1. Dr.Rohit kumar singh
1st yr ,P.G.Resident

2.  Rosacea ia a latin word (Like-ROSES)
 Rosacea is a disease lacking an entirely satisfactory
defination
 Chronic disorder
• Variable severity
 Variable presentation

3. Diagnostic criteria
Recent diagnostic criteria is by one of the primary and
one of many secondary criteria
PRIMARY CRITERIA
 Intermittent or persistent erythema
 Telangiectasia
 Papules
 Pustules
 Photosensitivity

4. SECONDARY CRITERIA
 Burning /stinging
 Elevated red facial plaques with or without
scales
 Dry/scaly skin
 Persistent facial edema
 Phymatous changes
 Ocular manifestations

5.  Site- central convexities of the face i.e mid-
forehead,nose,malar areas and chin
 Other sites where lesions can be seen are beard
regions , neck ,scalp , shoulders and upper
back
 Epidemiology- fair skin people(caucasians),but
people of african and asian descent can also have
the disease

6.  ROSACEA
 VASCULAR INFLAMMATORY
CHANGES CHANGES
FLUSHING PAPULES
TELENGIECTASIA PUSTULES
(Initial and constant
feature)

7.  LATE COMPLICATION
1.Chronic lymphoedema-
Thickening of the affected skin
Leonine facies
Peau d ‘ orange appearance
Morbihan’s disease:chr upper facial erythematous
oedema
2.Rhinophyma
3.Ocular blindness

8. Epidemiology
 Third to sixth decade, peak incidence in the
fourth or fifth decade of life
 Affects both genders, but M:F(1:3)…F> M
 Rhinophyma type afflicts mostly men.
Also can be seen in children
Acne rosacea affects white people, II-I-type
classification (Fitzpatrick) and is rare in Africans or
Asians.

9. Pathogenesis
1.Solar irradiation
2.Neurogenic aetiology
3.Oxidative stress
4.Abnormally high level of canthelicidin
5.Vasoactive mediators

10. 6.H.Pylori
7.Demodesidosis
8.HIV infection
9.Defect in trigeminal afferent pathway
defect(new speculation)

11. SOLAR IRRADIATION
dysfunction of unsupported facial blood
vessels
with endothelial damage
Leakage
Oedema
inflammation

12.  VEGF is increased
 Laser droppler- blood flow is increased markedly in
papulopustular
 Capillaroscopy- neoangiogenesis,telangiectasis
 In rosacea vascular abnormalities are confined to the face

13. NEUROGENIC AETIOLOGY
 Lowered neural threshold for reaction to noxious
stimuli may result in neurogenic inflammation
 Burning sensation
 Association with migraine

14. OXIDATIVE STRESS
 Reduced level of SUPEROXIDE DISMUTASE
 inflammatory Rosacea
 Response to metronidazole,tetracyclinsand
azithromycin and their antioxidant properties

15. CANTHELICIDIN
 Endogeneous antimicrobial peptide
 Component of the innate immune system
 Trigger inflammation - leukocyte and
angiogenesis

16.  CANTHELICIN
 Serine proteases

 IL-37
 PROINFLAMMATORY

17. VASOACTIVE PEPTIDES
 Proposed mediators
 Serotonin
 Bradykinin
 PGs
 Substance p
 Opioid peptides
 Gastrin
 As there is no associated sweating so it is stated that reason
being vasoactive mediators and not neural neural reflex
mechanism

18. H.PYLORI ( G-ve, microaerophilic)
 Increased level of gastrin( flushing)
levels of histamine,PGs,leukotrienes(other cytokines)
 More prevalent with papulo-pustular rosacea
 Inconclusive data in this regard
 Drugs used in eradications for the H.Pylori also
produces relief in rosacea patient

19.  DOMODEX MITES infestation(demodecidosis)
 Two species
 1.DEMODEX FOLLICULORUM
 2.DEMODEX BREVIS
 Present in demis, eyelid in hair follicles,eyelash
follicle,meibomian glands
 It is associated with the inflammatory
response(papulopustular)

20.  Presence of large number in the rosacea patient is
a common association
 Also plays an important role in ophthalmic
complication
 Metronidazole responsive

21. Found within follicular infundibula &
sebaceous ducts…

22.  HIV INFECTION ASSOCIATED
 Recent studies point out that rosacea has been
reported as a manifestation in the skin of HIV
infection

23. DEFECT IN TRIGEMINAL AFFERENT NERVE
PATHWAY
repeated facial flushing
ectatic vessels ,permanent vasodilation

24.  Also
 intake of hot liquids
 heat up the tissues
 leads to countercurrent heat exchange with carotid
artery
 signal relayed to hypothalamus
 dissipates heat through flushing and
vasodilation

25.  SUMMARY OF PATHOGENESIS
 Link ??? Between the vascular features and and the
inflammatory feature
link
Vascular
features
Increased
temperature
Inflammatory
feature

26.  This may be explained by different behaviour of
bacteria or perhaps folliculitis,at higher
temperature
 Improvement of inflammmatory lesions after
ablation of the telangiectatic vessels

27. Plewig-Kligman Stages
Stage 1
Stage 2
Stage 3

28. EARLY ROSACEA (STAGE I)
 “Flushers-blushers
 Often < Age 20
 Nose/cheeks
 Recurrent episodes of
flushing
 Eryhthema persists
 Few telagiectasias

29. STAGE I - TELANGIECTASIAS

30. STAGE I
 Telangiectasias
becomes more
prominent and widely
distributed over
central covexity of the
face

31. STAGE II
PAPULES & PUSTULES BEGIN, INCREASED ERYTHEMA AND
TELANGIECTASIAS

32. STAGE III
Dense erythema
Papule,pustules,
nodule
Telangiectasias,
severe,diffuse
Variable
erythematous
plaques

33. Subtypes of rosacea(NRS -2002)
 4 sub types
1.Erythematotelangiectatic
2.Papulopustular
3.Phymatous
4.Ocular
 One variant
1.Granulomatous rosacea

34. Erythemato-telangiectatic rosacea
 Central facial flushing ,burning or stinging
 Redness spares the periocular areas
 Skin with fine texture that lacks a sebaceous quality
characteristics (common in other types)
 Erythematous areas rough and scaly (chronic,low grade
dermatitis)
 Trigger factors –emotional stress,alcohol,spicy
food,exercise , hot liquids

36. Papulo-pustular rosacea
 Classic presentation of rosacea
 Typically in middle aged women
 Transient small erythematous papules
surmounted by pin-point pustules
 Telangiectasias present but difficult to
distinguish

38. Phymatous
 Marked skin thickening and irregular surface
nodularities of the nose (most often) , chin ,forehead ,
one or both ears and eyelids
 Careful evaluation for basal cell carcinoma
 4 distinct histological variant present
a) Glandular
b) Fibrous
c) Fibroangiomatosis
d) Actinic

40. RHINOPHYMA
Craggy,irregular,bulbous swelling of the nose
 Predominantly affects men
 Whisky nose
 Irregular skin thickening
 Hypertrophy of soft tissue masses centered about the tip of
the nose
PSEUDORHINOPHYMA- seen with heavy eyeglasses
,obstructing the lymphatics and venous drainage of the
nose
Rhinophyma in female in ctaneous B cell neoplasms

41. Ocular rosacea
 May precede the cutaneous sign by years
 Clinical features – eye stinging or burning , dryness ,
irritation with light or foreign body sensation
Manifestations-
 Blepharitis
 Conjunctivitis
 Inflammation of lids and meibomian glands(modified
sebaceous gland)
 Interpalpabralconjuctival hyperemia
 Conjunctival telangiectasias

43.  50 % cases of rosacea will have ocular involvement
 The severity of the eye involvement doesnot correlate
with the severity of the facial involvement

44. Lupoid or Granulomatous rosacea
 Is a varaint of rosacea
 Charaterized by – non-inflammatory
,hard,brown,yellow or red papules / nodules of the
central face
 In 15% cases they have extrafacial lesions

45. Not variants of rosacea(as considered earlier)
 Rosacea fulminans(pyoderma faciale)
 Steroid induced acneiform eruptions
 Perioral dermatitis

46. Rosacea fulminans(pyoderma
faciale)
 Most common in Women
 Age 15 – 46 yrs
 History of seborrhoea
 Characterized by rapid giant coalescent nodules on the face
 No comedones, telangietasias, erythema and
remission with little or no scarring

47. Pediatric rosacea
 Poorly defined condition
 It is familial
 Most likely underreported because of tendency to
recognize flushing and erythema as “
HEALTHY GLOW”
 Condition may persists and progress in adulthood

48. Histopathology of rosacea
 Depends upon the stage of the disease but vascular
dilation of upper and middermal vessels with perivascular
and perifollicular lymphohistiocytic inflammation is
generally present :PREDOMINANTLY DERMAL
CHANGES,SOLAR ELASTOSIS,INCREASED MAST CELL
DENSITY,LYMPHATIC CHANNELS MAY ALSO BE
DILATED IN THE DEEPER DERMIS
NON-PUSTULAR LESIONS
 Non-specific perivascular and perifollicular
lymphohistiocytic infiltrate,accompanied by ocassional
multinucleate d cells ,neutrophils and eosinophils

49. PAPULO-PUSTULAR LESIONS
 It demonstrate more pronounced granulomatous
inflammation, perifollicular abscessess ,sometimes
demodex may be abundant in nearby follicles
GRANULOMATOUS ROSACEA
 It has a striking feature of caseating and non-caseating
granulomata with negative stains for mycobacterium
and fungi

51. Differential diagnosis
Important ones are
Acne vulgaris
Acneiform eruption(steroid induced)
Lupus miliaris disseminatus faciei
Perioral dermatitis

52. Seborrhic dermatitis
Nasal sarcoidosis(lupus pernio)
Demodex folliculitis
Carcinoid syndrome

53. Cutaneous lymphocytic infiltration(dermis)
of the face includes “5Ls”
Jessner’s lymphocytic infiltrate
Lymphocytoma cutis
Polymorphic light eruptions
Discoid lupus erythematosus
Well-differntiated lymphocytic lymphoma

54. Jessner’s lymphocytic infiltrate
 Chronic benign T-cell lymphoproliferative disorder
 M > F , childrens can also be affected
 Lesions – smooth raised ,non-scaly erythematous nodules
or plaques usually on facial skin
 Usually asymptomatic(but some may complain burning or
pruritic sensation)
 May involute spontaneously
 Waxes and wanes in severity

57.  Winter exacerbations (in rosacea – summer )
 Histopathology
Large circumscribed aggregation of lymphocytes
around blood vessels and hair follicles
Sometimes infiltrate can extend to subcutaneous
tissue (fat)

59. Lymphocytoma cutis
 Also known as Spiegler-fendt sarcoid or
lymphadenosis benigna cutis of bafverstedt
 Benign cutaneous B- cell lymphoproliferative
condition
 Females > males

60.  Lesion- solitary or grouped ,asymptomatic
,erythematous or violaceous papules ,nodules or
plaques
 Site – head(specially on ear lobes),rarely on trunk and
limbs
 Can proceed to primary cutaneous B- cell lymphoma
 Can be in localized form or disseminated form

62. Histopathology
Epidermis
 Spongiosis
 Edema and transmural infiltration of lymphocytes and
plasma cells
 Granulomatous vasculitis
Dermis
 Nodular infiltrate of lymphocytes,histiocytes
eosinophils,plasma cells
 Germinal centres can seen

64. Polymorphic light eruptions
Genetically determined delayed (type IV)
hypersensitivity reaction to UVA > > UVB
F:M(2-3:1) F>M
Age of onset is 3rd decade
Lesions – papular (most common),papulovesicles
,plaques,vesicobullous,insect-bite like,erythema
multiforme like lesion associated with pruritis.

65.  Site – sun exposed parts(can be extra facial also)
 Symmetrical in distribution

66. Histopathology
Epidermis
Spongiosis
Dyskeratosis
Exocytosis
Basal cell vacuolization
Dermis
 Moderate to dense perivascular infiltration
 Predominant T-cell with neutrophil,eosinophils

68. Discoid lupus erythematosus
Benign disorder of the skin
F:M(2:1), F>M, age of onset 4th decade
Autoimmune disease
Lesions-well defined circumscribed or discoid type of red
scaly patches of variable size ,which heals with atrophy
,scarring and pigmentary changes(butterfly erythema)
Site- face (most common MALAR region),scalp,ear ,arms,
legs,trunk

70. History of joint pains,raynaud’s
phenomenon,chilblains,photosensitivity
In 15 % of the cases lesions on the face may appear similar
to rosacea( but no pustular lesions in rosacea)
In rosacea there may be low titre of ANA can be positive
finding(but it is insignificant)
No pustules as in rosacea
Histopatology can differentiates between the two diseases

71. Histopathology
Liquifactive degeneration of basal layer of the
epidermis
Atrophy of epidermis
Hyperkeratosis
Follicular plugging
Incontinence of pigment
A pachy dermal lymphocytic infiltrate with a few
plasma cells and histiocytes around appendages,which
may be atrophic

73. Sarcoidosis
 Multisystem disease defined by epitheloid cell granuloma
without caseation different organs
 M:F(2:1) M>F age 25 bto 35 yrs
 Lesions-
 maculopapular and erythematous forms
 Papular forms
 Plaque form
 Nodular form
 Erythema nodosum
 Lupus pernio(nasal sarcoidosis, more common in
women)

74.  Sarcoidaosis affect nasal septum(nasal
obstruction)
 Surface of nose is thickened(lupus pernio)
 Although telangiectatic ,is smooth but lacks the
rugose peau d’ orange surface(in rhinophyma)

75.  Site – face,extremities(extensor aspects) and rarely
trunk.
 Associated feature of
ocular,neural,skeletal,genitourinary ,cardivascular
system involvement.
 Histopathology
 Epidermis-hyperplasia,compact hyperkeratosis
 Dermis-lymphocytic infiltrate,granulomas in lower
dermis,
 Subcutaneous tissue – panniculitis (occasional)

77. ROSACEA VS. ACNE
 ADULTS
 PAPULES
 PUSTULES
 NO COMEDONES
 ERYTHEMA
 TELANGIECTASIAS
 TEENS
 PAPULES
 PUSTULES
 COMEDONES
 NO ERYTHEMA
 NO TELANGIECTASIAS

78. Other differential diagnosis
DISEASE SIMILARITY DIFFERENCE
ACNEIFORM
ERUPTIONS
ERYTHEMA,PAPULE,PU
STULE,TELANGIETASIS
AND INVOLVES
CENTRAL 3rd OF THE
FACE
MONOMORPHIC
,EXTRAFACIAL SITE
,DRUG
INDUCED,ATYPICAL
AGE AND SITE
SEBORRHEIC
DERMATITIS
BLEPHARITS
ERYTHEMA
SCALING,ECZEMATOUS
CHANGE
PARANASAL,NASOLABI
AL,EXTRAFACIAL
PERIORAL DERMATITIS
ERYTHEMA
PAPULES
PERIORAL
SMALLER LESIONS
NO TELANGIECTASIS,
FLUSHING,BLUSHING

79. Treatment
1.Avoidance of the trigger factors
2. Drugs both systemic and topical
3.Lasers
4.surgery

80. Triggers of rosacea
Ingested or iatrogenic
1.Foods and drinks 2.drugs
 Cheeze niacin
 Chocolate nitroglycerine
 Spicy foods tobacco
 Soy sauce alcohol based
 vanilla nifedipine
 Dairy products cyclosporine
 Liver bromocriptine

81.  3.beverages 4.topical agents
 Red wine topical steroids
 Hot drinks cosmetics
 Beer acetone
 Vodka

82. Environmental causes
1.temperature 2.weather
 Sun heat sunny
 Over-heating heat
 Sun lamp stong wind
 Humidity 3.emotions
 Hot bath anger
stress
embarrasment

83. 4.activity
 Exercise
 Menopause
 Chronic cough
 straining

84. Systemic drugs
1.Oral tetracyclin – first choice (200 mg bd)
 Also used in ocular rosacea
 Less efective for resistant lymphedema
 Marginally effective for rhinophyma
 Response in 7 to 14 days
 Continue upto 4wks or more
2.doxycycline(40 mg daily)
3.minocycline
4.oral metronidazole(200 mg bid)

85. 5.Azithromycin
6.Oral isotretinoin (10-60 mg /day)
Is alternative in resistant rosacea
Good response in rhinophyma
Improves quality of life
Not suitable for ocular rosacea
Prolonged treatment
7.Oral dapsone in granulomatous rosacea
8.Sulpha drugs – for demodex

86. Topical therapies
1.topical metronidazole gel( 1% ) is the major therapy in
rosacea
 Also used in blepharitis
2.adapalene
3.benzoyl peroxide
4.tacrolimus
5.Clindamycin,erythromycin,
6.azelaic acid 20% cream

87. 7.0.025% retinoic acid cream
8.10% sulphur cream
 Role of topical steroids are limited

88. Telangiectasia
 Vascular lasers
 Intense pulsed light
 PERT(post erythema revealed telagiectasia)
Lymphoedema of rosacea
 Antibiotic to decrease inflammation
 Low dose oral isotretoin0.1-0.2mg/day
 Oral ketotifen 1-2mg/day
 Prednisolone 30 mg daily
 Metronidazole initially 400 mg over 4 months
 200 mg /day for continuation phase

89.  Rhinophyma
 Surgical exision,lasers,dermabrasion
 Cryotherapy
 Radiofrequency
 Liquid nitrogen
Ocular rosacea
 Artificial tears
 Oral tetracyclines > doxycyclins,erythromycin
 Retinoids are avoided

90. Flushing
 Clonidine 50 micrgram bd
 Oxymetazoline 0.05% daily
 Rilmenidine 1 mg daily
 Beta - blockers

91. REFERENCES
 ROOK’S BOOK OF DERMATOLOGY 8TH EDITION.
 FITZPATRICK BOOK OF DERMATOLOGY.
 INDIAN ASSOCIATION OF DERMATOLOGIST,
VENEROLOGIST, AND LEPROLOGIST.
 LEVER’ HISTOPATHOLOGY OF THE SKIN