14.2 Integumentary System: Dermis, Appendages, Nail Unit & Cutaneous Receptors
Key Takeaways
Glabrous plantar skin has a thick stratum corneum and stratum lucidum, dermatoglyphics, the highest density of eccrine sweat glands, and no hair follicles or sebaceous glands.
The dermoepidermal junction contains laminin-332 in the lamina lucida, type IV collagen in the lamina densa and type VII collagen anchoring fibrils, whose defect causes dystrophic epidermolysis bullosa.
Eccrine sweat glands are merocrine and receive sympathetic cholinergic (M3) innervation, so diabetic autonomic neuropathy causes anhidrosis and fissuring; plantar hyperhidrosis predisposes to pitted keratolysis.
The nail plate is produced by the matrix (its visible distal part is the lunula); toenails grow about 1–1.5 mm per month, so a full hallux nail takes roughly 12–18 months to replace, and matrix injury causes permanent dystrophy.
Melanocyte number is similar across skin tones; pigmentation differences reflect melanosome size, number and distribution, and dermal arteriovenous anastomoses (glomus bodies) regulate heat loss in the digits.
14.2 Integumentary System: Dermis, Appendages, Nail Unit & Cutaneous Receptors
The general anatomy outline lists the integumentary system as its own topic. Section 14.1 covered the five epidermal strata and keratinocyte junctions. This section covers the rest of the skin organ: the dermoepidermal junction, dermis, subcutis, glands, hair, the nail unit and cutaneous blood flow. Podiatric practice is largely skin and nail care, so this anatomy explains calluses, ulcers, hyperhidrosis, onychomycosis and nail surgery.
Functions of the Skin
- Barrier: the stratum corneum lipid lamellae and corneocytes limit water loss and microbial entry.
- Immune surveillance: Langerhans cells, dermal dendritic cells, mast cells and antimicrobial peptides.
- Thermoregulation: sweating and control of cutaneous blood flow (16.6).
- Sensation: Meissner, Pacinian, Merkel and Ruffini receptors plus free nerve endings (13.5).
- Vitamin D synthesis: UVB converts 7-dehydrocholesterol to previtamin D3.
- Mechanical protection: the plantar skin and fat pad absorb repetitive load.
The Dermoepidermal Junction (Basement Membrane Zone)
| Layer | Main components | Disease when targeted or defective |
|---|---|---|
| Basal keratinocyte hemidesmosome | BP180 (type XVII collagen), BP230, integrin alpha-6 beta-4 | Bullous pemphigoid (tense subepidermal bullae) |
| Lamina lucida | Laminin-332 | Junctional epidermolysis bullosa |
| Lamina densa | Type IV collagen | |
| Sublamina densa (anchoring fibrils) | Type VII collagen | Dystrophic epidermolysis bullosa; epidermolysis bullosa acquisita |
Rete ridges interdigitate with dermal papillae to resist shear. They flatten with age, which is why elderly skin tears easily (14.4). Blisters from friction form within the epidermis, typically just below the stratum granulosum.
Dermis and Hypodermis
- Papillary dermis: loose connective tissue (type I and III collagen), capillary loops and Meissner corpuscles. Thinned suprapapillary plates over dilated capillaries explain the Auspitz sign in psoriasis (8.3).
- Reticular dermis: dense irregular type I collagen and elastic fibers. Collagen orientation creates relaxed skin tension lines; incisions parallel to them heal with narrower scars.
- Hypodermis (subcutis): adipose lobules separated by fibrous septa. On the plantar heel and metatarsal heads, vertical fibroelastic septa form closed fat chambers that act as hydraulic shock absorbers and anchor the skin to the plantar aponeurosis. This explains the limited mobility of plantar skin and the effects of fat pad atrophy (14.4) and steroid injection (11.3).
Skin Appendages
| Appendage | Secretion type | Distribution | Innervation and clinical notes |
|---|---|---|---|
| Eccrine sweat glands | Merocrine (exocytosis); watery hypotonic sweat | Whole body, densest on the palms and soles | Sympathetic cholinergic (M3). Diabetic autonomic neuropathy causes anhidrosis and fissures; plantar hyperhidrosis promotes maceration, tinea and pitted keratolysis (Kytococcus sedentarius: crateriform pits and malodor) |
| Apocrine glands | Apocrine; viscous, odor after bacterial breakdown | Axillae, groin, areolae; not on the soles | Adrenergic; active after puberty |
| Sebaceous glands | Holocrine (whole cell disintegrates) into hair follicles | Most of the body; absent on palms and soles | Androgen-driven; dry plantar skin relies on sweat and barrier lipids, not sebum |
| Hair follicles | Hair shaft from the matrix; anagen, catagen and telogen cycle | Absent from glabrous skin | Loss of hair on the toes and dorsal foot is a nonspecific sign of PAD |
The Nail Unit
| Component | Structure and function |
|---|---|
| Proximal nail fold and eponychium (cuticle) | Seals the space between the fold and the plate; loss of the cuticle allows chronic paronychia |
| Nail matrix (germinal matrix) | Produces the nail plate; its distal visible part is the lunula. The proximal matrix forms the dorsal plate and the distal matrix forms the ventral plate |
| Nail bed (sterile matrix) | Longitudinal ridges tightly bound to the plate; adds a thin ventral layer; very vascular |
| Hyponychium | Seal beneath the free edge; the entry point in distal lateral subungual onychomycosis (6.1) |
| Lateral nail folds | Soft tissue borders; involved in onychocryptosis (ingrown nail) |
| Nail plate | Compact layers of hard keratin made by onychocytes |
Growth rate. Fingernails grow about 3 mm per month, while toenails grow about 1–1.5 mm per month, so replacing a hallux nail takes about 12–18 months. This is why onychomycosis treatment courses are long and why cure is judged on clear nail growth months later. Growth slows with age, PAD and illness.
Matrix injury and nail surgery. Damage to the matrix (trauma, tumors, surgery) causes permanent dystrophy, splitting or a pterygium. Partial or total matrixectomy for recurrent ingrown nails deliberately destroys the matrix chemically (for example with phenol) or surgically so the involved strip does not regrow.
Nail Signs of Systemic Disease
| Sign | Appearance | Associations |
|---|---|---|
| Clubbing | Loss of the nail fold angle, bulbous digit | Lung cancer, chronic hypoxemia, inflammatory bowel disease (9.2) |
| Koilonychia | Spoon-shaped nails | Iron deficiency |
| Beau lines | Transverse grooves | Temporary matrix arrest after severe illness or chemotherapy |
| Terry nails | Mostly white nail with a distal pink band | Cirrhosis, heart failure, diabetes |
| Splinter hemorrhages | Longitudinal red-brown lines | Endocarditis (9.2), trauma |
| Pitting, oil-drop sign, onycholysis | Pits and salmon patches | Psoriasis (8.3) |
| Longitudinal melanonychia with periungual pigment | Dark band with Hutchinson sign | Subungual melanoma must be excluded (7.4) |
Pigmentation
Melanocytes come from the neural crest and sit in the basal layer at a roughly constant density across skin tones. Pigmentation differences reflect melanosome size, number, melanin type (eumelanin or pheomelanin) and distribution to keratinocytes. Tyrosinase defects cause oculocutaneous albinism, and autoimmune melanocyte loss causes vitiligo. Excess ACTH in Addison disease causes hyperpigmentation, including the palmar and plantar creases. Acanthosis nigricans marks insulin resistance.
Cutaneous Circulation
Two horizontal plexuses supply the skin: a superficial (subpapillary) plexus feeding the papillary capillary loops and a deep plexus at the dermis-subcutis border. In glabrous skin of the hands and feet, arteriovenous anastomoses (glomus bodies) bypass the capillaries. Sympathetic vasoconstriction closes them to conserve heat, and withdrawal of that tone opens them to lose heat. A glomus tumor arising from these bodies causes exquisite subungual pain, cold sensitivity and point tenderness. Skin wound healing follows the phases in 7.2.
Which feature is normally absent from the plantar skin of the heel?
Meissner corpuscles
Sebaceous glands
Eccrine sweat glands
Stratum lucidum
A hallux nail plate is avulsed after trauma, and the matrix is left intact. Approximately how long will a complete new hallux nail take to grow out?
About 2–3 weeks
About 12–18 months
About 3 months
About 5 or more years
Why does diabetic autonomic neuropathy cause dry, fissured plantar skin?
Loss of sympathetic cholinergic innervation of eccrine sweat glands causes anhidrosis
Destruction of sebaceous glands on the sole stops sebum production
Excess sympathetic adrenergic tone constricts the sweat ducts
Loss of parasympathetic innervation of plantar apocrine glands stops secretion
Sections you finish are checked off in the contents.