Lichen planus

Last updated: November 01, 2022

Lichen planus

Family Med/ ER PAEA

Family Med/ ER PAEA

Hemophilia
Bleeding disorders: Clinical
Disseminated intravascular coagulation
Immune thrombocytopenia
Thrombotic thrombocytopenic purpura
Heparin-induced thrombocytopenia
Hemolytic-uremic syndrome
Anemia: Clinical
Iron deficiency anemia
Anemia of chronic disease
Sickle cell disease (NORD)
Folate (Vitamin B9) deficiency
Lead poisoning
Sideroblastic anemia
Aplastic anemia
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Autoimmune hemolytic anemia
Vitamin B12 deficiency
Polycythemia vera (NORD)
Alpha-thalassemia
Beta-thalassemia
Acute leukemia
Chronic leukemia
Non-Hodgkin lymphoma
Hodgkin lymphoma
Lymphoma: Clinical
Antiphospholipid syndrome
Factor V Leiden
Protein C deficiency
Protein S deficiency
HIV (AIDS)
Influenza virus
Borrelia burgdorferi (Lyme disease)
Epstein-Barr virus (Infectious mononucleosis)
Salmonellosis
Shigella
Acne vulgaris
Rosacea
Folliculitis
Erythema multiforme
Stevens-Johnson syndrome
Alopecia areata
Onychomycosis
Bites and stings: Clinical
Pediatric infectious rashes: Clinical
Cellulitis
Erysipelas
Impetigo
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
Pediculus humanus and Phthirus pubis (Lice)
Sarcoptes scabiei (Scabies)
Poxvirus (Smallpox and Molluscum contagiosum)
Actinic keratosis
Seborrhoeic dermatitis
Skin cancer
Atopic dermatitis
Lichen planus
Pityriasis rosea
Psoriasis
Vitiligo
Burns
Pressure ulcer
Bullous pemphigoid
Hidradenitis suppurativa
Urticaria
Human herpesvirus 8 (Kaposi sarcoma)
Conjunctivitis
Corneal ulcer
Hordeolum (stye)
Orbital cellulitis
Age-related macular degeneration
Diabetic retinopathy
Pediatric ophthalmological conditions: Clinical
Glaucoma
Otitis externa
Vertigo
Pediatric ear, nose, and throat conditions: Clinical
Otitis media
Meniere disease
Nasal polyps
Allergic rhinitis
Sinusitis
Upper respiratory tract infection
Retropharyngeal and peritonsillar abscesses
Pediatric upper airway conditions: Clinical
Laryngitis
Sialadenitis
Parotitis
Bell palsy
Migraine
Tension headache
Meningitis
Essential tremor
Parkinson disease
Alzheimer disease
Delirium
Seizures: Clinical
Ischemic stroke
Transient ischemic attack
Lower urinary tract infection
Epididymitis
Mumps virus
Prostatitis
Acute pyelonephritis
Urethritis
Testicular cancer
Kidney stones
Benign prostatic hyperplasia
Nephritic and nephrotic syndromes: Clinical
Fibrocystic breast changes
Breast cancer
Cervical cancer
Miscarriage
Placental abruption
Placenta previa
Menopause
Pelvic inflammatory disease
Pregnancy
Gardnerella vaginalis (Bacterial vaginosis)
Trichomonas vaginalis
Osteoarthritis
Fibromyalgia
Gout
Osteoporosis
Reactive arthritis
Rheumatoid arthritis
Systemic lupus erythematosus
Bursitis
Chronic cholecystitis
Anal fissure
Pediatric constipation: Clinical
Hemorrhoid
Ulcerative colitis
Inflammatory bowel disease: Pathology review
Irritable bowel syndrome
Bowel obstruction
Colorectal polyps
Esophagitis: Clinical
Gastroesophageal reflux disease (GERD)
Gastritis
Peptic ulcer
Viral hepatitis
Cirrhosis
Gastroenteritis
Colorectal cancer
Chronic pancreatitis
Acute pancreatitis
Appendicitis
Jaundice
Chronic bronchitis
Emphysema
Pediatric lower airway conditions: Clinical
Pneumonia
Mycobacterium tuberculosis (Tuberculosis)
Lung cancer
Mesothelioma
Pneumothorax
Pulmonary embolism
Sleep apnea
Acute respiratory distress syndrome
Asthma
Wolff-Parkinson-White syndrome
Atrial flutter
Premature atrial contraction
Atrial fibrillation
Ventricular fibrillation
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular tachycardia
Bundle branch block
Atrioventricular block
Myocardial infarction
Unstable angina
Stable angina
Prinzmetal angina
Angina pectoris
Heart failure
Hypertension
Familial hypercholesterolemia
Endocarditis
Mitral valve disease
Tricuspid valve disease
Pulmonary valve disease
Aortic valve disease
Deep vein thrombosis
Chronic venous insufficiency
Thrombophlebitis
Hyperlipidemia
Aortic dissection
Aneurysms
Peripheral artery disease
Amenorrhea
Ovarian cyst
Ovarian torsion
Endometriosis
Mastitis
Erysipelas
Mallory-Weiss syndrome
Gastritis
Esophageal cancer
Gastric cancer
Pancreatic pseudocyst
Retinal detachment
Labyrinthitis
Tympanic membrane perforation
Meniere disease
Acute kidney injury: Clinical
Pediatric urological conditions: Clinical
Concussion and traumatic brain injury
Bell palsy
Cluster headache
Encephalitis
Multiple sclerosis
Myasthenia gravis
Carpal tunnel syndrome
Guillain-Barre syndrome
Epidural hematoma
Subdural hematoma
Subarachnoid hemorrhage
Intracerebral hemorrhage
Creutzfeldt-Jakob disease
Frontotemporal dementia
Dementia with Lewy bodies
Vascular dementia
Normal pressure hydrocephalus
Pleural effusion
Bronchiectasis
Septic arthritis
Osteomyelitis
Compartment syndrome
Osgood-Schlatter disease (traction apophysitis)
Ankylosing spondylitis
Cauda equina syndrome
Spinal disc herniation
Spinal stenosis
Thoracic outlet syndrome
Dislocated shoulder
Sprained ankle
Legg-Calve-Perthes disease

Transcript

Watch video only

With lichen planus, lichen means tree moss and planus refers to flat, and the reason it’s called that, is that lichen planus is a flat-topped skin rash that looks a bit like tree moss.

Lichen planus is an immune-mediated disorder, meaning that the immune system has started attacking its own skin, resulting in a skin rash.

Lichen planus can also affect mucous membrane.

Now, the skin is divided into three layers--the epidermis, dermis, and hypodermis.

The epidermis forms the thin outermost layer of skin.

Underneath, is the thicker dermis layer that contains the nerves and blood vessels.

And finally, there’s the hypodermis which is made of fat and connective tissue that anchors the skin to the underlying muscle.

The epidermis itself is made of multiple layers of developing keratinocytes - which are flat pancake-shaped cells that are named for the keratin protein that they’re filled with.

Keratinocytes start their life at the lowest layer of the epidermis called the stratum basale, or basal layer, which is made of a single layer of stem cells that continually divide and produce new keratinocytes.

These new keratinocytes then migrate upwards to form the other layers of the epidermis.

The stratum basale also contains another group of cells - melanocytes, which secrete a protein pigment, or coloring substance, called melanin.

As keratinocytes in the stratum basale mature and lose the ability to divide, they migrate into the next layer, called the stratum spinosum which is about 8 to 10 cell layers thick.

The next layer up is the stratum granulosum which is 3 to 5 cell layers thick. Keratinocytes in this layer begin the process of keratinization, which is the process where the keratinocytes flatten out and die.

Keratinization leads to development of the stratum lucidum layer which is 2 to 3 cell layers thick of translucent, dead keratinocytes.

Finally, there’s the stratum corneum, or the uppermost and thickest layer of the epidermis, which is like a wall of 20-30 layers, where the glycolipid acts like the cement and the dead keratinized cells are the bricks.

Now, the part of skin connecting the stratum basale of the epidermis to the underlying dermis is called the dermo-epidermal junction.

In healthy people, this junction looks like smooth waves between the epidermis and the dermis. But, if you look closely at this junction, there are two parts.

The first part is the lower portion of the plasma membrane of the keratinocytes in the stratum basale, which contains glue-like substances called hemidesmosomes.

These hemidesmosomes adhere keratinocytes of the stratum basale to the second component of this junction, which is called the basal lamina.

The basal lamina contains a group of molecules that provide structural and biochemical support to the keratinocytes.

Typically, when a cell becomes infected with viruses or mutated by cancer, antigens from inside this cell will be presented on MHC I molecules, which are found on all nucleated cells in the body.

If this were to happen, then a specific cell of the immune system called cytotoxic T cell would use its receptor to bind to the MHC class I molecule, which would cause it to release its payload of perforin and granzymes.

Perforin would perforate the target cell by forming pores, and these pores would allow the granzymes to enter into the cell. Once inside, the granzymes would induce apoptosis, or programmed cell death.

In lichen planus, some healthy non-infected keratinocytes start presenting antigens on MHC I molecules, and it’s unclear why they do that.

This antigen presentation on MHC I molecules enables cytotoxic T cells to attack these keratinocytes and kill them.

In killing the keratinocytes, these cytotoxic T cells also release cytokines, which recruit more cytotoxic T cells to the scene. That leads to more damage to the keratinocytes, as well as the surrounding tissue in the basal lamina.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Cutaneous and Mucosal Lichen Planus: A Comprehensive Review of Clinical Subtypes, Risk Factors, Diagnosis, and Prognosis" The Scientific World Journal (2014)
  6. "Lichen Planus" New England Journal of Medicine (2012)
  7. "Interventions for erosive lichen planus affecting mucosal sites" Cochrane Database of Systematic Reviews (2012)