• Describe the common oral diseases

Stomatitis: inflammation of the oral cavity

-Irritants: alcohol, tobacco, hot or spicy foods

-Infectious agents: Herpes virus, Candida albicans fungus, bacteria that cause trench mouth

¤ Aphthous Ulcers - canker sores

-Small,round, and superficial

-Grayish-white exudate

Stress, fever, foods

-Epidemiology: Most common oral ulceration. (10-40% population)

Puberty – 30 yrs of age. F>M

-Cause: NOT infectious/contagious/sexually transmitted.

-Predisposing factors: GENETICS, deficiency (Iron, folic acid, Vit B), GI disorders (celiac, Crohns), pernicious anemia, smoking

cessation, stress, hormones (↓progesterone in luteal phase), food allergies, immune deficiency, pharmaceuticals (NSAIDS,

alendronate, nicorandil)

-Duration: 7-10 days

-Rx: Pain relief, reduction of ulcer duration. Topical corticosteroids & antimicrobials.

¤ Herpes Virus - Herpetic Stomatitis, Cold Sore, Fever Blisters. HSV 1; HSV 2 (STD) -Small vesicles containing clear fluid

-Dormant in Ganglia; reactivated by Stress, fever, trauma, sun, infection

– Lips and nose

-Immunocompromised – more virulent. Gingivostomatitis. Conjunctiva. Esophagus

-Presentation: – Vesicles-bullae. Rupture produces painful ulcers

- Epidemiology - HSV-1 asymptomatic primary infection in children age 2-4 yrs, 10-20% of infections cause acute herpetic

gingivostomatitis

- HSV-2 w/sexual maturity, 2-4 outbreaks in first year

-Causes: HSV-1 & HSV-2, re-activation of virus results from stress and immunosuppression

-Duration: 3-4 weeks, infection for lifetime

-Rx: Topicals for pain & antivirals

¤ Candidiasis - Thrush, Monoliasis – due to Candida albicans

- Pseudomembranous, white, curd-like, circumscribed

- Diabetes, Antibiotics, Glucocorticoids, Anemia, Cancer, HIV

¤ Herpes Zoster (shingles) – Vesicles-bullae. Rupture produces painful ulcers

- Epidemiology: Usually self-limiting in children

-Increase risk w/ age & immune compromise

-Causes: Varicella Zoster virus (Chicken pox)

-Duration – Infection for a life. 3-4 weeks. 25% of Zoster patients have chronic neuropathic pain

(post herpetic neuralgia)

-Rx: Topicals for pain & antivirals

¤ Coxsackie (hand-foot-mouth) – Painful small vesicles on the hands, feet, and diaper area

- Small ulcers in the throat, tongue, soft palate

-Epidemiology - <10 years of age. Summer & Fall

-Causes – Coxsackievirus or Enterovirus

-Duration – Recovery in 5-7 days

-RX: Palliative (Tylenol & NSAIDS). No aspirin in kids – can be used in adults

¤ Leukoplakia – Whitish, well-defined patches. Hyperkeratosis (epidermal thickening) -Cannot be scraped off

-Strong association with tobacco usage

- Can be: - benign: no dysplasia

- Mild dysplasia to severe dysplasia

- Carcinoma-in-situ

-3% -25% transform into squamous cell carcinoma

AIDS and Kaposi Sarcoma -White, confluent patches

- “Hairy” Leukoplakia – corrugated

- Epstein-Barr

- Not related to the development of oral cancer

¤ Viral – Hairy leukoplakia (hairy tongue)

-Presentation: - Hyperkeratotic thickening of the lateral border of the tongue

- filiform papillae greatly elongated and resemble hairs

- elongated papillae become stained by food and tobacco and bacteria

-Epidemiology: - 80% of patients have HIV

- 20% of patients immunocompromised (cancer, transplants)

-Causes: - Epstein-Barr virus (EBV) found in lesions

-RX: Antivirals for HIV, tongue brushing, increased oral hygiene

¤ Erythroplakia – red, velvety

-Poorly defined borders

-Greater than 50% transformation to malignancy

¤ Oral Cancer

-Majority are squamous cell carcinoma

-Usually seen after age 40

-Lesions may cause localized pain or difficulty chewing, but most are asymptomatic

-If detected early, 90% survival rate

-Otherwise, only 20% - 40%

¤ Carcinoma of the Oral Cavity

-Arises from squamous epithelium:

Lips,

Cheeks,

Tongue,

Palate,

Back of throat

¤ Salivary Glands

Sialadenitis - Inflammation of salivary glands due to Trauma, Infection (Mumps), Autoimmune

- Due to rupture of salivary duct with leakage into surrounding tissue and Blockage of duct

- Chronic: decreased production of saliva or autoimmune due to sjorgren syndrome

¤ Tumors - pleomorphic adenoma

- Warthin Tumor – Benign; composed of epithelial and dense lymphoid tissue

Dermatological:

¤ Erythema Multiforme

-Presentation: - Skin & Oral tissue

- macules, papules, vesicles, bullae

- Red macule/papule w/pale vesicular or eroded center (bull’s eye/target)

- Crusting, ulceration, erythema of mucosal tissues and lips

-Epidemiology – uncommon, self-limited, most common 10-40 years

-Causes: Hypersensitivity to infections and drugs

- HSV, mycoplasma, histoplasmosis, coccidioidomycosis, typhoid, leprosy

- Sulfonamides, penicillin, barbiturates, salicylates, hydantoins, antimalarials

- Carcinomas, lymphomas, collagen disesases (lupus)

-Duration: - Mild: 2 - 6 weeks, may return

- Severe: Stevens-Johnson syndrome & toxic epidermal necrolysis have high death rates (usually due to

medication reactions)

-Rx: Rx: Treatment goals include:

1. Controlling the illness that is causing the condition

2. Preventing infection

3. Treating the symptoms: - Mild: Antihistamines (itch), antivirals (if viral), OTC for fever , OTC and topical

anesthetics for pain,

- Severe: antibiotics, steroids, IV Ig, hospitalization

¤ Geographic Tongue

-Presentation: - Multiple irregularly shaped but well-demarcated areas of desquamation

(loss) of the filiform papillae (eg. Smooth red patches and sores on the tongue)

- Smooth areas resemble a map

- Patches can move from day-day

-Epidemiology: uncommon (2%), self-limited, any age, less common in smokers – Harmless

-Causes: variant of psoriasis?, Vit B deficiency, irritation from hot/spicy food, alcohol

-Duration: days-weeks, smooth areas & whitish margins migrate across the surface of the

tongue by healing on one border & extending on another.

-RX: palliative (antihistamine gel, steroid mouth rinses, OTC for pain), avoid hot & spicy foods

¤ Lichen Planus

-Presentation: - dry and undulating, "lichen-like" appearance of affected skin

- Affects the mucous membranes (tongue and insides of cheek)

- Papules that form plaques

- Oral lesions can appear prior to the skin eruptions

- Can be tender or painful

- White, lace-Iike pattern is Wickham's striae

-Epidemiology: benign chronic disease, self limiting, 30-60 yrs, F>M, uncommon in children

-Causes: Unknown. Allergic or immune reaction, Hepatitis C, liver disease, pharmaceuticals

-Duration: self-limiting w/resolution at 1-2 yrs

-Rx: palliative (antihistamine, topical anesthetics, steroids, immunosuppressant’s)

¤ Pemphigoid

-Presentation - Bullae on mucous membranes, including the oral cavity.

- Itching & pain

- gingiva is desquamative

- Deposition of IgG and complement in the basement membrane

-Epidemiology: most frequent blistering disease of the skin (7-10/million/yr), elderly,

F>M

-Causes: autoimmune, antibodies to BPAG2 (collagen type 18) cause blistering, medications (penicillin, etanercept (Enbrel),

sulfasalazine (Azulfidine) and furosemide (Lasix).

-Duration: months-years, relapsing-remitting

-Rx: biopsy and steroids, immunosuppressants

Bacterial

¤ Acute necrotizing ulcerative gingivitis/periodontitis

-Presentation: Inflammation & infection of ligaments & bone that support the teeth

-Epidemiology: - very common, 30–50% of US population

- 10% have severe forms

- increased w/smoking, stress, poor oral hygiene, HIV, leukemia, Crohn’s,

diabetes, Down syndrome

-Causes: spirochetes, bacteroides, unknown

-Rx: good oral hygeine, antibiotics, smoking cessation, stress reduction, life style changes

____________________________________________________________________________________________________________

• Explain the causes of the nutritional diseases

-Lack of nutrition and over-nutrition are major health concerns.

-Healthy Diet:

-Sufficient Engergy: Carbohydrates, proteins, fats

-Essential Building Blocks: Amino Acids, fatty acids

-Vitamins and Minerals: Coenzymes, Structure (Calcium & Phosphate), Hormones

-Malnutrition

-Primary – Missing one or all factors of healthy diet

-Secondary – Dietary intake is adequate but malnutrition results from:

-Impaired absorption

-Impaired storage or utilization

-Excess loss

-Causes:

- Poverty: Homeless people, elderly persons, and children of the poor often suffer from protein-energy

malnutrition (PEM) as well as trace nutrient deficiencies. In poor countries, poverty, together with droughts, crop failure, and

livestock deaths, creates the setting for malnourishment of children and adults.

- Ignorance. Even the affluent may fail to recognize that infants, adolescents, and pregnant women have

increased nutritional needs. Ignorance about the nutritional content of various foods also contributes to malnutrition, as follows: (1)

iron deficiency often develops in infants fed exclusively artificial milk diets; (2) polished rice used as the mainstay of a diet may

lack adequate amounts of thiamine; and (3) iodine often is lacking from food and water in regions removed from the oceans,

unless supplementation is provided.

- Chronic alcoholism. Alcoholic persons may sometimes suffer from PEM but are more frequently lacking in

several vitamins, especially thiamine, pyridoxine, folate, and vitamin A, as a result of dietary deficiency, defective GI absorption,

abnormal nutrient utilization and storage, increased metabolic needs, and an increased rate of loss. A failure to recognize

thiamine deficiency in patients with chronic alcoholism may result in irreversible brain damage

- Acute and chronic illnesses. The basal metabolic rate becomes accelerated in many illnesses (in patients with

extensive burns, it may double), resulting in increased daily requirements for all nutrients. Failure to recognize these nutritional

needs may delay recovery. PEM is often present in patients with metastatic cancers.

- Self-imposed dietary restriction. Anorexia nervosa, bulimia, and less overt eating disorders affect a large

population of persons who are concerned about body image or suffer from an unreasonable fear of cardiovascular disease .

- Other causes. Additional causes of malnutrition include GI diseases, acquired and inherited malabsorption

syndromes, specific drug therapies (which block uptake or utilization of particular nutrients), and total parenteral nutrition.

• Describe the types of Protein-Energy Malnutrition and their significant features and explain

the mechanisms of the adverse effects of each

Protein-Energy Malnutrition (PEM)

-Common in low income countries. Up to 25% of children

-Developed countries. Elderly & debilitated patients

-Malnutrition:

-BMI <16 kg/m2

-(Normal BMI 18.5-25 kg/m2)

-Body weight <80% normal

-2 Protein Compartments which are Regulated differently

Primary: Marasmus, Kawashiorkor

Secondary: Cachexia

Marasmus

-Weight <60% of normal

-Catabolism/depletion: somatic protein & subcutaneous fat

-Normal serum albumin

- Low leptin – HPA release of cortisol –lipolysis

- Emaciated extremities

- Head appears too large for body

- Anemia and vitamin Deficiencies

Kwashiorkor

-Protein deprivation > calorie reduction

-Weaned too early, chronic diarrhea, nephrotic syndrome, extensive burns

-Loss of visceral protein, spared subcutaneous fat & muscle

-Hypoalbuminemia – edema

-Weight loss masked by fluid retention

Cachexia (Secondary Protein-Energy Malnutrition)

- Chronically ill, elderly, bedridden patients

- >50% of elderly nursing home patients in US

- Increases risk of infection, sepsis, impaired wound healing, mortality

-SIGNS:

-Depletion of subcutaneous fat in arms, chest, shoulders, metacarpal

- Wasting of quadriceps femoris & deltoid muscles

- Ankle or sacral edema

-Patients w/AIDS or advanced cancers (~50% cancer

patients)

-Extreme weight loss, fatigue, muscle atrophy, anemia, anorexia, edema

-Tumors produce cachetic agents

____________________________________________________________________________________________________________

• Explain the functions of Vitamin A, D and C and the clinical effects of the deficiency and

toxicity of each

FUNCTIONS OF VITAMIN A:

1. RETINA: retinal+opsin = rhodopsin

-Rhodopsin + light = neuronal activity = VISION

2. CELL GROWTH & DIFFERENTIATION: retinoids + retinoic acid receptors

-(RAR, RXR) = growth/ differentiation of mucus secreting epithelium

3. METABOLIC EFFECTS: fatty acid oxidation in fat tissue and muscle, adipogenesis, lipoprotein metabolism, obesity

4. IMMUNE SYSTEM: stimulate immune response in intestines, antioxidant

CLINICAL USE OF VITAMIN A:

1. Treat skin disorders (acne/psoriasis) – BEWARE TERATOGEN!

2. Acute Promyelocytic Leukemia

- Truncated RAR gene blocks myeloid cell differentiation

- Retinoic acid treatment overcomes the block causing leukemia cells to differentiate into neutrophils

VITAMIN A DEFICIENCY:

CAUSES:

1.Undernutrition

2.Malabsorption of fats:

-Infection in children,

-Absorption poor in infants

-Celiac disease, Crohn’s disease, colitis

-Bariatric surgery

-Elderly persons w/continuous use of mineral oil (laxative)

SYMPTOMS:

1. RETINA: impaired vision, night blindness especially

2. DIFFERENTIATION OF EPITHELIUM: epithelial metaplasia & keratinization

-EYES

1. Xerophthalmia: Dry eye - keratinization of lacrimal & mucus secreting epithelium

2. Bitot spots: Keratin debris in eye

3. Keratomalacia: erosin of corneal surface

-UPPER RESPIRATORY

1. Squamous metaplasia: predisposes to pulmonary infections, predisposes to renal and urinary stones

3. IMMUNE DEFICIENCY

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• Define obesity and describe the methods for measuring it

Obesity- State of increased body weight due to adipose tissue accumulation that is of sufficient magnitude to produce adverse

health effects. Obesity is associated with an increased risk of several important diseases (e.g., diabetes, hypertension).

Measured by BMI

-Weight in kg / (height in meters)2

- Normal: 18-25 kg/m2

- Overweight: 25-30 kg/m2

-Obese: over 30 kg/m2

-Skinfold measurements

-Circumferences (i.e. waist to hip ratio)

-Not only total body weight, but also Distribution

-Visceral Obesity

-Fat accumulation in trunk and abdomen

-Higher risk for disease

• Explain the function of Leptin, Ghrelin, Adipose tissue, and PYY

Leptin - Secreted by adipocytes

- Reduces food intake and enhances expenditures of energy

-Increases physical activity

-Thermogenesis

- Output is regulated by fat stores

-Abundance adipose tissue secretion is stimulated

-Low Body Fat secretion is diminished

- Acts on hypothalamus

Ghrelin - produced in stomach

- Increases food intake

- Normally rise before meals and falls 1-2 hours post

- Drop in levels is attenuated in obesity

Peptide YY – secreted from ileum and colon in response to food.

-Diminishes food intake

• Explain the clinical consequences of obesity

-Insulin Resistance

-Hypertension - risk of developing hypertension among previously normotensive persons increases proportionately with weight

-Hypertriglyceridemia and low HDL

-Cancer

-Gall Stones

-Nonalcoholic Steatohepatitis (fatty liver)

-Hypoventillation Syndrome

-Pickwickian Syndrome – constantly falling asleep

-Hypersomnolence

-Apnea

-Osteoarthritis

-Inflammation

- CRP

- Metabolic syndrome