1. Rosacea
MODERATOR: Dr. Vijay Paliwal Sir
PRESENTER: Dr. Sunil

2. INTRODUCTION:
• Rosacea is a chronic inflammatory skin disease predominantly affecting the central area of the face.
• Symptoms present in various combinations and severity, often fluctuating between periods of exacerbation
and remission.
• It is characterized by flushing, erythema, telangiectasia, papules, pustule, edema or a combination of these.
• Although rosacea can occur in anyone, it most commonly affects middle-aged individuals with fair skin,
less frequent in skin types V and VI.

3. Pathogenesis:
• Though the exact cause of rosacea is not known, its pathogenesis is multifactorial.
• Immune dysfunction
• Inflammatory reaction to cutaneous microorganisms
• UV damage
• Neurovascular dysfunction

4. Immune dysfunction:
• Role of innate immunity
• Triggers  increased TLR 2 expression :
 increased production of cathelicidin
 increased production of kallikrein 5
These peptides regulate and promate leukocyte
chemotaxis, angiogenesis and expression of extracellular
matrix components.

5. Role of Micro-organisms:
• Stimulate inflammatory reaction in the skin.
• Demodex folliculorum – resides in the sebaceous follicle, role in modulation of the host innate immune system,
these mites release chitin, which can activate TLR2 resulting in increased protease activity.
• Bacillus olenorius- which is thought to trigger the production of MMP-9, TNF- alfa and IL-8.
• H. pylori
• Staph. Epidermidis
• Chlamydia pneumoniae
Role is controversial

6. UV radiation:
• Both UVA radiation through its action on MMP and collagen denaturation and UVB radiation with its
effects of increasing the secretion of FGF 2 and VEGF 2 may contribute the hypervascularity of skin in
rosacea.
• Generates ROS – which can signal through TLR2 to propagate the kallikrein 5/cathelicidin inflammatory
cascade.

7. Neurovascular dysregulation :
Activation of TRPV (Transient Receptor Potential Vanilloid type ) 1-4 and TRPA1  release of neuropeptides like:
• Serotonin
• Bradykinin
• Prostaglandins
• Substance P
• Calcitonin gene-related peptide
• VIP
• Flushing & erythema
• Role in local immunity,
vasoregulation, nociception
and epidermal barrier
integrity.

8. Triggers of Rosacea
• Temperature- Heat, humidity,
hot baths
• Emotions- Anger, stress, rage,
embarassment
• Activity- exercise, straining
• Chronic cough
• Menopause
• Foods- Spicy food, dairy
products, soy sauce
• Beverages- hot drinks,
alcohol
• Drugs-Nitroglycerin,
niacin, tobacco
• Topical agents- Topical
steroids, retinoids,
acetone

9. Classification:
The American Rosacea Society Expert Committee has proposed a classification and staging system for rosacea.
• The following four subtypes have been described:
1. Erythemato-telangiectatic rosacea: Flushing
• Persistent facial erythema with telangiectases
• Skin sensitivity and dryness
Telangiectasias on a background of
erythema

10. 2. Papulopustular rosacea: Small, dome-shaped erythematous papules
• Some with surmounting pustules on the central aspects of the face on a
background of persistent erythema.
Erythema, papules and pustules on face

11. 3. Phymatous rosacea: Nodular, thickening of skin with irregular surface contours, patulous follicles
•Affects nose, chin, forehead, eyes, or eyelids

12. 4. Ocular rosacea: foreign body sensation, burning/stinging, dryness, itching, Light sensitivity, blurred vision,
telangiectasia of conjunctiva/lid margin, periocular erythema, blepharitis, meibomian dysfunction,
chalazion, and rarely loss of vision.

13. The following less common types of rosacea have also been described:
• Lupoid or granulomatous rosacea
• Steroid rosacea
• Halogen aggravated rosacea
• Gram-negative rosacea
• Rosacea conglobata
• Pyoderma faciale (rosacea fulminans)
• Edematous rosacea/ Morbihan disease
• Various phymas (rhinophyma, gnathophyma, otophyma, blepharophyma).

14. Pre-rosacea Frequent flushing
Stage 1
vascular rosacea
Transient facial erythema that becomes more persistent
Slight telangiectasias
Increased skin sensitivity
Stage 2
inflammatory rosacea
Persistent, spreading erythema
Edema, papules, pustules
Enlarged pores
Ocular changes
Stage 3
late rosacea
Large inflammatory nodules and furuncles
Tissue hyperplasia, fibroplasias
Rhinophyma
Stages:

15. • All clinical signs and symptoms have been grouped as:
1. Primary signs: Flushing (transient erythema), non-transient erythema, papules and pustules, and
telangiectasia.
• Presence of one or more features on the central face is indicative of rosacea.
2. Secondary signs: Burning, stinging, plaques, dry appearance, edema, ocular manifestations and
phymatous changes.
• These often appear with one or more primary features, but rarely can appear alone.

16. Grading:
• Rosacea can be graded as follows:
1. Primary signs : graded as-
Absent 0
Mild 1
moderate 2
Severe 3
2. Secondary signs : graded as –
present +
absent -

17. • In 2017, there was a shift from subtypes to phenotypes in the
diagnosis of rosacea
Diagnostic Phenotypes Major Phenotypes Minor Phenotypes
• Persistent facial erythema • Transient facial erythema • Burning
• Phymatous changes • Inflammatory papules and
pustules
• Stinging
• Telangiectasia • Edema
• Ocular changes • Dryness
Phenotypes According to the 2017 Consensus
At least one diagnostic or two major phenotypes are required in order to diagnose a patient with rosacea.

18. Complications:
Rhinophyma:
• It is a craggy, irregular, bulbous, swelling of the nose.
• More common in males.
• Earlier alcohol excess was blamed - “whisky nose”.
• Involves the ala nasi, columella & tip of the nose.
• Wide follicular openings are seen from which foul swelling keratinous debris may be expressed.

19. Rosacea lymphedema:
• More common in men.
• Persistent lymphedema.
• It involves the forehead, cheeks, and periocular zones.
• The involved area is firm and slightly erythematous.
• Usually resistant to treatment.
Solid facial
lymphoedema
involving
predominantly the
nose.
narrowing of the
nares.

20. Histopathology:
• The histopathological features depend upon the clinically predominant lesion.
• Vascular ectasia, dermal edema, and dermal connective tissue disorganization are seen in all cases.
ETTR :
• Presence of enlarged and dilated bizarre‐shaped capillaries and venules in the upper part of the dermis.
• Mild perivascular and interstitial lymphocytic infiltrate.
• Solar elastosis.
• Occasional demodex mites may be present within the follicles.

21. PPR:
• Prominent perivascular & perifollicular infiltrate of lymphocytes, neutrophils, plasma cells and less
commonly eosinophils.
• Increased numbers of mast cells have been reported.
• Ruptured follicles with granulomatous changes may be present in florid cases.
• Sometimes demodex mite remnants are seen within these granulomas.

22. Phymatous rosacea:
• Sebaceous gland hyperplasia
• Dermal thickening and fibrosis
• Dermal mucin
• Variable degree of perivascular lymphocytic/neutrophilic infiltration.
Ocular rosacea:
• The findings are non‐specific.
• Blepharitis mainly involves the posterior meibomian glands (posterior blepharitis).
• There is an inflammatory infiltrate (lymphocytic/histiocytic/neutrophilic) that varies according to the
severity of the condition.

23. ETTR
• Chronic photodamage
• Seborrhoeic dermatitis
• Facial contact dermatitis
• Lupus erythematosus
• Dermatomyositis
PPR
• Acne vulgaris
• Perioral dermatitis
• Tinea faciei
• Pityriasis folliculorum (demodicosis)
• Rosacea‐like dermatoses due to medications
(topical calcineurin inhibitors, topical or
systemic steroids)
PR
• Solid facial lymphoedema
• Infection (cutaneous tuberculosis)
• Sarcoid
• Chronic cutaneous lupus erythematosus of
the nose
• Granuloma faciale
• Malignancy (squamous carcinoma/lymphoma)
OR
• Other causes of chronic blepharitis
• dry eye syndrome
DIFFERENTIAL DIAGNOSIS;

24. Disease Similarities Differences
Acne vulgaris •Papules, pustules, erythema •Comedones
•Earlier onset
•Not limited to central third of face
•No telangiectasias or flushing
Steroid rosacea •Erythema, papules, pustules, telangiectasias
•Central third of face
•Related to topical application of corticosteroids, tacrolimus and
pimecrolimus
Seborrheic dermatitis •Blepharitis
•Erythema
•Scaling, eczematous changes
•Paranasal, nasolabial, extrafacial distribution
Perioral dermatitis •Erythema, papules •Perioral distribution
•Smaller lesions
•No telangiectasia, flushing, or blushing
Contact dermatitis •Erythema, papules, pustules
•Burning, stinging
•Follows size and shape of causal agent
•Scaling
•Spongiosis and parakeratosis on histology
Photodermatitis •Erythema, papules, plaques •Seasonal
•Usually extrafacial
Lupus •Erythema •Malar distribution
•Photosensitivity

25. Treatment:
• Historically, rosacea was treated by bloodlettings and application of leeches on rosacea-
affected skin.
• The therapy has changed since then, but a curative treatment approach has not yet been
developed.
• Current treatment focuses on symptom suppression to improve patients' quality of life, to
prevent progression, and to sustain remission.
• Usually a set of interventions is needed.

26. General measures:
• Educate the patient about:
• Chronic relapsing nature of the disorder
• Likelihood of exacerbations
• To avoid recognized triggers.
• Photoprotection- sun exposure avoidance and zinc oxide and titanium oxide based sunscreens.
• Facial cleansers - to remove excess sebum, exfoliated keratinocytes, environmental debris.

27. Specific measures:
Topical therapies:
• Metronidazole 0.75% (gel, cream, and lotion; twice-daily application).
• Metronidazole 1% (gel and cream; once-daily application).
• Azelaic acid 15% gel (twice-daily application).
• Ivermectin 1% cream (once-daily application).
• US FDA approved to treat inflammatory lesions of rosacea, and are well tolerated by most patients.

28. • Brimonidine tartrate 0.33% gel (once-daily application) –
 Approved by the FDA as the first medication for the topical treatment of persistent facial erythema associated with
rosacea.
 It is a selective α2-adrenergic receptor agonist with vasoconstrictive activity - reduces persistent facial erythema in the
majority of patients.
 The most common side effects are burning sensation, contact dermatitis, and rebound erythema.
 It should be used cautiously in patients with depression, cardiovascular disease, raynaud's phenomenon, and orthostatic
hypotension.

29. • Oxymetazoline 1% cream applied once daily
 It is an alpha 1 agonist that was approved by FDA for the treatment of persistent facial erythema.
 Morning application is recommended .
 Effect occurs within 1 to 3 hours.
 Duration of effect is 8 to 10 hours.
 Risk of post treatment rebound erythema is less.

30. • Sodium sulfacetamide 10%, with or without 5% sulfur in the form of cream, gel & lotion - have also been used for
papulopustular rosacea.
not approved by the FDA due to limited efficacy data.
• Various other topical off-label treatments for rosacea include:
• Macrolides
• Permethrin
• Retinoids
• Topical calcineurin inhibitors
• They may be helpful in specific patients based on the assessment of the physician.

31. Systemic therapies:
• Oral tetracyclines are the drug of first choice in treatment.
• The only FDA approved agent is a modified-release doxycycline -40 mg once-daily (30 mg immediate-release and
10 mg delayed-release), which was approved in 2006.
• Provides anti-inflammatory, without antimicrobial effects.
• It is effective for inflammatory lesions and in ocular rosacea.
• less effective for resistant lymphedema and marginally for rhinophyma.
• Minocycline & oral metronidazole are effective too.

32. • Beta-blockers - nonselective beta-blockers like propranolol and carvedilol have been found to reduce the incidence and
severity of rosacea associated erythema.
• These drugs block the beta-receptors- resulting in vasoconstriction and cause improvement in erythema and flushing.
• adverse effects - hypotension and bradycardia.

33. • Oral isotretinoin is indicated for the severe form of rosacea or for patients not responding to tetracyclines
and metronidazole.
• Dapsone is useful, safe, and cost-effective in granulomatous rosacea.
• After treatment of erythema, telangiectasia may still persist.
• This phenomenon of PERT (post-erythema revealed telangiectasia) must be explained to the patient.
• Otherwise, the patient may feel that the treatment has caused more telangiectasia.

34. Other drugs which have been tried :
• Oral ivermectin
• Octreotide
• Zinc sulfate
• Helicobacter eradication regimen - comprising omeprazole (40 mg/day), clarithromycin 500 mg to 1 g/day) and
metronidazole (1–2 g/day), for 1–2 weeks.

35. Ocular rosacea:
• Patients with mild ocular rosacea present with a dry gritty feeling in the eyes., they can be treated by lid hygiene and
lubricating eye drops.
• Patients with more severe ocular rosacea present with burning or stinging of the eyes, crusting of the lid margins, or
formation of chalazion and hordeolum,They need topical or systemic antibiotics, or cyclosporine.
• Topical cyclosporine 0.05% ophthalmic emulsion has been tried.
• For the more severe ocular rosacea, referral to an ophthalmologist is prudent.

36. • Phymatous rosacea:
• Mild rhinophyma may be responsive to systemic treatment with isotretinoin.
• It shrinks sebaceous glands, but long-term remission does not occur.
• More severe disease with deformity responds best to surgical excision, dermabrasion, radiofrequency,
electrosurgery, and CO2 laser therapy.

37. Physical and light based therapies:
• Telangiectasia and persistent erythema:
• Reduction in telangiectasia is not to be expected with any of the currently available topical agents.
• These features frequently become a psychological burden and impact on patient’s quality of life.
• Most commonly used are the pulsed dye laser (585–595 nm) and intense pulse light (IPL) devices.
• Rays are absorbed by oxyhaemoglobin, deoxyhaemoglobin and methemoglobin to generate heat energy resulting in
vascular destruction.
Emerging therapies – under trial
• Serine protease inhibitor - Topical epsilon-aminocaproic acid
• Mast cell stabilizer - Topical cromolyn sodium (4%)

38. Conclusion:
• The treatment of rosacea is not only difficult, but a challenge for the dermatologists.
• Although there are many modalities for different manifestations of the disease, the patients are usually
unsatisfied with the results.
• The relapsing nature of the disease decreases the chance of disease free survival.

39. Thank you