation on the left lateral trunk of the dog.

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Follicular dysplasia and interface dermatitis in Boxers

house and developed disease at the same time. Six of
the dogs were from New York State and had no known
previous travel history. Cases 2, 7 and 8 were from
the lower mainland British Columbia (Canada), West
Virginia and Massachusetts, respectively, and had no
previous travel history.
Most of the dogs had received previous therapeutic
agents (Table 1) with no benefit. Seven of the dogs
underwent simultaneous spontaneous clinical remission of both the follicular dysplasia and the interface
dermatitis after a course of five to seven months.
These dogs were not re-biopsied. One dog (case 5) had
persistent disease for 13 months prior to treatment,
and another dog (case 1) was lost to follow-up after a
4-month course of disease. Only four dogs were followed for over one year. Three of these four dogs (cases
3, 4 and 8) had recurrence of both the follicular dysplasia and interface dermatitis, followed by spontaneous
resolution, in the same way they had the year before.
These dogs were not re-biopsied.
One dog (case 5) had persistent follicular dysplasia
and interface dermatitis for 13 months. Tetracycline
(500 mg every 8 h orally) and niacinamide (500 mg
every 8 h orally) (see Table 1) treatment resulted in
resolution of the dermatitis within 8 weeks, but had no
affect on the follicular dysplasia as determined by
persistence of the alopecia. After 15 months of persistent alopecia (follicular dysplasia), this dog was treated
with 3 mg melatonin orally every 12 h, which resulted
in partial hair regrowth within 2 months, and complete
hair regrowth after 4 months. The dog continues to
receive melatonin and has maintained a normal hair
coat for eight months. After the hair coat had regrown,
the owner twice stopped the tetracycline and niacinamide, which resulted in the reappearance of the interface dermatitis within two weeks each time. The dog
has now been on tetracycline and niacinamide for
an additional five months with no recurrence of the
dermatitis.
Histopathological findings included features of
follicular dysplasia (specimens from clinical noninflammatory, alopecic areas) and interface dermatitis
(specimens from clinically inflamed, crusted areas).
Mildly or moderately dysplastic hair follicles were
present in 66.7 and 22.2%, respectively, of these dogs.
One dog had no dysplastic hair follicles. Moderate or
small numbers of dysplastic hair follicles were present
in 66.7 and 22.2%, respectively, of the dogs. Sebaceous
gland melanosis was present in 44.4% of these dogs. In
all cases, the interface dermatitis (Fig. 4) was characterized by mild to severe hydropic degeneration of
epidermal basal cells (Fig. 5), mild to severe apoptotic
keratinocytes predominantly in the basal layer, mild to
severe subepidermal pigmentary incontinence (Figs 4
6), and a variably intense subepidermal infiltration
of lymphocytes, plasma cells and macrophages. Epidermal hyperplasia (predominantly due to acanthosis)
was mild to moderate and regular. Orthokeratotic
hyperkeratosis was typically diffuse and laminated.
Most cases had a concurrent perifollicular accumulation

163

Figure 4. Photomicrograph of an area of interface dermatitis (case

5). Note the subepidermal band of inflammatory cells consisting of
lymphocytes, plasma cells, macrophages and pigmentary incontinence (bar = 95 m).

Figure 5. Photomicrograph of an area of interface dermatitis (case

3). Note the hydropic degeneration of basal epidermal cells, the
pigmentary incontinence, the infiltration of lymphocytes, plasma
cells and macrophages, and the extravasation of erythrocytes (bar
= 48 m).

of lymphocytes, plasma cells and macrophages. Two

cases (22.2%) had minimal superficial dermal extravasation of erythrocytes and subepidermal fibrosis
(Fig. 7). Interface mural folliculitis was not seen.
Skin biopsies from the dogs contained lymphocytes
and plasma cells that stained positive for IgA, IgG and
IgM (78, 100 and 44%, respectively) in the superficial
dermis and perifollicular areas. Positively staining cells
were absent in the epidermis of all sections. Positive
immunoglobulin staining of the superficial dermal
interstitial spaces and the endothelium of small blood
vessels also was seen in 78 and 100% of the cases,
respectively. Immunohistochemical staining for complement was rarely positive in the superficial dermis or
within blood vessels (11 and 33% of the cases, respectively). Immunoglobulin or complement staining of
the basal lamina at the dermoepidermal junction was
absent in all nine cases. Patterns of immunohistochemical staining were similar in the three dogs with inflammatory skin disease (Table 2), and dissimilar to what
would be expected in dogs with cutaneous lupus
erythematosus.

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M. A. Rachid et al.

Figure 6. Photomicrograph of an area of interface dermatitis (case

4). Note the hydropic degeneration of epidermal basal cells, the
infiltration by lymphocytes, plasma cells and macrophages, and the
subepidermal and perifollicular pigmentary incontinence (bar
95 m).

DISCUSSION
Although follicular dysplasia is well-recognized in
Boxers, the cause is unknown. Affected dogs typically
have no associated hormonal imbalance.1,5,6,8,9 Because
most of the dogs experience recurrent, seasonal hair
loss, it has been suggested that photoperiod working
through pineal levels of melatonin and pituitary levels
of prolactin may be involved.46 In fact, typical clinical
and histological findings were reproduced in one Boxer
by keeping it in a dark room for one month during the
summer.10 Lastly, because the disorder is seen with
such frequency in Boxers, a genetic or breed predisposition probably plays a role.26
To our knowledge, the interface dermatitis associated with recurrent and persistent follicular dysplasia
in Boxers reported herein has not been described
previously. We recognized our first clinical case at the
CUHA in January 2001, and had examined or received
biopsy specimens on another five dogs by the end of
the year. Our retrospective histopathological study
revealed that biopsy specimens from three other cases
had been received between 1991 and 2000, but not

recognized as something unique. We could find no

analogous clinicopathological syndrome reported in
the human literature.
Data on age, sex, seasonality of the disease and
histopathological features of the follicular dysplasia in
our Boxers are similar to those described in previous
reports.16 Two of our dogs were siblings that lived in
the same household and experienced simultaneous
and parallel courses of recurrent seasonal disease.
Although apparently rare, recurrent follicular dysplasia has previously been reported in unrelated dogs
living in the same house.2,11 The lesions which were
eventually diagnosed as interface dermatitis were
described by owners as being initially papular, pustular
or vesicular. When seen by veterinarians, the dermatitis
was predominantly crusting and localized to the areas
of follicular dysplasia. Hence, the histopathological
features of the interface dermatitis reported herein are
potentially incomplete, insofar as no primary lesions
(papules, pustules, vesicles) were biopsied. The most
common diagnosis made by veterinarians was bacterial folliculitis, but appropriate antibiotic therapy was
ineffective. The most common causes of annular, alopecic, crusted skin lesions in dogs are bacterial folliculitis, demodicosis and dermatophytosis.6 However, the
histopathological findings in these three disorders are
diagnostic and quite different from the interface dermatitis described herein.6
The clinical and histopathological resemblance of
the interface dermatitis to cutaneous lupus erythematosus6,13 prompted us to perform immunohistochemical investigations. Typical immunohistochemical
findings in cutaneous lupus erythematosus include the
deposition of immunoglobulins and complement at the
basement membrane zone.6,12,13 Immunohistochemical staining for immunoglobulin was positive in skin
biopsies from the nine dogs with concurrent follicular
dysplasia and interface dermatitis. However, the pattern of staining resembled that of a typical inflammatory response and was likely due to leakage of
globulins from vessels in inflamed areas. There was no
immune complex or complement deposition in the
basement membrane zone or blood vessel walls, and
the condition is unlikely to be autoimmune or related
to cutaneous lupus erythematosus.
Although there are numerous clinical disorders in
dogs6 and humans12 that are characterized histopathologically by interface dermatitis, none are clinically
analogous to the dermatosis described herein. Because
most of the Boxers developed lesions during the winter
and were from the northern USA or Canada, chronic
radiant heat dermatitis (erythema ab igne) is a diagnostic consideration.14,15 However, the lesions of chronic
radiant heat dermatitis occur in areas of skin exposed
to a heat source (heating pad, heated kennel mat, heat
lamp, heat register, electric blanket, wood stove, etc.),
and the lesions are typically irregular, linear, branching, drip-like or lattice-like in configuration.14,15 None
of our Boxers had known chronic exposure to heat
sources (indeed, two dogs had disease in the summer),

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Follicular dysplasia and interface dermatitis in Boxers

and the lesions were annular in configuration. In addition, the characteristic histopathological findings in
chronic radiant heat dermatitis (keratinocyte karyomegaly, rarefaction of dermal collagen and wavy, eosinophilic fibres in the superficial dermis) were not present
in our Boxers.14,15
A remarkable aspect of this new syndrome is the
apparent temporal association of the alopecia and the
dermatitis. Seven dogs had recurrent, seasonal disease,
wherein the alopecia and dermatitis simultaneously
appeared and disappeared. In the three dogs with
known seasonally recurrent disease, once again the alopecia and the dermatitis ran identical clinical courses.
One dog had persistent alopecia and dermatitis.
We attempted treatment only in the dog with persistent disease. Owing to the histopathological resemblance of the dermatitis to lupus erythematosus, we
discussed the various therapeutic options for cutaneous lupus erythematosus with the owner.6 The owner
wished to avoid glucocorticoids, so we used tetracycline and niacinamide. This drug combination has
been used successfully in many cases of canine cutaneous lupus erythematosus.6 The dermatitis resolved
completely when tetracycline and niacinamide were
administered, and relapsed both times when treatment
was stopped. The owner also wanted us to address the
alopecia therapeutically, so we recommended melatonin.46 Complete hair regrowth occurred within four
months, and the owner has not wanted to stop melatonin therapy to see if relapse would occur.
The cause of this syndrome is not known. Because of
the recurrent and seasonal nature of most of the cases,
photoperiod appears to play a role. The exclusive
occurrence in Boxers, two of which were siblings, suggests genetic predisposition. An association with drug
administration or vaccination could not be established.
In summary, we describe herein a new syndrome of
concurrent follicular dysplasia and interface dermatitis
in Boxers. The two dermatoses run identical recurrent
(seasonal) or persistent courses. Tetracycline and
niacinamide may be of benefit for the interface dermatitis, and melatonin may be useful for the follicular
dysplasia.

165

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1. Scott, D.W. Seasonal flank alopecia in ovariohysterectomized dogs. Cornell Veterinarian 1990; 80: 18795.
2. Miller, M.A., Dunstan, R.W. Seasonal flank alopecia in Boxers
and Airedale Terriers: 24 cases (198592). Journal of the
American Veterinary Medical Association 1993; 11: 156772.
3. Rothstein, E., Scott, D.W., Miller, W.H. Jr. et al. A retrospective study of dysplastic hair follicles and abnormal melanization in dogs with follicular dysplasia syndromes or endocrine
skin disease. Veterinary Dermatology 1998; 9: 23541.
4. Guagure, E. Les alopcies dorigine gntique chez le
chien. Point Vtrinaire 1996; 28: 5438.
5. Paradis, M. Alopcies acquises chez le chien. Mdecin
Vtrinaire Du Qubec 2000; 30: 1027.
6. Scott, D.W., Miller, W.H. Jr, Griffin, C.E. Muller and
Kirks Small Animal Dermatology, 6th edn. W.B. Saunders, Philadelphia, 2001.
7. Mauldin, E.A., Scott, D.W., Miller, W.H. et al. Malassezia dermatitis in the dog: a retrospective histopathological and immunopathological study of 86 cases
(199095). Veterinary Dermatology 1997; 8: 191202.
8. Curtis, C.F., Evans, H., Lloyd, D.H. Investigation of the
reproductive and growth hormone status of dogs affected
by idiopathic recurrent flank alopecia. Journal of Small
Animal Practice 1996; 37: 41722.
9. Daminet, S., Paradis, M. Evaluation of thyroid function
in dogs suffering from recurrent flank alopecia. Canadian
Veterinary Journal 2000; 41: 699703.
10. Ando, J., Nagata, M. Seasonal flank alopecia in a Boxer.
Japanese Journal of Veterinary Dermatology 2000; 6: 1720.
11. Fontaine, J., Beco, L., Paradis, M. Alopcie rcidivante
des flancs: tude de douze cas chez le griffon Korthals.
Point Vtrinaire 1998; 29: 4459.
12. Elder, D., Elenitsas, R., Jaworsky, C. et al. eds. Levers
Histopathology of the Skin VIII. Lippincott-Raven,
Philadelphia, 1997.
13. Dahl, M.V., Gilliam, J.N. Direct immunofluorescence in
lupus erythematosus. In: Beutner, E.H., Chorzelski, T.P.,
Kumar, V., eds. Immunopathology of the Skin, 3rd edn.
Churchill Livingstone, New York, 1987: 499518.
14. Declercq, J., Vanstapel, M.J. Chronic radiant heat dermatitis (erythema ab igne) in 2 dogs. Veterinary Dermatology 1998; 9: 26975.
15. Walder, E.J., Hargis, A.M. Chronic moderate heat dermatitis (erythema ab igne) in 5 dogs, 3 cats, and 1 silvered
langur. Veterinary Dermatology 2002; 13: 28392.

Rsum Une dysplasie folliculaire rcidivante ou persistante, associe une dermatite dinterface est rapporte
chez neuf Boxers. Les donnes relatives lge, au sexe, la saisonnalit de lalopcie et les images histopathologiques de la dysplasie folliculaire de ces neuf Boxers sont comparables celles rapportes dans les rapports prcdents. La dermatite dinterface est caractrise par des lesions multifocales, annulaires, croteuses,
confines aux zones de dysplasie folliculaire. Les lsions inflammatoires ne sont jamais prurigineuses ou douloureuses, et ltat general est bon. Sur un plan histopathologique, les lsions inflammatoires sont caractrises
par une dermatite dinterface. Des tudes immunohistochimiques nont pas permis de mettre en vidence des
immunoglobulines ou du complment au niveau de la membrane basale, ou dans les parois des vaisseaux sanguins. Chez les chiens prsentant une maladie rcidivante ou permanente, les images de dysplasie folliculaire et
de dermatite dinterface ont galement prsent des episodes de gurison spontane puis de rcidive ou ont persist. Un chien a t trait aves succs par lassociation de ttracyclines et de nicotinamide pour la dermatite
dinterface et de mlatonine pour la dysplasie folliculaire. Bien que ltiopathognie de cette maladie nouvelle et
que les relations entre les deux types de modalits ractionnelles microscopiques restent peu claires, la photopriode et une predisposition gntique pourraient jouer un role.
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M. A. Rachid et al.
Resumen Se describe una displasia folicular recurrente o persistente y una dermatitis de interfase en nueve Boxers. Los datos sobre edad, sexo, estacionalidad de la alopecia y caractersticas histopatolgicas de la displasia
folicular en estos nueve Boxers son similares a otros casos descritos en trabajos anteriores. La dermatitis de interfase fue caracterizada por lesiones multifocales anulares y costrosas confinadas a las reas de displasia folicular.
Las lesiones inflamatorias no eran ni prurticas ni dolorosas y los perros afectados se encontraban en buen estado
de salud. Histopatologicamente las lesiones clnicamente inflamatorias se caracterizaron como una dermatitis
de interfase. Los estudios inmuno-histoqumicos no pudieron demostrar inmunoglobulinas o complemento en
la zona de la membrana basal o en las paredes de los vasos sanguneos. En perros con enfermedad recurrente o
persistente, la displasia folicular y la dermatitis de interfase siguieron cursos idnticos, concurrentes en la remisin
espontnea y la repeticin, o la persistencia, respectivamente. Un perro con enfermedad persistente fue tratado
con xito: tetraciclinas y niacinamida para la dermatitis de interfase y melatonina para la displasia folicular.
Aunque la etiopatogenia de esta nueva condicin descrita y la relacin entre los dos patrones histolgicos no se
conocen, factores como el fotoperodo y la predisposicin gentica parecen desempear un papel.
Zusammenfassung Rezidivierende oder persistierende follikulre Dysplasie und Dermatitis der Grenzzone
wird bei neun Boxern beschrieben. Alter, Geschlecht, Saison und histopathologische Befunde der follikulren
Dysplasie bei diesen neun Boxern ist mit denen frherer Berichte vergleichbar. Die Dermatitis der dermalenepidermalen Grenzzone war durch multifokale, annulre, krustige und auf die Bereiche der follikulren Dysplasie
begrenzte Lsionen beschrnkt. Die entzndeten Bereiche waren weder juckend noch schmerzhaft und betroffene Hunde waren ansonsten gesund. Histopathologisch waren die klinisch entzndeten Lsionen als Dermatitis
der Grenzzone charakterisiert. Immunhistochemische Studien zeigten weder Immunglobuline noch Komplement in der Basalmembranzone oder den Blutgefsswnden. Bei Hunden mit rezidivierender oder persistierender
Erkrankung zeigten die follikulre Dysplasie und Dermatitis der Grenzzone einen identischen Verlauf von Spontanremission und Rezidiv oder Persistenz. Ein Hund mit persistierender Dermatitis wurde erfolgreich behandelt:
Tetrazyklin und Niacinamid fr die Dermatitis der Grenzzone und Melatonin fr die follikulre Dysplasie.
Obwohl die tiopathogenese dieses neu beschriebenen Syndroms und die Beziehung zwischen den beiden
histologischen Reaktionsschemata nicht bekannt sind, scheinen Photoperiode und genetische Prdisposition
eine Rolle zu spielen.

2003 European Society of Veterinary Dermatology, Veterinary Dermatology, 14, 159166