Glands

1. PILOSEBACEOUS UNIT
DR. PREKSHA DUGAR

2.  INTRODUCTION
 HAIR
 ANATOMY
 HISTOLOGY
 SEBACEOUS GLAND
 EMBRYOLOGY
 HISTOLOGY
 LOCATION AND TYPES OF SEBACEOUS GLANDS
 BIOCHEMISTRY OF SEBUM
 FUNCTION OF SEBACEOUS GLANDS
 REGULATION OF SEBACEOUS GLAND
 APPLIED ASPECTS
 REFERENCES
INDEX

3. INTRODUCTION
 Pilosebaceous unit is a 3-dimensional complex structure present on surface of mammalian
skin
 It is composed of hair follicle, hair shaft, arrector pili muscle and sebaceous gland

4. HAIR
 Hair is a protein filament that grows from follicles found in the dermis, or skin. Hair
is primarily composed of protein, notably keratin
 The human body except for some areas of glabrous skin, is covered by hair follicles
which produce either thick terminal or fine vellus hair

5.  Hair follicle is histologically divided into 2
regions in relation to insertion of arrector
pili muscle-
1. The Upper Part- which consists of the
infundibulum and the isthmus
2. The Lower Part- which comprises the stem
and the hair bulb

7. ANATOMY OF HAIR
 The hair follicle is divided into 4 parts from deep to
superficial
1) Hair bulb- Consists of 5 major portions from inside to
outside
(a) Dermal Hair Papilla
(b) Hair Matrix
(c) Hair consisting of medulla , cortex and cuticle
(d) Inner Root Sheath consisting of inner root sheath cuticle,
Huxley’s and Henle’s layers
(e) Outer Root Sheath

8. 2) Suprabulbar- Area/Stem- from the hair matrix to insertion of arrector
pili muscle. It consists of hair, inner root sheath and outer root sheath
3) Isthmus- Extending from insertion of arrector pili muscle to sebaceous
gland entrance. Isthmus lacks inner root sheath. It consists of hair and
outer root sheath only
4) Infundibulum- Extending from sebaceous gland to the follicular orifice.
It is nearly identical to the epidermis and is not a component of root
sheath

9.  Layers of hair (within outwards)
• Hair shaft- medulla, cortex, cuticle
• Inner root sheath – IRS cuticle, huxley, henle
• Outer root sheath
• Glassy membrane
• Connective tissue/ dermal sheath

10. HISTOLOGY

12. SEBACEOUS GLAND
 EMBRYOLOGY
 HISTOLOGY
 LOCATION AND TYPES OF SEBACEOUS GLANDS
 BIOCHEMISTRY OF SEBUM
 FUNCTION OF SEBACEOUS GLANDS
 REGULATION OF SEBACEOUS GLAND

13. INTRODUCTION
• Lipid producing , Multi lobular structures of
epithelial origin
• Consists of : Acini connected to a common
excretory duct ( ductus seboglandularis )
• Associated with hair follicles all over the body
• Holocrine gland (fully differentiated secretory
cells burst  release both cytoplasmic content
and cell membranes into their ducts)
• Secretion: Sebum formed from autolysis of their
cells HOLOCRINE GLAND

14. DEVELOPMENT
 Sebaceous glands first appear as hemispherical protuberances on the posterior surfaces of the hair
follicle at the junction of future infundibulum and isthmus
 The cells contain moderate amount of glycogen
 As the cells move from the periphery to the centre they lose glycogen and lipid accumulates
 13th – 16th week - glands are clearly distinguishable
 17th week – Lipid drops are visible, lumen formed, gland becomes multiacinar, duct formed

15.  3rd trimester – becomes functional
 At the end of fetal life the gland is well developed.
 At birth it becomes a part of vernix caseosa
 After birth , the size decreases and enlarges again to become functional only after puberty(under the
influence of androgens).

17. • Two or three (in some hair pegs) epithelial
swellings appear on the posterior wall.
• The uppermost bulge becomes the rudiment of
the apocrine glands
• The middle one becomes the rudiment of the
sebaceous gland
• The lower bulge is the site of arrector pili
muscle attachment

18. TRANSCRIPTION FACTORS
 The bulge region of the follicle contains the epidermal stem cells that generate
multiple cell lineages
 Earliest known signal necessary for sebaceous gland development is SOX9
STEM CELL (TCF3)
 Epidermal and follicular
keratinocytes
 Sebaceous glands

19. • As daughter cells migrate from the bulge
region, changes in the expression patterns of
numerous transcription factors determine
their final cell lineage.
• Transcription factors such as-
1.Wnt/wingless (Wnt) promotes placode
formation
2.Sonic Hedgehog (Shh) signaling pathways
are intricately involved in embryonic
patterning and cell fate decisions.

21. SEBACEOUS DUCT
 Sebaceous ducts are lined by Undifferentiated Keratinocytes
 The duct of the sebaceous gland marks the transitional zone between-
1. Stratified squamous epithelium of follicular infundibulum
2. Lipid producing cells of sebaceous lobules

22.  The granular layer of the ductal epithelium gradually disappears due to-
1. Thinning of wall of the duct
2. Lipid producing sebaceous cells become evident
 The epithelium of the sebaceous duct is thin, and its thin cornified layer is compactly
arranged with a scalloped surface
 They are associated with hair follicles composed of stratified squamous epithelium

25. HISTOLOGY
• Sebaceous glands are uni- or multi-lobular
structures of pale eosinophilic staining cells
with lipid droplets in their cytoplasm
• Surrounding the glands are connective tissue
capsules composed of collagen fibers that
provide physical support
• The sebaceous ducts are lined by stratified
squamous epithelium

28. DISTRIBUTION
 Sebaceous glands are associated with hair follicles all over the body
 They are largest and most dense on the scalp, followed by face , neck and shoulders –
400/cm² to 900/cm²
 They are relatively sparse on the torso and limbs - <100/cm²
 They are not present over palms and soles

29.  4 classes of pilosebaceous unit
1. Terminal – scalp and beard
2. Apopilosebaceous – axilla and groin
3. vellus – majority of skin
4. sebaceous – chest , back and face

30. VELLUS, SEBACEOUS AND TERMINAL FOLLICLES

31.  Sebaceous glands are found in some non hairy sites
• Eye lids — Meibomian glands , Tarsal glands
• Nipples — Montgomery tubercles , Areolar glands
• Genitals – Tyson glands
• Buccal mucosa & vermilion border of lip — Fordyce spots

32. COMPOSITION OF SEBUM
 Sebum production is a continuous event
 When sebum leaves sebaceous gland , it contain neutral lipids, mainly triglycerides, wax esters,
squalene and some amount of cholesterol and cholesterol esters
 During the passage of sebum through hair canal, bacterial enzymes hydrolyse some triglycerides

33. • Triglycerides , diglycerides & FFA – 40-60%
• Wax esters – 25 – 30%
• Squalene – 12- 51%
• Cholesterol esters – 3-6%
• Cholesterol – 1.5 – 2.5%

34. FUNCTION
• Barrier function
• Sebum reduces water loss from the skin
• It protects skin and its surface lipids from oxidation by delivery of vitamin C
• It has mild anti bacterial action & protects skin from bacterial and fungi as it contain anti-
inflammatory lipids & IgA

35. • Antimicrobial peptides like Cathelicidin , psoriasin , B-defensin 1, B-defensin 2 are expressed
within sebaceous gland
• Free fatty acids in sebum are bactericidal against gram +ve organisms
• Vitamin D precursor

36. EFFECT OF HORMONES ON SEBACEOUS GLAND
Entirely under hormonal control
 Regulated by sebaceous gland cell receptors like :
1. Androgen and estrogen receptors
2. PPAR (peroxisome proliferator activated receptors)
3. LXR (liver x receptor),retinoid and vit D receptor

37. • ANDROGENS
• Enlargement of sebaceous gland at puberty
• most effective androgens are Testosterone , 5alpha dihydrotestosterone and 5alpha-androstane-3beta-17
beta -diol
• Increases proliferation of sebocytes and increase sebum production.

38. • Estrogen – Decreases the size of the gland and sebum production (only in high concentration)
Acts at pituitary-gonadal axis , thus reducing endogenous androgen production
• Cortisone – suppress secretion by suppressing the adrenal androgens
• ACTH – Increases proliferation of sebocytes
Increase sebum production

39. • Pituitary gland – Directly or indirectly control the sebum production
• Thyroid gland – Plays a role in sebum production.
-Thyroidectomy causes decrease in sebum production which is reversed by
thyroxine supplementation

40.  Antiandrogens :Norpogesterone
17-alpha methyl-beta-nortestosterone
Flutamide
Spirinolactone
Ranitidine
Cimetidine
• Retinoids : Isotretinoin is most potent pharmacological inhibitor of sebum secretion
• Decreases proliferation of sebocytes
Inhibitors of Sebaceous activity :

41. RESIDENT MICROFLORA WITHIN THE
PILOSEBACEOUS UNIT

42. APPLIED CONCEPTS

43. DISEASES OF SEBACEOUS GLANDS
 Increased activity/ volume
 Acne Vulgaris
 Rosacea
 (Hyper) Seborrhoea
 Periorificial Dermatitis
 Hair follicle Naevus
 Congenital sebaceous gland hyperplasia
 Senile sebaceous gland hyperplasia
 Sebaceoma (sebaceous gland epithelioma)
 Sebaceous Carcinoma

44.  Decreased activity/ Volume
 Senile xerosis cutis
 Psoriasis
 Lichen planopilaris
 Pseudopelade Brocq
 Hidradenitis Suppurativa
 Linear Morphea
 Chemotherapy induces diffuse alopecia

45. ACNE VULGARIS
 Common disorder of the pilo-sebaceous unit
 Etiopathogenesis :
1. Androgens
2. Sebaceous hyperplasia with seborrhoea
3. Altered cornification and differentiation

46. 4. Colonization of duct by microbial
flora
4. Inflammation and Immune
response
6. Other factors like climate , stress
diet, etc

48. • Generally, occurs in sebaceous rich body regions – face , mid chest , back , shoulders and
arms
• Present with pleomorphic eruptions
• Lesions can be-1. Inflammatory – Papules
Pustules
Nodules
Cyst
2. Non-inflammatory- Comedones – open and closed

49. KERATOSIS PILARIS
 Follicular keratotic papules in
the hair-bearing areas
 Most commonly seen in
proximal extremities

50. GRAM-NEGATIVE FOLLICULITIS
 Mostly as a complication of long-term oral or less
frequently topical antibiotic therapy used to treat
acne
 Overgrowth of gram-negative organisms including
Klebsiella, E.Coli , Serratia marescens , Proteus
mirabilis or Pseudomonas aeruginosa

51. MALASSEZIA FOLLICULITIS / PITYROSPORUM
FOLLICULITIS
 Caused mainly by Malassezia globosa

52. FIBROFOLLICULOMAS
 They are 2-4mm dome shaped
papules
 Seen most commomnly on the face,
neck and upper trunk

53. COMEDO NAEVUS/NAEVUS COMEDONICUS/NAEVUS
FOLLICULARIS/NAEVUS UNILATERALIS COMEDONICUS
 Pilosebaceous naevoid disorder
 Developmental defect of hair follicle usually
involving the scalp, face and trunk and
occasionally genitalia

54.  Associated sebaceous glands may be
normal hypoplastic/ hyperplastic
 Lesions consist of keratin filled pits,
grouped or in linear arrangement

55. SEBACEOUS NEVUS/NEVUS SEBACEOUS OF JADASSOHN
 It is an organoid naevus consisting of a
mixture of relatively normal-looking dermis,
sweat and sebaceous glands.
 Usually involves scalp
 At puberty sebaceous gland enlarges and
epidermis becomes verrucous

56. SEBACEOUS ADENOMA
 Benign tumour of incompletely
differentiated sebaceous cells
 Waxy pink/yellow tumours, usually
<10 mm in size
 When associated with multiple visceral
carcinomas, it is referred to as Muir-Torre
syndrome(MTS)

57. SEBACEOUS CARCINOMA
 Rare malignant tumor arising from the
sebaceous gland
 Firm , solitary yellow-orange lesion
 Mainly face and scalp

58. SEBACEOUS CYST/EPIDERMOID CYST
 It is a retention cyst
 It is due to the blockage of the sebaceous duct causing
a cystic swelling
 Common in face, scalp, scrotum
 Painless, fluctuant, non transilluminating with a
punctum over the summit

59. FOLLICULITIS KELOIDALIS
 Chronic form of folliculitis
 Nape of neck involved
 Associated with cicatricial alopecia

60. SCALP FOLLICULITIS
 Caused by bacteria (Cutibacterium acnes,
Staphylococcus aureus ), yeast (Malassezia spp.)
and mites (Demodex folliculorum)

61. FOLLICULITIS DECALVANS/TUFTED
FOLLICULITIS
 Chronic disorder of the hair bearing areas on the
scalp that leads to scarring, alopecia and atrophy
 Maybe the result of an abnormal host response to
toxins from S.aureus

62. FOLLICULAR OCCLUSION TETRAD
 It is a symptom complex consisting of four conditions having a similar
pathophysiology
 The tetrad includes :1. Hiradenitis suppurativa
2. Acne Conglobata
3. Dissecting cellulitis of scalp
4. Pilonidal sinus
 Pathophysiology : Follicular occlusion in apocrine gland bearing areas

63. HIRADENITIS SUPPURATIVA
 It is a chronic inflammatory recurrent debilitating follicular disease
 Usually presents after puberty
 Painful, deep seated inflamed lesions in the apocrine gland – bearing areas of the body (axilla, anogenital
and inguinal region)

64. ACNE CONGLOBATA
 Rare but severe form of acne
 Hypersensitivity reaction of the skin to
Propionibacterium acne
 Presents with deep burrowing abscesses which
interconnect via sinus tract

65. REFERENCES
 Rook’s textbook of dermatology(9th edition)
 Dermatology textbook – Jean L. Bolognia , Julie V . Schaffer , Lorenzo Cerroni(4th
edition)
 IADVL textbook of dermatology (5th edition)
 Fitzpatrick’s dermatology (9th edition)
 Lever’s textbook of Histology