REVIEW

Standard classification and

pathophysiology of rosacea: The 2017
update by the National Rosacea Society
Expert Committee
Richard L. Gallo, MD, PhD,a Richard D. Granstein, MD,b Sewon Kang, MD,c Mark Mannis, MD,d
Martin Steinhoff, MD, PhD,e,f Jerry Tan, MD,g and Diane Thiboutot, MDh
San Diego and Sacramento, California; New York, New York; Baltimore, Maryland; Doha, Qatar;
Dublin, Ireland; Windsor, Ontario, Canada; and Hershey, Pennsylvania

In 2002, the National Rosacea Society assembled an expert committee to develop the first standard
classification of rosacea. This original classification was intended to be updated as scientific knowledge and
clinical experience increased. Over the last 15 years, significant new insights into rosacea’s pathogenesis
and pathophysiology have emerged, and the disorder is now widely addressed in clinical practice.
Growing knowledge of rosacea’s pathophysiology has established that a consistent multivariate disease
process underlies the various clinical manifestations of this disorder, and the clinical significance of each of
these elements is increasing as more is understood. This review proposes an updated standard
classification of rosacea that is based on phenotypes linked to our increased understanding of disease
pathophysiology. This updated classification is intended to provide clearer parameters to conduct
investigations, guide diagnosis, and improve treatment. ( J Am Acad Dermatol http://dx.doi.org/10.1016/
j.jaad.2017.08.037.)

Key words: comorbidity; erythema; ocular; papules; pathophysiology; phenotypes; phymas; pustules;
rosacea; telangiectasia.

R osacea is well established as a chronic

cutaneous syndrome, encompassing various
combinations of potential signs and symp-
toms that manifest primarily on the convexities of the
Abbreviations used:
NRS:
RosaQoL:
National Rosacea Society
Rosacea Quality of Life Index
central face (cheeks, chin, nose, and central part of
forehead) and are often characterized by repeated
remissions and exacerbations. Rosacea is commonly
diagnosed in certain demographic groups, and in Latin Americans, African-Americans, and Africans
epidemiologic studies of whites, its prevalence has (Figs 1 to 4).5-8 The disorder is identified more often
been 10% or higher.1-4 Although it has been most in women than in men, and although it may occur at
frequently observed in patients with fair skin, any age, the onset typically occurs at any time after
rosacea has also been diagnosed in Asians, age 30.1,2

From the Department of Dermatology, University of California-San
Diegoa; Department of Dermatology, Weill Cornell Medical
College, New Yorkb; Department of Dermatology, Johns
Hopkins School of Medicine, Baltimorec; Department of
Ophthalmology & Vision Science, University of California Davis
Eye Center, Sacramentod; Department of Dermatology, Qatar
University, Dohae; Department of Dermatology, University
College Dublin Charles Institute of Dermatologyf; University
of Western Ontario, Windsorg; and Department of Derma-
tology, Pennsylvania State University, Hershey.h
Supported by the National Rosacea Society.
Disclosure: Dr Granstein is a Galderma consultant and Elysium
investigator and advisory board member; Dr Kang is a
Galderma advisory board member. Dr Tan is a Galderma
advisory board member, consultant, speaker, and investigator;
a Bayer advisory board member; and a Cipher Roche advisory
board member. Drs Gallo, Mannis, Steinhoff, and Thiboutot
have no conflicts of interest to declare.
Accepted for publication August 7, 2017.
Reprint requests: National Rosacea Society, 196 James St,
Barrington, IL 60010. E-mail: info@rosacea.org.
Correspondence to: Richard L. Gallo, MD, PhD, 3350 La Jolla Village
Drive, 111 B, San Diego, CA, 92161. E-mail: rgallo@ucsd.edu.
Published online October 28, 2017.
0190-9622/$36.00
Ó 2017 by the American Academy of Dermatology, Inc.
http://dx.doi.org/10.1016/j.jaad.2017.08.037

1
2 Gallo et al J AM ACAD DERMATOL
n 2017

In 2002, the National Rosacea Society (NRS) have been treated successfully for their papules
assembled an expert committee to develop a and pustules, the erythema and flushing often
classification system to provide standard criteria remain.18
essential for performing research, analyzing results, The following updates have been developed by
and comparing data from different sources, as well as the committee and reviewed by a panel of 21rosacea
to serve as a diagnostic reference in clinical practice.9 experts worldwide and are intended tobe useful to
The classification system also established standard clinicians and researchers byproviding clearer and
terminology to facilitate clear more meaningful parameters
communication among a to conduct new investiga-
broad range of basic, clinical, CAPSULE SUMMARY tions, as well as to build on
and other researchers; prac- existing findings while offer-
d In 2002, the National Rosacea Society
ticing dermatologists; primary ing a more meaningful guide
assembled an expert committee to
care physicians; ophthalmol- to diagnosis and treatment.
develop the first standard classification
ogists; other medical special-
of rosacea.
ists; regulatory authorities; DIAGNOSTIC
health and insurance admin- d New scientific investigations have CRITERIA
istrators; patients; and the yielded significant insights into rosacea’s The original standard
general public. Because the pathogenesis and pathophysiology. classification of rosacea
etiology and pathogenesis of d The current update provides clearer identified the most common
rosacea were unknown at parameters to conduct investigations patterns or groupings of
that time and there were no while offering a more meaningful guide signs and symptoms and
histologic or serologic markers to diagnosis and treatment. designated them as follows:
for the disease, the system subtype 1, erythematotelan-
was based on morphologic giectatic; subtype 2, papu-
characteristics alone to provide a framework that lopustular; subtype 3, phymatous; and subtype
could be readily updated as new discoveries were 4, ocular. Although didactically successful, the
made. The standard classification was proposed as a subtype designations were widely utilized individ-
provisional system, and it was hoped that with ually and construed as distinct disorders, ignoring
increased scientific knowledge and experience in the frequent simultaneous occurrence of more
clinical practice, the definition of rosacea would than 1 subtype and the potential progression
ultimately be based on pathophysiology. from one subtype to another.18 Moreover, the
Over the 15 years since the classification’s focus on subtypes tended to limit consideration
development, scientific investigations have yielded of the full range of potential signs and symptoms
significant insight into rosacea’s pathogenesis and that may occur in individual patients and that,
pathophysiology, whereas clinical experience has in some cases, may confound the assessment of
suggested a need for an updated approach to severity.
diagnosis, classification, and treatment.10,11 To Because rosacea can encompass a multitude of
fulfill the directive of the original authors of the possible combinations of signs and symptoms, the
2002 classification system, the NRS convened a following updated classification system is based
committee to update the standard classification of on phenotypesdobservable characteristics that
rosacea, including new parameters for its diag- can result from genetic and/or environmental
nosis, assessment, and common presentations. The influencesdto provide the necessary means of
revised standard diagnostic features were adopted assessing and treating rosacea in a manner that is
on the basis of their positive predictive value as consistent with each individual patient’s experi-
supported by rosacea experts.12 In addition, new ence (Table I). The phenotypes and diagnostic
scientific evidence has shown that rosacea’s diverse criteria are largely in agreement with those
features may be part of a continuum of inflamma- recommended by the global rosacea consensus
tion that may not be clinically visible but is detect- panel in 2016, and at least 1 diagnostic or 2 major
able histologically and biochemically.13-16 This phenotypes are required for the diagnosis of
suggests that the common presentations of flushing rosacea.12
and fixed centrofacial erythema may progress to
include papules and pustules and potentially lead Diagnostic phenotypes
(in a small proportion of cases) to subsequent A diagnosis of rosacea may be considered in the
development of phymas.17,18 This is further sup- presence of 1 of the following diagnostic cutaneous
ported by the observation that in patients who signs.12
J AM ACAD DERMATOL
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Fig 1. A, Erythema of rosacea on white skin. B, Papules and pustules of rosacea on white skin.
Fig 2. Erythema of rosacea on Asian skin.
Fixed centrofacial erythema in a characteristic
pattern that may periodically intensify. Persistent
redness of the facial skin is the most common sign of
rosacea in Fitzpatrick phototypes I to IV; however,
erythema may be difficult to detect in the darker
phototypes (V and VI). In patients with type V or VI
skin, papules and pustules may be the first clearly
visible signs of rosacea. A personal history, drug
history, and complete physical examination are helpful
to clinicians in excluding other entities in the possible
differential diagnoses such as lupus erythematosus,
steroid-induced rosacea, or seborrheic eczema.13 In
rosacea, a history of flushing or blushing is common in
phototypes I to IV.
Phymatous changes. These can include patu-
lous follicles, skin thickening or fibrosis, glandular
hyperplasia, and a bulbous appearance of the nose.
Rhinophyma is the most common form, but other
phymas may occur.
Major phenotypes
Major cutaneous signs often appear with 1 or
more of the diagnostic features, although some
can occur independently. Without a diagnostic
phenotype, the presence of 2 or more major features
may be considered diagnostic.12 Major phenotypes
include the following.
Gallo et al 3
Fig 3. Erythema and papules and pustules of rosacea on
Latin American skin.
Papules and pustules. Dome-shaped red
papules with or without accompanying pustules,
often in crops and dominant in the centrofacial
area, are typical. Nodules may also occur.
Although patients with concomitant acne may
exhibit comedones, comedones should be
considered part of an acne process unrelated to
rosacea, as has been supported by recent
transcriptome analyses in acne and rosacea.13,19-21
Flushing. Frequent and typically prolonged
flushing (sometimes blushing) is common except
in darker skin tones, in which case flushing may be
subjectively experienced without obvious erythema.
In contrast to other erythematous changes, in
rosacea flushing can occur within seconds to
minutes in response to neurovascular stimulation
by trigger factors.13-15,19,22
Telangiectasia. Telangiectasias, which are
common signs of rosacea and are predominantly
centrofacial in phototypes I to IV, are rarely seen
in the darker phototypes V and VI. Use of
a dermatoscope may allow for detection of
telangiectasias in patients with darker skin types.
Ocular manifestations. Ocular manifestations
occur in many patients. These are outlined in detail
in the following section.
4 Gallo et al
Fig 4. Phymatous changes of rosacea on African skin.
Secondary phenotypes
Secondary signs and symptoms may appear with
1 or more diagnostic or major phenotypes and may
include the following.12
Burning or stinging. Burning or stinging
sensations may occur typically on erythematous
skin without scales, although scaling may also occur,
especially on malar skin.23 Pruritus (itch) is not a
typical characteristic of rosacea but may also occur.
Edema. Facial edema may accompany or follow
prolonged erythema or flushing as a result of post-
capillary extravasation during inflammation.24
Sometimes soft edema may last for days or be
aggravated by inflammatory changes. Solid facial
edema (persisting hard, nonpitting edema) can occur
with rosacea, often as a sequela of papules and
pustules, and also independently of redness, papules
and pustules, or phymatous changes. Commonly, a
combination of blood and lymphatic vessel edema
occurs, although the dominance may vary.13
Dry appearance. Central facial skin may be
rough and scaly so as to resemble dry skin and
suggest an eczematous dermatitis, and rosacea may
often include the coexistence of seborrheic
dermatitis. This ‘‘dry appearance’’ may be associated
with burning or stinging sensations and may be
caused by irritation rather than the disease process.
Ocular rosacea
Ocular rosacea can occur in the context of mild,
moderate, or severe dermatologic disease and may
also appear in the absence of diagnostic skin
manifestations (Fig 5). Ocular signs strongly
suggestive of ocular rosacea include (1) lid margin
telangiectases, (2) interpalpebral conjunctival
injection, (3) spade-shaped infiltrates in the cornea,
and (4) scleritis and sclerokeratitis.
Common symptoms that may suggest ocular
rosacea but are not specific to the disorder include
(1) burning, (2) stinging, (3) light sensitivity, and
(4) foreign object sensation.
Ocular signs that commonly appear in rosacea
but are not specific to the disorder include
(1) Meibomian gland dysfunction (‘‘posterior’’
J AM ACAD DERMATOL
n 2017
blepharitis) characterized by inspissation and
inflammation of the Meibomian glands (chalazia);
(2) conjunctivitis; and (3) ‘‘honey crust’’ and
cylindrical collarette accumulation at the base of
the lashes,25 irregularity of the lid margin
architecture, and evaporative tear dysfunction (rapid
tear breakup time).
The external ocular signs that will be readily seen
by the dermatologist include (1) lid margin
telangiectases, (2) characteristic interpalpebral
conjunctival telangiectases, (3) inspissation of the
Meibomian glands, and (4) chalazia.
The ocular signs that will likely require slit-lamp
examination by the ophthalmologist include
(1) keratitis, including a range of disease severity
from epithelial defects to corneal infiltrates and
thinning; (2) corneal spade-shaped infiltrates and
vascularization; and (3) scleritis.
Disease severity can be categorized as follows:
(1) mild (blepharitis), (2) mild to moderate
(blepharitis plus conjunctival injection [indicating
more diffuse ocular surface dysfunction]), (3)
moderate to severe (involvement of the cornea
with punctate keratitis, infiltrates, and vasculariza-
tion), and (4) severe (scleritis or keratitis).
OTHER CONSIDERATIONS
Major presentations
Although the new classification’s common
patterns or groupings of signs and symptoms
are not to be considered subtypes or units for
research or individual diagnosis and treatment,
they may now be referenced in updated terms that
reflect current knowledge of their pathophysiology,
including neurovascular, inflammatory, phymatous,
and ocular. For example, it is proposed that
the original erythematotelangiectatic subtype be
considered a primary neurovascular inflammatory
response (neurovascular inflammation), whereas
the papulopustular subtype would encompass
both neurovascular and enhanced innate and
adaptive immune systemeassociated inflammatory
responses. Of note, both are inflammatory mecha-
nisms that lead to different signs.
Progression
Although rosacea’s various phenotypes may
appear in different combinations and at different
times, research suggests that all may be
manifestations of the same underlying inflammatory
continuum13-16 and that rosacea may progress not
only in severity but to include additional
phenotypes.17,18 Recent studies point to a
multivariate set of pathogenic pathways, including
defects in the innate and adaptive immune systems,
J AM ACAD DERMATOL
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Table I. Phenotypes of rosacea
Diagnostic* Majory
Fixed centrofacial erythema Flushing
in a characteristic pattern Papules and pustules
that may periodically intensify Telangiectasia
Phymatous changes Ocular manifestations
d Lid margin telangiectasia
d Interpalpebral conjunctival injection
d Spade-shaped infiltrates in the cornea
d Scleritis and sclerokeratitis
*These features by themselves are diagnostic of rosacea.
y
Two or more major features may be considered diagnostic.
Fig 5. Ocular rosacea. Blue arrows indicate ‘‘honey crust’’
and cylindrical collarette accumulation at the base of the
lashes; red arrows indicate lid margin telangiectases.
mast cells and related biochemical mechanisms, and
the neurovascular system.13-16,26-28
It now appears likely that initial erythema and
vascular manifestations such as telangiectasia may be
in a continuum initiated by a combination of
neurovascular dysregulation and innate immune
responses, including increased LL37 and serine
proteases.13,20,22,26,29,30 Papules are characterized
by increased Th1 and Th17 cells, as well as by
plasma cells, mast cells, and macrophages,22,26
whereas pustules are characterized by increased
production of neutrophil-recruiting chemokines.22
Although the immune response gene expression
levels peak in rosacea with papules and pustules, a
marked infiltrate and upregulation of genes involved
in innate and adaptive immune responses are
also present in neurovascular and phymatous
presentations of rosacea, suggesting a continuum
of inflammation through different molecular
pathways and cell activities that are reflected in
the different clinical signs and symptoms.
Moreover, studies indicate a marked upregulation
of mast cell density as a common factor in all
major presentations, but the greatest increase
Gallo et al 5
Secondary
Burning sensation
Stinging sensation
Edema
Dryness
Ocular manifestations
d ‘‘Honey crust’’ and collarette
accumulation at the base of the lashes
d Irregularity of the lid margin
d Evaporative tear dysfunction
(rapid tear breakup time)
occurs in rosacea characterized by papules
and pustules, demonstrating a link between the
neurovascular, inflammatory, phymatous, and ocular
presentations.13,26,27
Because various inflammatory pathways appear
to be more operative in some individual
presentations than in others, more epidemiological
studies are needed to clarify this clinical impression.
For example, although phymatous changes (a
diagnostic feature of rosacea) may appear without
erythema in some patients, biopsies reveal an
inflammatory infiltrate and transcriptome analysis
demonstrates the presence of inflammatory
mediators, suggesting that subclinical inflammation
is present.20-22 Consequently, a current working
hypothesis is that early phymatous rosacea without
a clear history and clinical presentation of erythema
may be associated with subclinical neuroinflamma-
tion and adaptive or innate immune responses that
then progress to fibrosis and glandular hyperplasia.
This is supported by the fact that all patients
with phymatous rosacea in the transcriptome
analysis showed increased expression levels of
genes associated with inflammation and immune
responses.13,15,20,22 Thus, although phymatous
changes may not occur in all patients, subclinical
fibrotic changes may have already occurred on the
molecular level before they become clinically
evident in neurovascular and inflammatory rosacea,
leading to the conclusion that fibrosis in rosacea may
start much earlier than might be expected through
clinical observation.13
Severity
Various instruments (Table II) have been used to
assess each of the standard phenotypes as well as for
global assessment of rosacea. Examples of tools in
existence for the various phenotypes include the
6 Gallo et al
Table II. Scales to assess rosacea phenotypes
Phenotype Scale
Flushing FAST, GFSS
Persistent erythema CEA/PSA
Telangiectasia None
Papules/pustules Lesion counts, IGA scales
Phymatous changes None
Psychosocial effects RosaQoL
CEA, Clinician’s Erythema Assessment; FAST, Flushing Assessment
Tool; GFSS, Global Flushing Severity Score; IGA, Investigator’s
Global Assessment; PSA, Patient’s Self-Assessment; RosaQoL,
Rosacea Quality of Life Index.
Flushing Assessment Tool31 and the Global Flushing
Severity Scale32 for flushing, the Clinician’s Erythema
Assessment33 and the Patient’s Self-Assessment34
for persistent erythema, lesion counts and an in-
vestigator’s global assessment35 for papules and
pustules, and the Rosacea Quality of Life Index
(RosaQoL)36 for psychosocial effects. In 2004, the
NRS expert committee published a standard grading
system for rosacea in which primary and secondary
features of rosacea are graded as absent, mild,
moderate, or severe and that also provides for a
global assessment on the same scale.37 There is a
need for a single updated scale that includes
standardized severity assessments of the diagnostic,
major, and secondary phenotypes of rosacea and can
be used for all phototypes.
Psychosocial effects
A multitude of surveys over the last 15 years have
documented rosacea’s adverse impact on emotional,
social, and occupational well-being, including its
link to severity.38-48 The psychologic burden alone
includes depression, anxiety, and worry, and
appropriate severity scales to measure this
dimension include the RosaQoL, the Dermatology
Quality of Life Index,49 the Depression Anxiety Stress
Scale,50 and the Penn State Worry Questionnaire,51
among others. With the exception of the RosaQoL,
which excludes phymatous changes and establishes
no minimal important difference, the scales are
nonspecific for rosacea, and further research may
be needed to adequately measure its distinct
dimensions, as well as to precisely measure the
impact of rosacea on social and occupational
interactions of disparate ethnic groups.
CONCLUSION
This updated classification of rosacea is intended
to provide accuracy and flexibility appropriate for
the study, diagnosis, evaluation, and treatment of
rosacea within the context of current scientific
J AM ACAD DERMATOL
n 2017
understanding and clinical experience. Growing
knowledge of rosacea’s pathophysiology has
increasingly found that a consistent multivariate
disease process appears to underlie the various
potential manifestations of the disorder, and its
clinical significance may increase substantially as
more is understood about the many comorbidities
reported in recent studies. As with the original
classification of rosacea, this updated standard
system is considered provisional and may require
modification as the etiology and pathogenesis of
rosacea become clearer and its relevance and
applicability are tested by investigators and
clinicians. The authors welcome reports on the
usefulness and limitations of these criteria.
The committee thanks the following individuals who
reviewed and contributed to this document: Dr Luiz
Almeida, Faculdade de Ci^ encias Medicas de Minas
Gerais, Belo Horizonte, Brazil; Dr Mats Berg, Department
of Dermatology, Uppsala University, Sweden; Dr Anthony
Bewley, Whipps Cross University Hospital and Royal
London Hospital, United Kingdom; Dr Ncoza
Dlova, Department of Dermatology, University of
KwaZulu-Natal College of Health Sciences, Durban,
South Africa; Dr Mark Dahl, Department of Dermatology,
Mayo Clinic-Arizona, Scottsdale; Dr James Del Rosso,
Department of Dermatology, Touro University Nevada
College of Osteopathic Medicine, Henderson, Nevada; Dr
Michael Detmar, Institute of Pharmaceutical Sciences,
Swiss Federal Institute of Technology, Zurich,
Switzerland; Dr Anna Di Nardo, Department of
Dermatology, University of California-San Diego; Dr Zoe
Draelos, Department of Dermatology, Duke University,
Durham, North Carolina; Dr Lynn Drake, Department of
Dermatology, Harvard Medical School, Boston,
Massachusetts; Dr Alexander Egeberg, Department of
Dermato-Allergology, Herlev and Gentofte University
Hospital, University of Copenhagen, Hellerup, Denmark;
Dr Fabienne Forton, Dermatology Unit, Universit
e Libre de
Bruxelles, Brussels, Belgium; Dr Yolanda Helfrich,
University of Michigan Department of Dermatology, Ann
Arbor; Dr Marian Macsai, Department of Ophthalmology,
Northwestern University, Chicago, Illinois; Dr Richard
Odom, Department of Dermatology, University of
California-San Francisco; Dr Daniel Popkin, Department
of Dermatology, Case Western Reserve University,
Cleveland, Ohio; Dr Martin Schaller, Department of
Dermatology, Universitatsklinikum, Tubingen, Germany;
Dr Linda Stein Gold, Division of Dermatology, Henry Ford
Health System, Detroit, Michigan; Dr Esther Van Zuuren,
Department of Dermatology, Leiden University Medical
Centre, the Netherlands; Dr Guy Webster, Department of
Dermatology, Thomas Jefferson University, Philadelphia,
Pennsylvania; and Dr Edward Wladis, Department of
Ophthalmology, Albany Medical College, New York. The
final document does not necessarily reflect the views of
any single individual, and not all comments were
incorporated.
J AM ACAD DERMATOL
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