Spring 2019: Derm System Final Exam

Lecture One: Henson (02/22/2019)

• Functions of the Skin
o The skin functions bi-directionally to keep the good things in and keep the bad things out.
o Skin holds in water to protect us from: dehydration, radiation, chemicals, microorganisms, and physical trauma
o The skin contains receptor organs that provide communication and protection from impact and friction injuries
§ Touch and vibration: rapidly adapting mechanoreceptors
• Meissner corpuscle end-organs
• Pacinian corpuscle end-organs
• Hair follicle receptors
§ Pressure: slowly adapting mechanoreceptors
• Merkel corpuscle end-organs
• Ruffini corpuscle end-organs
§ Thermoreceptors:
• A-delta & C fibers
§ Pain:
• Free nerve ending nociceptors
o Production of melanin
§ Protection against UV rays of sun
§ Produced by melanocytes in the basal layer
§ Aggregate of smaller component molecules such as pheomelanin and eumelanin (most abundant)
§ Melanin can dissipate more than 99.9% of absorbed UV radiation as heat, preventing indirect DNA damage
o Thermoregulation
§ Thermoreceptors and sweat glands à evaporative heat loss
§ Hypothalamus controls cutaneous arteries and sweat glands to retain or dissipate heat
o Synthesis of Vitamin D3
§ Exposure to UV light causes the skin to make Vitamin D
§ Liver and kidney turn Vitamin D à calcitrol
• Calcitrol regulates calcium and phosphorus production
o Psychological and social functions
§ Appearance, facial expression, and non-verbal communication
§ Dermatoglyphics: skin patterns by ridges and sulci that are unique for each individual (fingerprints)
• Innate vs. Adaptive

o Assuming no infection, our skin looks like A. Langerhans found in the epidermis in spinosum layer. Langerhans are dendritic cells.
When you see them in the dermis, they are called dermal dendritic cells. There is ability to present antigens and the other aspect
is that they may have macrophage like features. These cells reside here in the epidermis, waiting for a problem.
o Once you have breach in skin (antigen/injury) you see influx of antigen and cytokines are produced from the inflammation and what
happens is that these Langerhans are activated when injury/antigen happens, and they accumulate antigen in the cell itself.
When antigen arrives inside the cell, it releases cytokines/chemokines into the dermis. Down in the dermis we have DC and those
are activated as well. Once you start to get cytokine soup and chemokines, we can recruit other WBC to deal with what has
happened in the skin. Innate ability = first time you’ve been exposed. When you recruit granulocytes à neutrophils. Neutrophils
clear out tissue so if you’ve injured the skin, you have something to clear it out = pus (protein, dead cell, due to the neutrophil
breaking down). Monocytes à macrophages. These dendritic cells in dermis can accumulate antigen and shuttle it away and takes
it over to the LN. So this can chew up/recycle tissue but also to remove the cause of whatever started this in the first place.
o CLA + cells = skin. CUTANEOUS LYMPHOCYTE ASSOCIATED ANTIGEN. If we say they are CLA + T cells, these T cells have a
honing mechanism so they can circulate as needed and if you have injury, they can be recruited to that particular area of the skin.
The way they hone to the skin deals with surface markers that are bound to resident dendritic cells in the dermis. Chemokines
are sent into the blood and that stimulates CLA cells to migrate to that region. Once they arrive, they engage with DC and the
DC can bind to CLA cells. The DC would have presented antigen prior to this. The second time you’re exposed to this, you have
more cells primed and ready to go.
Spring 2019: Derm System Final Exam
• Skin is functionally a unit with three parts:
o Epidermis
§ Avascular (no blood vessels) and is nourished by diffusion from the dermis
§ Main type of cells in the epidermis are:
• Keratinocytes
• Melanocytes
• Langerhans cells
• Merkel cells
§ Considered to be keratinized stratified squamous epithelium
§ The epidermis is divided into many layers where cells are formed through mitosis at the innermost layers
§ They move up the strata changing shape and composition as they differentiate and become filled with keratin
• The outermost layer interacts with the environment, so we need it to be protective = filled with keratin
• The innermost layer has a different arrangement of keratin (intermediate filaments = weak) and as we
migrate upwards, those filaments become bound together (tonofilaments = strong)
§ They eventually reach the top layer (stratum corneum) and become sloughed off (desquamated)
• This process takes place within weeks (keratinization)
§ The outermost layer of epidermis consists of 25-30 layers of dead cells
§ Layers of the Epidermis: (outermost to innermost)
• Stratum Corneum
o AKA: Horny Layer
o Composed of dead cells that lack nuclei
o As these dead cells slough off, they are continuously replaced by new cells from the stratum basale
o Cells contain keratin
o The thickness of the stratum corneum varies according to the amount of protection and/or grip
required by a region of the body
• Stratum Lucidum
o Thin, clear layer of dead skin cells in the epidermis and is named for its translucent appearance
under a microscope
o It contains a clear substance called eleidin that eventually becomes keratin
o This layer is found beneath the stratum corneum of thick skin and is only found on the palms of the
hands/soles of the feet
o The keratinocytes of the stratum lucidum do not feature distinct boundaries and are filled with
densely packed keratin filaments in dense matrix \LOOSEY GOOSEY\
• Stratum Granulosum \granular layer\
o Typically contains 3-5 rows of squamous cells with many small basophilic granules in their cytoplasm
(precursor for keratin)
o Also contain large amounts of filaggrin which is a protein that serves to bundle keratin
o Membrane-coated lamellar granules are also present and contain lipids
o Lamellar granules are exocytosed in this layer to generate waterproof barrier to prevent life-
sustaining nutrient transport and leads to the characteristic cell death of the outer layers of
keratinized epithelium
o Nucleus begins to break down
• Stratum Spinosum
o Multi-layered arrangement of cuboidal cells that sit beneath granulosum layer
o Adjacent cells are joined by desmosomes giving them the spiny appearance when they shrink and are
stained (shows the desmosomes holding firm)
o Nuclei are darkened (pyknosis) which is an early sign of cell death
o Cells actively synthesize intermediate filaments called cytokeratins that are composed of keratin
§ They anchor to the desmosomes to join adjacent cells to provide structural support to
help the skin resist abrasion
• Stratum Basale (germinativum)
o Layer of keratinocytes that lies at the base of the epidermis and is immediately above the dermis
o Consists of a single layer of tall, simple columnar epithelial cells
o These cells undergo rapid cell division (mitosis) to replenish the regular loss of skin by shedding from
the surface
o About 25% of the cells are melanocytes that produce melanin which provides pigmentation for the
skin and hair (send out projections through the different layers to deposit the melanin)
o Dermis
§ The dermis contains the hair follicles, sweat glands, sebaceous glands, apocrine glands, and blood vessels
• Blood vessels provide nourishment and waste removal to its own cells
§ Also found in the dermis are lymph vessels, nerve endings, collagen, and elastin
§ Layers of the Dermis
• Papillary Layer
o Composed of loose areolar connective tissue
o Named for its fingerlike projections (papillae) that extend towards the epidermis
o The papillae provide the dermis with a bumpy surface that will interdigitate with the epidermis to
strengthen the connection between the two layers of skin
Spring 2019: Derm System Final Exam
• Reticular Layer
o Usually thicker
o It is composed of dense irregular connective tissue with some elastic fibers and adipose tissue
o It receives its name from the dense concentration of collagenous, elastic, and reticular fibers that
weave through it
o These proteins give the dermis its strength, extensibility, and elasticity
o Located in this region are the hair roots, sebaceous glands, sweat glands, receptors, nails, and blood
vessels
o Basement Membrane Complex
• Thick vs. Thin Skin
o Thick
§ Glabrous and non-hairy
§ Founds on the palm of the hands and soles of the feet
§ It contains 4-5x the normal number of sweat glands, lacks hair follicles and sebaceous glands
o Thin
§ Hairy
§ Epidermal layers are not well defined due to each layer being either:
• Reduced = Spinosum
• Discontinuous = Granulosum
• Absent = Lucidum
• Accessory organs of the skin constitute: hair, nails, and cutaneous glands
• Hair
o Functions
§ Sensation
§ Protection
• Barrier
• Hairs in nose
• Eyebrows
§ Thermoregulation
o Characteristics
§ Stratum corneum of the skin is made of pliable soft keratin, whereas with hair/nails, it is composed of hard keratin due
to tougher bonds between the proteins
§ Hair is found almost everywhere on the body
§ Three types:
• Lanugo: fine, unpigmented fetal hair
• Vellus: fine, unpigmented children’s hair
• Terminal hair: coarse, long, pigmented hair of the scalp, pubic, and axillary regions
o Structure of Hair & Follicle

§ Hair is a filament of keratinized cells

§ The shaft is visible above the skin while the root is below and is found within the hair follicle
§ The follicle is an oblique tube within the skin
§ There is a bulb swelling found at the base of the hair follicle where the hair originates
§ The vascular tissue (hair papilla) at the distal portion of the bulb is what provides
nutrients
§ Epithelial root sheath (external root sheath) is an extension of the epidermis while the
connective root sheath (internal root sheath) is derived from the dermis
§ Hair receptors will entwine each follicle
§ Arrector pili muscles are smooth muscles that cause goosebumps
• Glands
o Sweat glands/Cutaneous
§ Filtrate of blood plasma containing waste products like lactic acid
§ Types:
• Merocrine
o Millions of them
o Cool the body
Spring 2019: Derm System Final Exam
o Product moves through the cell membrane via exocytosis and the
products are moved to the apical surface where the vesicles coalesce
with the membrane on the apical surface to release the product
o Most glands release their products like this
• Apocrine
o Produce sweat containing fatty acids
o Found ONLY near hair follicles and respond to stress and sexual arousal
o Fatty acids are used as food to produce different gases (body odor)
o Product is cytoplasm at the tip of the cell
o The apical portions of the cells are pinched off and lost during the secretory process
o Sebaceous glands
§ Oily, waxy secretion called sebum that contains broken-down cells
§ Lipid content:
• 25% wax monoesters
• 41% triglycerides
• 16% free fatty acids
• 12% squalene
§ Helps to maintain the flexibility of the skin
o Ceruminous glands (ear wax)
o Mammary glands
• Embryology
o Epidermis
§ At 4 weeks, the surface ectoderm has organized over the mesoderm

§ At 7 weeks, the epidermis is made up of basal cells (cuboidal) and the periderm consists of a single cell layer.
Mesenchymal cells begin to aggregate below a presumptive hair follicle

• Periderm is a specialized embryonic structure that covers the epidermis until keratinization occurs. It
degenerates (separates at 24 weeks). It holds cells attached via tight junctions and are studded with
microvilli (blebs)
§ At 11 weeks, the cells of the stratum intermedium are appearing above the basal layer. Melanoblasts begin to form as
well as epidermial ridges. The cells of the periderm undergo keratinization and desquamation (exofoliated peridermal
cells form part of the vernix caseosa)

§ Newborn à all layers are formed

o Dermis
§ Dermal cells situated under the epidermis by 6-8 weeks
§ Embryonic fibroblasts are pluripotent cells that create adipocytes, fibroblasts, and cartilage-producing cells
§ At this stage, they are able to make collagen but the ratio of Type 3 to Type 1 is 3:1 (reversed in adults)
§ At about 9-10 weeks, superficial mesenchyme becomes distinct from skeletal components
§ At 12-15 weeks, we can distinguish fine weave pattern of papillary dermis from reticular dermis
§ Large collagen fibers accumulate in 2nd and 3rd trimester
§ At 22-24 weeks, elastic fibers are detected
o Differences between embryonic vs. adult DERMIS
Spring 2019: Derm System Final Exam
§ Embryo
• Watery, cellular
• Extracellular gel-like matrix of large well-hydrated proteoglycans
§ Adult
• Fibrous, acellular
• Rigid and fibrous
o At the end of the 2nd trimester, we shift from non-scarring to scarring dermis and at birth, it is thick and organized by still
thinner than adults
• Defense Properties of the Skin
o Physical barrier is 10mm thick
o Relatively dry which deters the growth of microorganisms in the skin
o Resident flora may prevent colonization by pathogens
o Langerhans cells in the epidermis can present antigens
o Antibodies are present in the skin
o Shedding of cells of the epidermis occurs constantly but increased during inflammation
• Biofilms

o Biofilm is an aggregate of microorganisms in which cells are stuck to each other and/or to a surface (solid substrate)
o These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS) which is
referred to as slime (polymeric jumble of DNA, proteins, and polysaccharides)
o Biofilms are characterized by structural heterogeneity, genetic diversity, and complex community interactions and an extracellular
matrix of polymeric substances
o Biofilms are a common mode of bacterial growth in nature and they have tremendous impact on our lives (sewage, corrosion, food
contamination, dental plaque, chronic infections, or medical implants)
o Formation begins with the attachment of free-floating microorganisms to a surface and these first colonists adhere to the
surface through weak, reversible Van der Waals forces
o If the colonists are not immediately separated from the surface, they can anchor themselves more permanently using cell
adhesion structures (pili)
o Bacteria growing in biofilms are up to 1000x more resistant to antibiotics than bacteria not growing on biofilms which means
that standard antibiotic therapy is useless
• Diseases
o Impetigo
§ Superficial epidermal vesiculopustule
§ Most often begins near the nose/mouth
§ S.Aureus & Group A Strep
§ Highly communicable and is inoculated into the skin via minor trauma
§ Face and extremities are most commonly affected
o Bullous Impetigo
§ Localized infection with blisters
§ S.Aureus
§ Blisters form when the adhesion molecule desmoglein 1 is cleaved
§ Occurs in newborns
§ Occurs in diaper region, axilla, or neck
§ 30% of all impetigo cases are bullous impetigo
o Folliculitis
§ Infection of the hair follicle
§ Small erythematous papules
§ S.Aureus, P.Aeruginosa, and Malssezia Furfur
§ May drain blood and/or pus
o Furuncles
§ Deep, inflammatory nodule developed from a previous folliculitis
§ Infection envelops the whole hair follicle, adjacent subcutaneous tissue
Spring 2019: Derm System Final Exam
§ S.Aureus
§ Common in skin areas that are exposed to friction and perspiration
§ Warm and painful; ranges from the size of a pea to a golf ball
o Cellulitis
§ Acute, severe and rapidly spreading infection
§ Seen in skin and subcutaneous tissues
§ Previous trauma or skin lesions (predisposing) or a breach in the skin
§ S.Pyogenes and S.Aureus
§ Severe Infection:
• Malaise, chills, fever
• Lymphangitic spread
• Circumferential cellulitis
• Pain disproportionate to examination findings
• Change in skin color
o Odontogenic Cellulitis
§ Polymicrobial
§ Can see anaerobic Prevotella or Peptostreptococcus
§ Treatment:
• IV clindamycin or ampicillin
• Oral clindamycin or amoxicillin
o Acne Vulgaris
§ Small cysts form in the hair follicles due to blockage of orifices by retention of sebum
§ Malssezia Furfur and P.Acnes are common
§ Release of free fatty acids from the sebum that leads to inflammation
§ P.Acnes can form biofilms = hard to treat
o P.Humanus var. Capitis (Lice)
§ Common in the US
§ Not a vector for human disease
§ Life cycle = 1 month
§ Eggs hatch in 8 days
§ Transmitted by close personal contact
• Dermal Mycoses
o Superficial = outermost layers; low immune response
o Cutaneous = infections that are deeper in the epidermis, hair, nails; immune response is present
§ Skin, hair, nails
§ Infecting organisms = dermatophytes
§ Keratinases break down keratin
§ Clinical manifestations referred to as “ringworm” or “tinea”
§ Activated T cells and macrophages = inflammation
§ If CMI is weak à skin is chronically infected
o Subcutaneous = dermis, subcutaneous, muscle, fascia
• Human Papilloma Viruses
o Background
§ HPV is the most common sexually transmitted viruses (nearly all sexually active men and women get it at some point in
their lives)
§ About 79 million Americans are currently infected and roughly 14 million become newly infected each year
§ >11 million women in the US get cervical cancer each year
• Mechanism for HPV carcinogenesis was first identified via cervical cancer
§ >90% of cervical cancers are related to HPV infection (high risk 16 and 18)
§ 20% of adults become infected with HPV 16 at some point
o Structure
§ Non-enveloped ds-DNA (circular)
§ Contains 9 open reading frames
§ 7 early phase genes (E) and 2 late phase genes (L)
• E genes = regulate txn of DNA
• L genes = encode for proteins involved in viral spread (capsid proteins)
§ >120 types of HPV
o High Risk vs. Low Risk
§ If the genome exists as a circular episomal DNA separate from the host cell DNA à benign or low risk (HPV 6 and 11)
that results in oral squamous papillomas, dermal warts, and laryngeal papillomas
§ If HPV genomes are integrated into the host cell DNA à malignant or high risk (HPV 16 and 18) that results in
cervical, laryngeal, or oral types of cancers
§ Integration = hallmark for malignant transformation
• Insertion of E6 and E7 = immortalization of cells à cancer
o Tumor Locations
§ Majority are located on the tonsils and the base of the tongue
§ Check for deviated uvulas
Spring 2019: Derm System Final Exam
o Vaccination
§ Gardasil
§ Since mid-2006, licensed HPV vaccine is available
§ Adminster 3-dose series on a schedule of 0, 1-2, and 6 months to all adolescents between 11-12 years (can be started
as early as 9 years)
• Immunology
o Non-Allergic Drug Reactions
§ Some drug reactions are a result of overdosage, accumulation of drugs, or unwanted pharmacological effects (stretch
marks with systemic steroids)
§ Other reactions are idiosyncratic (an odd reaction peculiar to one individual), or a result of alterations of ecological
balance.
§ Cutaneous reactions can be expected from the nature of some drugs. These are normal but unwanted responses.
§ Mouth ulcers frequently occur as a result of the cytotoxicity of methotrexate.
§ Silver-based preparations, given for prolonged periods, can lead to a slate-grey color of the skin (argyria).
§ Acute vaginal candidiasis occurs when antibiotics remove the normal resident bacteria from the female genital tract
and so foster colonization by yeasts.
§ Dapsone or rifampicin, given to patients with lepromatous leprosy, may cause erythema nodosum leprosum as the
immune response to the bacillus is re-established.
§ They affect many, or even all, patients taking the drug at a sufficient dosage for a sufficient time.
o Allergic Drug Reactions
§ Occur in only a minority of patients and even with low doses
§ Usually appear after the latent period required for an immune response (1-10 weeks)
§ Chemically related drugs may cross-react
§ Fortunately, allergic drug reactions present in only a limited number of forms; urticaria and angioedema, vasculitis,
erythema multiforme, or a morbilliform erythema.
§ Rarer allergic reactions include bullae, erythroderma, pruritus, toxic epidermal necrolysis and the hypersensitivity
syndrome reaction.
o Toxic (reactive) Erythema
§ Common type of drug eruption
§ Looks like measles or Scarlet Fever
§ Shows prominent urticarial or erythema multiforme-like elements
§ Itching and fever accompany the rash
§ Drugs include:
• Antibiotics (ampicillin)
• Sulphnoamides
• Diuretics
• Hypoglycemics
• Barbiturates
• Phenylbutazone
• Paraminosalicylate (PAS)
o Urticaria
§ Salicylates are most common, often working non-immunologically as histamine releases
§ Insect repellants and nitrogen mustards cause this on contact
§ May be part of severe/generalized reaction (anaphylaxis) that includes bronchospasm and collapse
o Erythema Multiforme
§ Target-like lesions that appear on extensor aspects of limbs
§ Bullae may form
§ Stevens-Johnson syndrome à patients are ill and mucus membranes are affected
§ Caused by:
• Sulphonamides
• Barbiturates
• Lamotrigine
• Phenylbutazone

Large Group One: Henson (02/25/2019)

Case 1: Contact Dermatitis
• Should a patient present with an “allergic reaction” after you have prescribed a certain abx, make sure you ask if the patient has taken
this drug before; if they’ve never taken the drug before, it may not be an allergic reaction
• Febrile Eruptive Papules:
o Impetigo
§ Group A Strep & S.Aureus
o St. Anthony’s Fire (Erysipelas)
§ S. Pyogenes
• Non-Febrile Eruptive Papules
o Scabies
o Lice
o Dermal fungal infections
Spring 2019: Derm System Final Exam
o Ringworm (tinea)
• Patient used Blistex which contains camphor & phenol that could potentially cause swelling of the lips
• Incidence & Prevalence
o 13.6 cases per 10000 using physical examinations by dermatologists
o The National Ambulatory Medical Care Survey conducted in 1995 estimated 8.4 million outpatient visits to American physicians
for contact dermatitis
o This is considered to be the 2nd most frequent dermatologic diagnosis
o Of office visits to dermatologists, 90% are for dermatitis
• Hypersensitivity Reactions
o Type 1: This reaction is rapid and occurs within minutes to hours and includes allergic reactions. This is characterized by the
involvement of IgE
o Type 2: This reaction occurs within hours to days and is due to antibodies binding to particulate antigens resulting in complement
activation and damage to the host
o Type 3: this reaction occurs within hours to days and is due to complement activation induced by soluble antibody-antigen complex
that occurs in the serum
o Type 4: This reaction occurs within 2-4 days and is also known as “delayed-type hypersensitivity reaction” where macropahges
and T cells are active participants
§ THIS IS WHAT OUR PATIENT HAS
• Complications & Treatment
o Potential complications include: 1) chronic dermatitis and 2) bacterial infection due to scratching
o Pharmacologist treatment includes: 1) topical corticosteroid (use oral corticosteroid if severe) and 2) topical immunomodulators
for some instances
§ Doctor can also prescribe antihistamines for the patient
• Dental Management
o Discontinue the cause of the allergic reaction (gloves, meds, etc)
o Topical corticosteroids
o Antihistamines
o Refer to dermatologist (you have 2 days from when they take the topical to decide if it’s out of our scope to treat)
• Anaphylaxis
o Rare but is considered to be the most serious drug allergy reaction and is a medical emergency
o Symptoms start within minutes after exposure to the drug
o Signs & Symptoms include:
§ Tightening/constriction of the airways/throat à trouble breathing
§ Shock with severe drop in BP
§ Weak, rapid pulse
§ Nausea, vomiting, diarrhea
§ Dizziness, lightheadedness or loss of consciousness
• Table to Memorize
Antibiotics • Aminopenicillins (ampicillin, amoxicillin)
• Beta-lactams
• Beta-lactamase inhibitors (amoxicillin/clavulanate)
• Cephalosporins, all 4 generations
• Extended spectrum penicillins
• Monobactams (aztreonam)
• Penems (imipenem)
• Pencillins
• Semi-synthetic penicillins (dicloxacillin)
Sulfonamides • Sulfamethoxazole/trimethoprim combination
• Sulfapyridine
• Sulfasalazine
• Sulfones (dapsone)
Anti-inflammatory • Aspirin
• NSAIDs
Anticonvulsants
Antiretroviral

• Useful Rules
o Determine if the drug in question is on the list of frequent offenders (see above)
o The longer the patient has been on the drug without a problem, the less likely it is that a problem will ever develop
o The rash must appear within the “Window of Opportunity” (1-10 weeks)
§ Immediate reaction = patient has previously taken the drug and they are allergic to it
§ If the patient has been taken the drug for more than 10 weeks without a reaction, he/she will likely not have a
problem
Case 2: Basal Cell Carcinoma
• Considered to be the most common cancer on earth
Spring 2019: Derm System Final Exam
• Clinically the ulcer can appear as a “rodent ulcer” and appear hypervascularized in the beginning in order to provide nutrients to the
carcinoma
• 90% of us can get basal cell carcinoma if it is a single incident; however, some patients can develop palmar pitting which is now part of the
Gorlin Syndrome (key feature for Gorlin!)
• Looking at a panoramic radiograph of a patient with Gorlin, we notice multiple radiolucencies present in the jaw. These are characteristic of
OKC.
• Most of the patients with Gorlin will have developed multiple OKCs by the time they’re 19. In patients with single instances of OKC
development, removal of the cyst will not have recurrences; however, in patients with Gorlin, removal of the cysts can have recurrences
• Further diagnostic tests to help with diagnosis include: 1) geneticist 2) biopsy the skin and odontogenic lesions and 3) refer to physician
o Biopsy confirmation includes: nests of epithelium with basaloid cells around the periphery
• The incidence and prevalence for this condition is 1 per 60,000
• Gorlin syndrome is considered to be an AD inherited condition that exhibits high penetrance and variable expressivity
o Due to mutations in patched (PTCH) which is a tumor suppressor gene that has been mapped to chromosomes 9q22.3-q31
• Systemic Manifestations of Gorlin Syndrome
o Multiple OKC
o Multiple basal cell carcinomas (can appear in places where sun may not directly hit it)
o Calcified falx cerebri
o Mild ocular hypertelorism
o Rib anomalies (splayed, fused, missing, bifid)
o Spina bifida occulta of the cervical or thoracic vertebrae
o Mandibular swelling
o Palmar/plantar pitting
o Enlarged head circumference
o Epidermal cysts of the skin
• Possible complications include: 1) basal cell carcinoma at an early age 2) OKC at a younger age 3) medulloblastoma
• Medical management for this condition includes: 1) genetic counseling 2) surgical excision of basal cell carcinoma 3) avoid UV
• Dental implications include: 1) removal of OKC that includes wide surgical excision with peripheral ostectomy 2) jaw deformities and 3)
recurrence
Case 3: Herpes
• Herpetic lesions usually begin to erupt around the vermillion border of the lip. First time lesions usually appear in the oral cavity (primary
herptetic gingival stomatitis)
• Follow-up questions for patients with herpetic outbreaks:
o Have you ever had oral ulcers?
o When was the last time you saw your physician?
o How often do you have recurrences?
o How severe are the eruptions?
• The incidence and prevalence of this condition is roughly 90% of adults are exposed to HSV-1 with herpes labialis persisting as 15-45%
• HSV-1 is spread predominantly through infected saliva or active perioral lesions (spreads via viral shedding)
• HSV-1 is best adapted and performs more efficiently in the oral, facial, and ocular areas
o However, the pharynx, intraoral sites, lips, eyes, and skin above the waist is involved most frequently
• Recurrence for HSV-1 is the vermillion border and adjacent skin of the lips. Virus can be reactivated by:
o UV Light
o Stress
o Trauma
• 15% of cases of HSV infection are associated with erythema multiforme
o Acute and self-limiting inflammatory disorder
o Symmetrically distributed nodular, popular, vesicular, and bullous lesions of variable distribution
o Caused by: 1) infections 2) drugs 3) malignant disease 4) collagen vascular diseases
• Treatment
o Systemic acyclovir
o Penciclovir, Docosanol, or Acyclovir Cream
o Long-term suppression of recurrences with an antiviral medication is reserved for patients with:
§ More than 6 recurrences per year
§ Those suffering from HSV-triggered erythema multiforme
§ Immunocompromised
o We as dental practitioners would be able to treat this condition in a normal immunocompetent adult; those that are
immunocompromised need to be referred to an MD
Case 4: Psoriasis
• Psoriatic lesions are typically erythematous plaques surrounded by silvery keratotic scales
• It is considered to be an inflammatory condition with unknown cause and may have an autoimmune component to it but it is not necessarily
an autoimmune disorder
o Characterized by an increased proliferative activity of the cutaneous keratinocytes
o Worse in the winter
• Other family members could have a history of psoriasis
• Clinical signs to narrow diagnosis:
o Koebner effect à lesions appear in areas where you cause trauma, such as elbows and knees
Spring 2019: Derm System Final Exam
o Auspitz’s sign à if you pull some of the superficial scale off, the underside will show blood (pinpoint) due to dermal papilla
exposure
• Asthma and arthritis are systemic manifestations that can also be associated with psoriasis
• Lichen planus & discoid lupus are two look-a-like lesions associated with psoriasis
• Lichen Planus Histology
o Hyperkeratosis
o Langerhans Cells Hyperplasia
o Lymphocytes found near the dermal-epidermal junction
o Saw-toothed deformation of rete ridges
• The incidence and prevalence of this condition is 2% of the US have this occurring in the 2nd decade of life that can persist for years
• Psoriasis Histology
o Elongation of rete ridges
o Hyperkeratosis
o Inflammation of the papillary dermis
• Treatment
o Manage with pharmacotherapy and UV radiation (mild psoriasis usually has no treatment)
o Use topical corticosteroids for moderate psoriasis
o Other topical drugs have proven to be effective:
§ Calipotriene = vitamin D3 analog
§ Tazarotene = retinoid (Vitamin A) compound
o Severe cases of psoriasis warrant psoralen and ultraviolet A therapy (PUVA) or ultraviolet B (UVB) therapy
o Methotrexate or cyclosporine may also be used as systemic treatments for severe disease
• Oral Manifestations
o Erythema Migrans
§ Appears to be slightly greater in psoriasis but there is no proven direct correlation between the two
Case 5: Melanoma
• The incidence and prevalence of this condition is roughly 62,000 per year, commonly diagnosed in males aged 55-60
• ABCDE’s of Melanoma
o Assymetry
o Borders
o Color
o Diameter >5mm
o Evolving lesion
• In melanoma lesions, roughly 75% occur de novo and 25% occur from a dysplastic nevus
• Direct sunlight, exposure to carcinogens, or hereditary factors are possible risk factors attributed to melanoma
• Dysplastic nevi are larger than most (>5mm) and have variable pigmentation with irregular borders
• Malignant Melanoma Growth
o Radial: indicates the tendency of melanoma to grow horizontally within the epidermal and superficial dermal layers
o Vertical: with time, the pattern of growth assumes a vertical component and the melanoma now grows downward into the deeper
dermal layers
§ Concern with this as there are lymphatic and blood vessels in the dermis layer
• Invasion Level = Clark’s
o Level 1: Confined to the epidermis (malignant melanoma in situ); Five year survival = 100%
o Level 2: Confined to the papillary dermis; Five year survival = 90%
o Level 3: Infiltration penetrating but not beyond the junction between the papillary and reticular dermis; Five year survival = 50-
65%
o Level 4: Infiltration into reticular dermis; Five year survival = 30-50%
o Level 5: Infiltration into subcutaneous panniculus; Five year survival = 10-30%
• Medical Management
o Surgical excision with 1-3cm of clean margins in small lesions; wide surgical excision in large lesions
o Depth of invasion predicts some prognosis
o Better prognosis in younger patients
o Refer the patient to a dermatologist
• Oral Manifestations
o Melanoma in the mouth always warrants a biopsy!
o Poor prognosis with oral melanoma; Five year survival = 13-22%
o Radical surgical excision if found in the mouth
Case 5: Pemphigus Vulgaris
• Clinical Tests to help with diagnosis include: 1) biopsy 2) DIF 3) Serum Ab testing
o DIF = direct immunofluorescence to detect ab bound to antigen
o Antibodies found in DIF = IgG and C3
o Antibodies found in serum = Desmoglein 1 and 3
o Results for Serum Test: Anything positive >20 for desmoglein 1 and 3
• Nikolsky’s Sign:
o As you examine the mouth, the tissue reflects easily with slight pressure (epidermal layer sloughs off)
• The incidence and prevalence of this condition is 0.42 per 100,000 in the US with a mean age of 50-60 years
Spring 2019: Derm System Final Exam
• Systemic Manifestations of this condition include:
o Oral first to show last to go
o Skin
o Eyes
o Other mucosae
• Associated with high morbidity and significant mortality
• Pathophysiology

o Auto-antibodies (IgG) are directed against the extracellular protein desmoglein 3 which is one of the cadherins
o Desmoglein 3 is treated as an antigen and this produces the separation of the cells of the spinous layer with the formation of
vesicles and bullae
o The process of destruction (lysis) of the intercellular connections (desmosomes) of the epithelial cells is known as acantholysis
o The union between epithelium and CT is not affected in this condition
• Pemphigoid
o Blister-like lesions that present on areas of the skin that rub together (intertriginous) that is characterized by destruction of
hemidesmosomes
o Supepidermal clefts
o Usually seen in the elderly
o Involvement of the mucosa is mild
o Chronic ciatricial mucosal pemphigoid confined to the oropharynx
o Less serious than pemphigus
• Treatment
o Oral Agents
§ Dapsone = systemic corticosteroid
§ Methotrexate = immunosuppressive agent
§ Mycophenolate Mofetil = chemotherapeutic agent against lymphocyte proliferation
§ Chlorambucil = alkylating immunosuppressive agent against B cells
§ Rituximab Therapy = chimeric monoclonal Ab that targets B cell differentiation Ag CD20
o Plasmapheresis = removal of ab in plasma through filtration
o IV Ig therapy = newest therapy with less side effects but fewer clinical trials
• Patients on systemic steroids need to manintain adequate Vitamin D and calcium intake with diet/supplementation
• Patients with long-term systemi corticosteroid therapy should be evaluated by a rheumatologist within the first 30 days of treatment for
osteoporosis risk assessment and consideration of a bisphosphonate for prophylaxis against osteoporosis
• Management of patients with PV requires coordination of care between the dermatologist the patient's primary care physician & the
dentist
o An ophthalmologist should evaluate patients with suspected ocular involvement and those requiring prolonged high-dose steroids.
• Patients with oral disease require a dentist for evaluation and care.
• Our patient:
o Predinosone short or long term
o Dexamethasone elixir
o Lidex gel
o Good oral hygiene and careful not to traumatize
Erythema Nodosum
• Primarily involve the subcutaneous tissue
• Associated with infection and inflammatory conditions
• Often self-limited
• Perivascular inflammatory infiltrates: eosinophils, giant cells
• Very tender
• NOT associated with pemphigus vulgaris