Dental Medicine

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CHAPTER 1 ANTIBIOTIC PROPHYLAXIS.

YES NO
Previous infective endocarditis Joint replacement
(However, for patients with a history of complication
associated with joint replacement surgery who are
undergoing invasive dental procedures prophylactic
antibiotics will only be considered after consultation
with pts and the orthopedic surgeon.
Prosthetic cardiac valve (transcatheter implanted Mitral valve prolapse (with or without regurgitation) or
prosthesis and homografts) or prosthetic material used thickening valve leaflets
for cardiac valve repair (such as annuloplasty rings and *although mitral valve prolapse is the most common
cords) underlying condition that increase risk for IE.
Cardiac transplant with valvular regurgitation Rheumatic heart disease – heart is permanently
damaged by rheumatic fever
Some congenital conditions All other congenital conditions
- Unrepaired / not fully repaired - Atrial septal defect
cyanotic heart disease (such as - Ventricular septal defect.
palliative shunts and conduits - Hypertrophic cardiomyopathy etc.
used for temporary
stabilization)
- Any repaired congenital heart
defect with residual shunts or
valvular regurgitation
Dental procedures that are eligible when the patients Bicuspid valve disease
are in the yes column Calcific aortic stenosis : calcium deposit form on the
- Manipulation of gingival tissue or periapical region aortic valve.
or perforation of oral mucosa
- Extraction
- Cleaning, SRP
- Fitting orthodontic bands
- Placing TADs (temporary anchorage device),
- Biopsy
- sutures

Cyanotic (5T) Acyanotic


R -> L shunts (deoxygenated blood enters the systemic L -> R shunts
circulation) (less severe compare to cyanotic)
Tetralogy of fallot Atrial septal defect (ASD)
Truncus arteriosus Ventricularr septal defect (VSD)
Transposition of great vessels Hypertrophic cardiomyopathy (HCM)
Tricuspid atresia Patent ductus arteriosus (PDA)
Total anomalous pulmonary vascular return. Coarctation of aorta
*Congenital heart defects may lead to formation of pathological connections called shunts between the left and
right heart chamber.
Most common types of congenital heart defects: VSD – ASD – tetralogy of Fallot - single ventricle defects
For pediatric patients, all of these + repaired congenital heart defects that have been completely repaired with a
prosthetic device, antibiotics are recommended for the first 6 MONTH!!

OTHER (gray areas of antibiotic prophylaxis) – antibiotics can be considered.


Severely immune- HIV with CD4 <200 or AIDS- related opportunistic infection, bone marrow or solid
compromised states organ transplant recipents, neutropenia, cancer chemotherapy or history of head and
neck radiotherapy. , RA (rheumatoid arthritis) taking biological response modifiers or
predinisone >10mg/day, SCID (severe combined immunodeficiency), autoimmune
disease
Hyperglycemic states HbA1c >8% or random blood glucose >200mg/dL
(uncontrolled diabetes)
*Dental procedures such as routine local anesthetic through non-infected tissue, placing RPD/ orthodontic
appliances, orthodontic brackets, shedding deciduous teeth, and even bleeding from trauma to the lips or oral
mucosa, even pts on yes column DO NOT need an antibiotic prophylaxis.

Prescription Writing
FIRST CHOICE Adult Amoxicillin 2g 1hour before tx
Children Amoxicillin 50mg/Kg 1hour before tx
PCN allergy (alternative of Adult Azithromycin 500mg 1hour before tx
clindamycin, due to Children Azithromycin 15mg/kg 1hour before tx
growing concern of
Clostridium difficile)
PCN allergy (NO LONGER Adult Clindamycin 600mg 1hour before tx
RECOMMENDED) Children Clindamycin 20mg/kg 1hour before tx
Non-oral (IV or IM) Adult Ampicillin 2g 30mins before tx
Children Ampicillin 50mg/kg 30mins before tx
* Simple trick to remember: divide the adult dose by 30 ~ 40 to get the pediatric dose.

 Sample questions
 Pts forgets to take antibiotic b4 treatment, what to do
You can ask the patient to take the antibiotics up to 2 hours after the procedure, no need to reschedule.
 What if patients is taking antibiotics for some other condition, but also needs antibiotic prophylaxis
Select antibiotics from different class that the ones the patient are already taking
 Patients has prosthetic heart valve and is coming in to have an occlusal restoration done.
If no clamping of rubber dam and straightforward occlusal restoration, DO NOT NEED antibiotics.
 Orthopedic surgeon recommends antibiotic for prosthetic hip joint, but did not prescribe it
as long as the dentist have on file what the recommended antibiotics is, the dentist himself can prescribe.
 Placing orthodontic bands often causes significant gingival manipulation and bleeding hence the risk of a
bacteremia event.
Placing local anesthetic via a block or infiltration is of less risk due to the size and location of the
puncture. The exception to that might be an intraligamental or PDL injection which I could argue would
require prophylaxis in the appropriate patient.
 Endodontic procedures
If the rubber dam clamp is placed at the line angles of the tooth and does not disrupt the gingival tissue,
then not needed--if however, you anticipate manipulation of the gingival tissues in properly placing the
clamp, then antibiotic prophylaxis may be a good idea.
 amoxicillin is bactericidal and macrolides and lincosamides are bacteriostatic
The ADA specifically recommends a lincosamide if someone is already on amoxicillin. The reason is, while
technically their mechanisms compete with one another, a single dose designed for prophylaxis will not
significantly interfere with the other antibiotic.
 IMPRESSION
Not for alginate impressions, but go if retraction cord is placed as part of the impression procedure

HYPERTENSION

1. Acute: caused by some stimulus, such as physical exertion, anxiety or stress and subsides when the stimulus is
away.
Chronic: remains higher than normal with or without stimuli.
White coat: elevation in a health care setting.

2. Hypertension categories
Blood pressure category Systolic Diastolic Treatment
Normal Less than 120 And Less than 80
Elevated 120~129 And Less than 80 Change in lifestyle
Hypertension stage I 130~139 Or 80~89 1 antihypertension medication
Hypertension stage 2 140 or higher Or >90 2 antihypertension medication
within different classes.
Hypertensive crisis Higher than And/ Higher than 120 Changes in medication or immediate
180 or hospitalization if there are signs of
organ damage.

3. Risk factors: obesity, smoking, lack of physical activity, diet (sodium, alcohol), age, familial history/genetics/
pain/ medications (stimulants, decongestants, immunosuppressants, corticosteroids, contraceptives), diseases
(chronic kidney disease, hyperthyroid, acromegaly sleep apnea).
*Essential/primary hypertension is high blood pressure that is not due to another medical condition. 90~95% of
cases will fall into essential hypertension.

4. Blood pressure reading


① Rest for 5 mins before measuring.
② Length should be 80% arm circumference, width should be 40% arm circumference. Most common error
is caused by wrong cuff size.

③ Record in both arms and use the arm that gives higher reading.

5. Hypertension medication
Category Mechanism Drug names Side effects
a-adrenergic blocker Alpha 1 receptor is Prazosin, doxazosin, Dry mouth, taste
vasoconstrictor and its terazosin. changes and ulcerations
blocker related to hypertension
medications -> can be
relieved by frequent
sips of water, biotin
rinse, etc.
a-adrenergic agonist (a2 Sympathetic NS decreases, Clonidine, guanfacine,
in CNS) which leads to a drop in BP methyldopa.
and heart rate.
Direct vasodilator Act directly on smooth Hydralazine, minoxidill Gingival bleeding
msucle of vessel wall to
open K channels and cause
vasodilation
Peripheral adrenergic Block adrenergic receptor Guanadrel, reserpine.
inhibitors in indirect way
Beta adrenergic blocker. Beta 1receptor is Atenolol, bisoprolol,
responsible for activating metoprolol, propranolol,
heart contracction, timolol.
blocking the receptor will
relax the heart.

Alpha and beta Combination of alpha and Carvedilol, labetalol.


adrenergic blocker bete adrenergic blocker
Calcium channel blocker Blocks calcium influx into Nifedipine, amiodipine, Gingival hyperplasia
smooth muscle cells at the ditiazem, verapamil. (esp. nifedipine) ->
vessel walls to cause surgical excision but
vasodilation. recurrence is common.
Diuretic Blocks reabsorption of Hydrochlorothiazide,
sodium in the kidney, furosemide, torsemide,
decreasing blood volume amiloride, triamterene,
spironolactone.
Direct renin inhibitor Block renin-angiotensin- Allskiren Angioedema : rapid
Angiotensin-converting aldosterone system. Lisinopril, enalapril, swelling beneath the
enzyme inhibitor captopril, fosinopril. skin or mucosa
Angiotensin II receptor Losartan, candesartan, presenting big puffy lips
blocker irbesartan, valsartan

6. Patient management with uncontrolled hypertension


① 120/80
A. Short AM appointments
B. Stress management (exlain procedure, short acting bensodiazepine before the appointment or N2O
during the appoitnment)
C. Slow chair movements (patients who are older adults or diabetics may exp. orthostatic
hypertension)
D. Limit epinephrin to 0.04mg (1 cartridge in 1:50,000 or 2 cartridge in 1:100,000 or 4 cartridges in
1:200,000)
Epinephrine helps LA to work longer and prevent pain, however there are concerns with inadvertent
intravascular injection -> aspirate repeatedly + minimize epinephrin +
E. A void epinephrine retraction cord.
② 160/100 -> all of the above and repeat measurement, monitor BP during procedure (every 10~15mins)
③ 180/120
A. Elective – defer tx
B. Urgent
a. Aysmptomaitic (hypertensive urgency) :call physician b4 procedure and do some convervativ
treatment and referral to doctor.
Such as giving antibiotics or incising and draining an abscess
b. Symptomatic (hypertensive emergency where symptoms include altered mental status, blurred
vision, chest pain,difficulty breathing, dizziness, and numbness in extremeties) –> immediate
referal to ER. (IV BP medication, antibiotics etc)
Obese, diabetic, smoker, high colesterol, older age, reduced functional capacity tip the scale to refer to the
physicians.
DIABETES

1. Diabetes insipidus
① Condition where kidneys are unable to retain water
② Body can’t produce or react to ADH properly. (ADH – antidiuretic hormone )
③ Polydipsia and polyuria
④ Tx: synthetic ADH, low salt diet and or IV fluids.

2. Diabetes mellitus
① Glucose is a high energy reactive molecules that can cause oxidative damage to the endothelial cells that
lie in the blood vessels -> can lead to atherosclerosis -> hypertension/ heart attack/stroke /peripheral
vascular disease
② Damage to capillaries can cause neuropathy (aka diabetic nerve pain), retinopathy and nephropathy.
③ Polydipsia, polyphagia, and polyuria
④ Types
A. Type 1 diabetes (Insulin dependent- autoimmune disease killing the beta cells, thus insulin deficiency
)
a. Juvenile onset
b. Ketone breath (fruity smell) : no glucose inside the cells that needs energy, which burns lipid as
energy producing toxic ketone bodies.
- Ketosis: more mild
- Ketoacidosis: more severe.
c. Require insulin injections.
B. Type 2 diabetes
a. 85~90% of all diabetes
b. Adult onset – obesity, poor diet, lack of physical activity
c. Insulin resistance
d. Most cases can be prevented
e. Last-stage cases require insulin injections.
C. Gestational
a. Due to placental hormones
b. Combination of type I and type II: insulin deficiency + insulin resistance
c. Usually resolves after delivery

3. Diabetes measurements
① Blood glucose
A. Measures with glucometer.
B. Not very reliable as the blood sugars goes up and down
② HbA1c
A. Measures glycosylated hemoglobin
B. The modification is permanent for the entire life span of the RBC and it is stable for 3months.

4. Categories
Types of test Normal Prediabetes Diabetes Comments
HbA1c <5.7% 5,7~6,4% >6,5% Well controlled diabetes are
<7% that is taken within
3month.
Fasting blood sugar test < 99mg/dl 100~125mg/dl >126mg/dl Not eaten or drink except
(impaired fasting water for at least 8 h.
glucose)
Glucose tolerance test 139 mg/dl 140~199mg/dl >200mg/dL Fasting for 8 hours and drink
(impaired glucose drink and check blood
glucose glucose 2 hours later
tolerance) Alternatively, can just take 2
hours after a meal
* Comorbidity occurs when a person has more than one disease or condition at the same time

5. Insulin injections : common prescription combine 1 rapid acting form of insulin right before eating meals with
one long acting form of insulin per day to have a basal effect

Synthetic derivatives
Rapid-acting Lispro, aspart, glulisine
Short-acting Human insulin
Intermediate-acting NPH
Long acting Detemir, glargine

6. Diabetes medications
Antidiabetic category Mechanisms Drug names
Sulfonylurea/ insulin Taken 30mins before meals. Glipizide, glyburide glimepiride
secretagogues. Enhance insulin secretion
(insulin secretion ↑)
Biguanide Taken with meals. Metformin
(↓glucose production) Reduce glucose production by decreasing
gluconeogenesis, uptake from intestine,
glucagon production
Dipeptidyl peptidase-4 Taken once daily regardless of meals Sitagliptin, linagliptin, saxagliptin
inhibitor Inhibits the dipeptidyl peptidase 5 which
(indirectly ↑ insulin breakdowns natural secretagogues, glp-1 and
secretion) gip that stimulate insulin secretion. (indirectly
increasing insulin)
Thiazolidinedione/ GLUT Taken with meals, improve insulin sensitivity Proglitazone, rosiglitazone
(↓blood glucose by esp. for fat and muscle cells.
↑glucose transporters) It produces more glucose transporters.
Alpha-glucosidase inhibitor Just before meals Acarbose, miglitol
(loosing glucose) Delay carbohydrate digestion in the gut,
(blocks the breakdown of polysaccharide into
glucose. Excrete glucose instead of absorbing.
However bacteria can ferment with these
extra glucose and can cause abdominal pain,
nausea, diarrhea.)
SGLT2 are expressed almost exclusively at the Canagliflozin, dapagliflozin,
proximal convoluted tubule in the kidney. empagliflozin.
inhibiting it, urinate glucose -> can feed
bacteria, causing urinary tract

7. Hypoglycemia
① Blood sugar <70mg/dL
② If conscious -> orange juice or glucose tab
③ If unconscious -> call 911 IV dextrose or IM glucagon
④ Signs and symptoms : TIRED (tachycardia, irritability restlessness, excessive hunger, diaphoresis)

8. Hyperglycemia
① Blood sugar;≥126mg/dL for fasting or ≥200mg/dL for postprandial
② Can lead to life-threatening complications like diabetic ketoacidosis or hyperosmolar hyperglycemic state
③ Signs and symptoms

9. Patient management
① Well controlled
A. Short AM appointments
B. Avoid NSAIDS with sulfonylureas -> worsen hypoglycemia
C. Avoid glucocorticoids if possible -> increase blood glucose levels and insulin resistance. Making
diabetes and hyperglycemia worse.
D. Avoid levofloxacin if possible -> lower blood glucose level, and worsen hypoglycemia
E. Normal insulin and meals -> take usual insulin dose and normal meals.
F. Use glucometer prior to dental procedure.
G. Have glucose source available.
H. Slow change in dental chair.
② Poorly controlled
A. Elective: defer tx
B. Urgent
a. Asymptomatic: call DR, remove infection aggressively, and refer to DR.
b. Symptomatic : ER -> intravascular antibiotics and insulin level.
*Brittle diabetes: 200mg/dL of fasting glucose, and hba1c>9%, go for antibiotic prophylaxis before proceeding.

10. Oral manifestations


Dry mouth, burning mouth, delayed wound healing, increased incidence and severity of infections, caries, oral
candidiasis, parotid gland enlargement (compensatory hyperactivity of the salivary gland), gingivitis and
periodontal disease.

Sample questions
1. Patient with diabetes is undergoing general anesthesia, what do you do ?
Severe diabetic does not recommend going to GA.
IV sedation and GA: fasting from midnight the night before the procedure, and using only half the usual
dose of insulin dose, supplementing with IV glucose during the procedure as needed.
2. Patient has trouble remembering if they took their insulin today.
Depend on the Hba1c and the glucometer record prior to the procedure.
3. Ketosis is generally not harmful, and is the presence of higher than normal ketones in the blood and urine
due to the burning of stored fat (can happen in fasting states as well as type I diabetics). Ketoacidosis on
the other hand is potentially life-threatening and is the presence of high levels of ketones AND sugar in
the blood making it too acidic, which can cause serious harm to the liver and kidneys.

ASA CLASSIFICATION

ASA Definition Examples Dental consideration


1 Normal healthy Non-smoking, no or minimal alcohol use No special modification
patient
2 Patient with mild Current smoker, pregnancy, well-controlled Minor treatment modification.
systemic disease hypertension, well-controlled
diabetes(<7%), social alcohol drinker,
obesity, well-controlled epilepsy, asthma,
thyroid dysfunction
3 Patients with severe Stable angina pectoris, history (>3month) Major modifications in treatment
systemic disease MI, CVA, or TIA, exercise induced asthma,
that limits activity end stage renal disease undergoing dialysis,
but is not alcohol abuse or dependence, morbid
incapacitating obesity(BMI≥40) , COPD, poorly controlled
hypertension (140/90 above), poorly
controlled diabetes, poorly controlled
epilepsy, symptomatic thyroid dysfunction.
4 Patient with severe Unstable angina pectoris, recent Elective care is contraindicated, for
systemic disease (<3months) Mi, CVA (stroke) or TIA, ESRD emergency care -> go for non-
that is a constant not undergoing dialysis, uncontrolled invasive treatment such as
threat to life seizures, septic shock, symptomatic medication.
hypertensive emergency. Invasive treatment in hospital env.
5 Moribund patient End stage cancer, end stage organ Only palliative care beyond the
not expected to dysfunction, massive trauma necessary surgery is advised.
survive the next 24
hours.
6 Declared brain-dead
patient whose
organs are being
removed for donor
purposes.

CPR

1. 5As
① Appraise scene safety
② Assess responsiveness: tap the victim on the shoulder and ask if the patient is okay.
③ Alert for help
④ Assess breathing and pulse simultaneously in 10s.
⑤ Activate ems. (emergency medical services) calling 911, AED (automated external defibrillator)

2. 3 possible scenarios for victims who is unresponsive


Pulse Breathing What to do
Yes Normal Monitor until emergency
responders arrive.
Yes Abnormal (asthma attack/ Maintain patent airway and begin
anaphylactic shock/ choking/ rescue breathing
drowned) -> respiratory arrest.
No (cardiac arrest) Abnormal Start CPR
No Normal Extreme rare case but if it happens
start CPR.
*cardiac arrest is electrical problem where the heart is malfunctioning and stops breathing properly. Heart attack is
circulation problem where blood flow to the heart is physically blocked lacking oxygen.

3. CPR guidelines (CAB in order)


① Compression = 30 compressions in each cycle of cpr.
A. Victim faceup on firm surface, compress on the lower half of the sternum between the nipples.
B. Compress 2 inches at a rate of 100~120 compressions per minute.
C. Limit interruptions in chest compressions to less than 10s.
D. Allow chest to fully recoil after each compression

② Airway
A. Head tilt-chin lift position. (Stretches the anterior neck muscles and lifts the tongue away from the
back of the throat.)
B. Use jaw thrust if trauma is suspected when suspecting cervical spine injury.
Placing the fingers of both on either side of the mandible, and apply forward and upward pressure to
slide the mandible into protrusive position, while

③ Breathing
A. 2 breath and each one lasting 1s.
B. Just enough air to make the chest visibly rise

4. AED (automated external defibrillator)


① Designed to stop an abnormally beating heart.
A reset button -> the patient might have undetectable pulse
② Need clean dry skin
③ Turn on and attach pads to UR and LL of chest
④ Use adult pads on children >8 years old.
⑤ Witnessed cardiac arrest -> use AED on arrival.
⑥ Unwitnessed cardiac arrest -> use AED after about 5 cycles/2minutes of CPR.

5. Children/infant CPR
① For children and adult: use carotid artery
For baby: brachial artery -> since infants don't have much of a neck, finding the carotid artery can be
difficult,
② Start CPR immediately if unwitnessed collapsed. (do CPR immediately before checking things like pulse or
breathing)
③ Force: Use 1 hand for small children and 2 fingers for infants
Compress 1/3 depth of chest cavity for children and infants.
④ 15 compressions for every 2 breaths for children and infants if you have 2 rescuers. (unlike 30
compressions 2 breaths in adults), as younger patients are more air hungry.

6. Rescue breathing: for someone with pulse but abnormal breathing. (respiratory arrest)
kid: 1 breath every 3s.
Adult: 1breath every 5s.
*memory trick: kid is 3 words, adult is 5 words.

7. Choking/foreign body obstruction.


① Universal sign: both hands clutched to the throat, but if the person isn’t giving that signal, then inability to
talk, difficulty breathing. Noisy labored breathing and/or frantic pointing to their throat.
A. 1st thing: encourage coughing
B. Otherwise: abdominal thrusts if conscious.
Push the back of dominant hand’s thumb between the xiphoid process and the navel, pushing in and
up (J)
② Infants 5 back slaps followed by 5 chest thrusts for infants.
③ If unconscious, check the mouth (finger sweep if visible and obtainable) before delivering breaths.
④ Brain can only survive for 6mins without oxygen.

COPD and Asthma


COPD

1. COPD(chronic obstructive pulmonary disease): most COPD patient may exhibit both of chronic bronchitis and
emphysema
① Chronic bronchitis (blue bloater)
A. Chronic inflammation in the airways – producing too much mucous.
B. Difficult for the patient to breathe BOTH in and out.
C. Cause: cigarette smoking. Air pollution and dust or toxic gases can also contribute.
D. Diagnose: daily productive cough for 3month or more in at least 2 consecutive years.
E.
Main S/Sy
a. Chronic productive cough with lots of sputum
b. Noisy chest – Rhonchi and wheezing.
c. Normal chest xray
d. Elevated hemoglobin, peripheral edema, cyanotic and tends to be overweight.
② Emphysema (pink puffers)
A. Enlarged alveoli (involves only the alveoli)
B. Difficulty in Expiration
C. Cause: smoking, exposure to air pollution, marijuana smoke, rarely AAT deficiency –related
pulmonary emphysema.
Damages the lung epithelium releasing inflammatory mediators and enzymes (elastase) -> loosing
elastic recoil.
D. Diagnose: permanent enlargement and destruction of airspaces distal to the terminal bronchioles.
E. Main S/Sy
a. No much cough or sputum with quiet chest
b. Barrel shaped chest (due to over inflated lungs -> flattened diaphragm, smaller heart)
c. Weight loss due to work of breathing
d. Severe dyspnea.
e. Pursed-lip breathing.

2. Diagnostic aids and supplements


① Spirometer: measures amount of air person can breathe out.
A. FEV1(forced expiratory volumes in 1s)/FVC (forced vital capacity) <70% is COPD diagnosis.
B. Stages
Stage1 (mild) ~ stage 4 (severe)
② Pulse oximeter: measures percentage of Hb saturated with oxygen. 95~100% is normal.
③ Arterial blood gas measurement
④ Chest xray
3. COPD medications : slowing progression or manage the disease.
① Anticholinergics –> bronchodilators
A. Reduce mucus secretion and relax smooth muscle to open up the airway by blocking acetylcholines
B. Ipratropium and tiotropium.
② Beta –adrenergic agonists -> bronchodilators.
A. Relax smooth muscle of the airways by increasing C-amp levels
B. Epinephrine, isoproterenol, albuterol, indacaterol.
*Anticholinergic and beta-adrenergic agonists are commonly used in combination, as it is from different class of
drug and allows lower doses but same effects.
③ Corticosteroids
Fluticasone (inhaled), predinisone (oral)
④ Phosphodiesterase inhibitors- Theophylline (a last resort, many side effects)

*memory tips: ABCD, and the strategy of prescribing the drugs follows the exact same order.
 Stage 1 COPD starts with anticholinergic
 Stage 2 COPD adds long-acting beta-adrenergic
 Stage 3 COPD adding corticosteroids.
 Stage 4 COPD using phosphodiesterase inhibitors.

4. Patient considerations for COPD


① Well controlled
A. Encourage smoking cessation -> nicotine replacement and bupropion therapy.
B. Avoid pulmonary irritants -> isolation and suction.
C. Semisupine or upright chair position -> prevent difficulty breathing.
D. Bilateral blocks such IAN or greater palatine block can cause unpleasant airway constriction feeling,
avoid it whenever possible.
E. Avoid rubber dam as it can also constrict breathing ability.
F. Avoid narcotics and barbiturates (respiratory depressants)
G. Avoid macrolides (e.g erythromycin) and ciprofloxacin with patients taking theophylline.
These antibiotics can reduce the metabolism of theophylline and can cause toxicity -> nausea,
vomiting, insomnia, headache, arrhythmia, and convulsion
* Not all seizures(epilepsy) are characterized by convulsions. Convulsions involve uncontrollable shaking, but if you
have a seizure you can simply feel confused without a physical reaction.
H. Avoid nitrous oxide -> might accumulate at the airspaces
I. Use general anesthesia cautiously.
Patients, who are taking corticosteroids, require supplement procedures due to concern for adrenal
suppression.
J. Low flow O2 (2L/min) if oxygen saturation is <95%
*patients should not be given of O2 as for COPD patients respiratory drive depends on decreased
oxygen, but in emergency cases, oxygen can be given for a very short period till the emergency
episode resolves or to the hospital.
K. Use pulse oximeter.
② Poorly controlled
A. Someone who is symptomatic: shortness of breath at rest, productive cough, upper respiratory
infection or an oxygen saturation <91%.
B. Defer and refer to medical doctor.
* For COPD patients, look out for cardiovascular comorbidities, which is very common in COPD patients.

5. Oral manifestations of COPD


① Halitosis, staining, nicotine stomatitis, periodontal disease and oral cancer related to smoking.
② Poor oral hygiene may lead to aspiration pneumonia. (such as bacteria in saliva)
③ Dry mouth due to anticholinergic medication.
④ Stevens-Johnson syndrome linked to theophylline.

ASTHMA
1. Asthma: reversible episodes of breathing difficulty, coughing or wheezing.
① Bronchiolar tissue is sensitive to different stimuli, it is imp. to know what triggers an asthma attack or
flare-up (it can be respiratory infection, cold air, exercise, NSAIDS, and anxiety/stress)
② Pathophysiology: can be smooth muscle spasm/ inflammation of the bronchial mucosa and/or goblet cell
hyperplasia (too many goblet cells) that is seen in chronic bronchitis.
③ Diagnosis: spirometry -> gold standard.

2. Asthma medications: used either for long term control or short-term immediate relief, and combination of
these are usually used to improve lung function
① Antihistamines: blocks histamine receptors.
A. Histamines is responsible for 3 things in the classic allergic response: redness, swelling and itchiness
B. Diphenhydramine, fexofenadine
C. Not prescribed for asthma, but instead for allergies, however if allergies trigger asthma,
antihistamines can be used to help control asthma and prevent asthma attack.
② Beta-adrenergic agonists – just like COPD
For an acute asthma attack, the first line of defense is going to be short-acting bronchodilator like
albuterol via an inhaler or nebulizer. If the symptoms does not improve or worsen, epinephrine subcu.

③ Corticosteroids
A. Inhaled corticosteroids are currently the most effective anti-inflammatory medication for treating
persistent asthma.
B. Prednisone, budesonide, fluticasone.
Combination of corticosteroids and long acting beta-adrenergic agonist, such as formoterol + budesonide =
symbicort. Salmeterol + fluticasone = advair
④ Decongestants: reduce nasal congestion..
A. Pseudoephedrine is an a1 selective agonist (vasoconstrictor), reducing nasal swelling and
inflammation.
B.
Mostly used to treat cold, flu, allergies, or sinusitis. In patients with allergies, it can indirectly manage
the asthma.
⑤ Leukotriene receptor antagonists.
A. Block leukotriene(pro-inflammatory mediatos) that the body releases
B. Montelukast, zafirlukast.

3. Patient considerations for asthma


① Well controlled - Prevent acute asthma attack
A. Stress management such as short acting benzodiazepine, NO2, etc.
B. Asthma medication taken.
C. Have inhaler and Epipen ready.
D. Excellent isolation to minimize tooth enamel dust or any other pulmonary irritants.
E. Avoid NSAIDS as it can precipitate asthma attacks in small populations.
F. Avoid narcotics and barbiturates
G. Use pulse oximeter, and if <95% low flow oxygen (2L/min)
② Poorly controlled -> defer and refer.

4. Oral manifestation of asthma


① Dry mouth due to inhalers.
② Caries
③ GERD – exacerbated by bronchodilators
④ Oral candidiasis – 5% of inhaled corticosteroids in long period of time.
⑤ Enamel defects -> associated asthma children.
⑥ Periodontal disease -> associated with severe asthma adult
⑦ Higher rate of malocclusion (excess overjet, posterior crossbite, high palatal vault) associated with
habitual mouth breathing.

USE OF NO2
YES Contraindications
Dental anxiety COPD - for severe COPD, difficult to get out of the lung,
Also they have respiratory drive triggered by decreased
O2, as NO2 are given alongside with lots of oxygen, can
decrease the patient’s drive to breathe.
Gag reflex Nasal obstruction*
Asthma as long as the patient DO NOT has Multiple sclerosis * for patients with MS, chronically high
symptoms. levels of nitric oxide may have detrimental effects on the
vascular health of the brain
Pregnancy (1st trimester esp.)
NO2 can readily enter fetal circulation and can be toxic to
cells undergoing mitosis.
Psychiatric disorder” – consult first with psychiatrist.
Communication barrier – NO2 administer should be done,
confirming with the patient that they are at the right
stage.
Otitis media – avoided in children who have otitis
mediadue to pressure buildup and gas diffusion
Sickle cell disease – regular use of NO2 can interfere B12
metabolism. Sickle cell disease have B12 deficiency.
*relative contraindication

O2
Okay to use: Relative contraindications (also contraindicated for
NO2 as O2 is administered in large amount)
Humidified low flow oxygen can be provided to Bleomycin (chemotherapeutic agent) that can
COPD to help alleviate unpleasant airway damage the lungs
Asthma patients. Paraquat poisoning : toxic herbicide

STEROIDS AND ADRENAL INSUFFICIENCY

1. Steroids: are derived from cholesterol.


① Secreted by a steroid gland (adrenal cortex, testes, ovaries, placenta)
② Categories
A. Corticosteroids – secreted from adrenal cortex.
a. Glucocorticoids = cortisol
b. Mineralcorticoidds = aldosterone.
B. Sex steroids
a. Progestogens = progesterone
b. Androgens = testosterone
c. Estrogens = estradiol

2. Cushing’s syndrome – elevated cortisol level.


① Cause
A. Endogenous: due to benign tumor
a. Primary: ↑ cortisol at adrenal cortex.
b. Secondary: ↑ACTH at anterior pituitary. = Cushing disease
c. Tertiary: ↑CRH at hypothalamus.
B. Exogenous: due to taking too many glucocorticoids.
a. Most common form of cushing syndrome
b. If a patient has taken 20mg of exogenous cortisol for at least 2 weeks within the last 2
years, suspect adrenal cortex function SUPPRESSION
c. 20mg Exogenous cortisol (is usually administered as hydrocortisone) = 5 mg prednisone
= 0.75 mg dexamethasone.
② Symptoms
A. Moon facies: round, red and full face
B. Buffalo hump: collection of fat between shoulders
C. Central obesity: protruding abdomen and thin extremities.
D. Hypertension and hypercalcemia
E. Mood changes and chronic tiredness.

3. Addison’s disease/ adrenal insufficiency


① Cause - Endogenous: due to immune-mediated destruction of tissue
A. Primary↓cortisol, ↑ACTH to compensate for the decreased cortisol
B. Secondary
C. Tertiary.
② Symptoms
A. Hyperpigmentation: bronzing, brown macular pigmentations also on the lips and mucosa.
B. Immunocompromised.
C. Fatigue.
D. Muscle weakness
E. Weight loss

4. Addisonian Crisis/ adrenal crisis/ acute adrenal insufficiency


① Corticosteroid levels are critically low.
② Primary cause: autoimmune destruction of the adrenal gland.
Secondary cause: atrophy due to constant inhibition of exogenous steroids.
③ Stresses lead to hypotension, vomiting, and possibly lethal hypovolemic shock.
④ Solution: activate 911, monitor vital signs, start IV saline solution (to help with hypotension,
hypovolemia) and give IV hydrocortisone.

5. Patient considerations for adrenal insufficiency- primary goal: prevent addisonian crisis.
① Well controlled
DO DON’T DO
Stress management GA generally contraindicated.
Increases glucocorticoid demand and could render
adrenal insufficient patient susceptible to adrenal
crisis.
Epinephrine use. Avoid phenobarbital, midazolam, phenytoin,
rifampicin (antibiotic for tuberculosis),
ketoconazole, fluconazole, imipramine
(antidepressant), and etomidate. (GA)
Monitor BP during procedure (<100/60mmHg
consider fluid replacement or steroid
supplementation)
Supine chair position if hypotension
Provide adequate steroid supplementation
Routine dental tx does not require any, but
stressful surgery would require preoperative (or
possibly postoperatively as needed)
② Poorly controlled – symptomatic who have uncontrolled or undiagnosed adrenal insufficiency

BISPHOSPHONATES

1. Bisphosphonates: prevent bone resorption by inducing osteoclasts to undergo apoptosis.


① Other effects
A. Increases bone density
B. Slows tooth movement: lengthen ortho. tx time.
C. Impairs bone healing
D. May lead to osteonecrosis.
② Uses
A. Osteopenia
B. Osteoporosis
C. Fibrous dysplasia
D. Hyperparathyroidism
E. Paget’s disease
F. Multiple myeloma
G. Metastatic bone lesions of various cancers.
H. Malignancy associated hypercalcemia.
I. Osteogenesis imperfect
J. Gaucher’s disease
K. Rett’s syndrome.
③ Pharmacokinetics
A. Oral (2%)has much lower bioavailability than IV(100%).
B. A lot of the oral drugs are lost
a. Bisphosphonate has high binding affinity to calcium, iron and magnesium in the
intestinal tract. Esp. orange juice, milk or antacids.
b. Excreted from kidney
C. The drug is attracted to hydroxyapaptite binding sites on bony surfaces undergoing active
turnover.
D. Concentrates higher in trabecular bone than cortical bone.
E. Half-life can vary from 10 hours for iabndronate to 10 years for alendronate
④ Pharmacodynamics/ mechanism of action.
A. Synthetic analogue of inorganic pyrophosphate that has high affinity for calcium → It gets
integrated and sequestered in bone, when osteoclasts resorb bone impregnated with the
drug → impairs the osteoclasts and induce apoptosis.
B. Reduces function and number. (decrease the development and recruitment of the
osteoclasts and promote their apoptosis reducing the numbers )
C. When given long term, also decrease osteoblast activity, due to coupling effect through
intracellular mediators bet. osteoclasts and osteoblasts.
→causing impaired bone healing due to decreased bone and capillary formation
2. Medications: – nate
Generic name Brand name Type Use Relative Comments.
potency
Etidronate Didronel Oral Paget’s disease 1
Tiludronate Skelid Oral Paget’s disease 10
Clodronate Bonefos Oral/iv Osteoporosis 10
Pamidronate Aredia IV Bone metastases 100
Multiple myeloma
Alendronate Fosamax Oral Osteoporosis 1000
Risedronate Actonel Oral Osteoporosis 5000
Zoledronate Zometa IV Bone metastases 10000
Multiple myeloma
*From pamidronate down to zoledronate, have –N side group increase potency of the drug by inhibiting
farnesyl pyrophosphate synthase. (the enzyme crucial to the production of cholesterol and lipids causing
osteoclast apoptosis)

3. Medication-related osteonecrosis of the jaws.


① Medications such as bisphosphonate, denosumab, or bevacizumab. (-mab, monoclonal
antibody that is used to treat osteoporosis, treatment induced bone loss, metastases to bone.
these are anti-angiogenic)
② Osteonecrosis: Dead bone due to lack of blood supply (due to the anti-angiogenic properties of
these drugs)
③ May start asymptomatic, but progresses to dehiscence with paresthesia or pain.
④ More common in mandible (less vascular), posterior. (constant masculatory forces)
(Most commonly on the lingual posterior near the mylohyoid ridge and on the mandibular tori)
⑤ Higher dose, more frequent administration, longer duration and IV administration have higher
risk and higher severity of MRONJ.
 HIGH-YEILD FACTS - Risk factors of MRONJ
 Concomitant use of estrogen or glucocorticoids
 Over 65 y.
 Only the more portent nitrogen containing bisphosphonates tend to cause MRONJ
 Jaw bones are more at risk, due to the constant micro-trauma caused by continuous mastication.
⑥ DIAGNOSIS of MRONJ
A. Current or previous tx with a causative medication
B. Exposed bone in the maxillofacial region that has persisted for more than 8w.
C. No history of radiation therapy to the jaws – Osteoradionecrosis.
⑦ Prevalence: average case appears 1 year after administration
A. IV -> 1% spontaneous, 10% after extraction
B. Oral -> 0.1% spontaneous 0.5% after tooth extraction.
⑧ Patient considerations for MRONJ
 Comprehensive exam, establish excellent periodontal health, extract all non-restorable/
questionable teeth, eliminate dental caries, and maintain excellent oral hygiene before patient
starts high risk drugs.
A. Prevent at risk patient from developing MRONJ
a. Treat all active infections such as sinus tracts, purulent periodontal pockets, or active
abscesses.
b. Nonsurgical preferable to surgical approaches
c. If surgery are required, go for conservative surgical technique. Ex) for multiple tooth
extraction, have 2month in between those extractions.
d. Antibiotic coverage such as Amoxicillin 500mg for a week.
e. Consider alveolectomy – eliminate sharp edges.
f. Drug holidays*
- Can be considered in patients who have IV bisphosphonates for 1 y or more, or an
oral bisphosphonates for 5 years or more.
- Consult physician.
- 3 month prior to the dental surgery, and recontinue after the surgery with a less
potent non-nitrogen containing bisphoshphonates
B. Treatment for active MRONJ
a. 0.12% chlorhexidine rinse.
b. Local surgical debridement*
- Can be done if the MRONJ is from oral bisphosphonate but not recommended
from IV.
- It can help prevent trauma to soft tissues by removing the sharp edges of the
bone.
c. Hyperbaric oxygen*
d. Aggressive use of systemic antibiotics
- Most of the microbes involved in the MRONJ are sensitive to penicillin, also
metronidazole, clindamycin, doxycycline, and erythromycin are effective as well.
- Depending on the symptoms it may require combination of antibiotics, and even IV
antibiotics
e. Irrigation with local antibiotics*
*Still have insufficient evidence
 Routine dental care with a local anesthetics can and should be performed.

INR AND BLEEDING

1. Hemostasis
① Vascular : vasoconstriction
② Primary: Platelet plug
③ Secondary: coagulation = fibrin clot.
④ Fibrinolytic

2. Vascular wall defects: rarely have severe bleeding episode after a tooth extraction.
① Disease: Both of Marfan syndrome and Ehlers-danlos syndrome affects connective tissue, which
in turn affects vascular wall.
A. Marfan syndrome
B. Ehlers –danlos syndrome
C. Osler –weber –rendu syndrome/ hereditary hemorrhagic telangiectasia: affects blood
vessels more directly.
② Management
A. Consult with hematologist
B. Minimally invasive dentistry
C. Local hemostatic measures
D. Avoid NSAIDs.

3. Platelet pathway : end result is platelet plug tethered to the endothelium via vWF
① Steps (3A)
A. Adhesion: Damage on the endothelium layer of the blood vessels causes the release of von
Willebrand factor, which attaches to circulating platelets via GP1b.
B. Activation
Binding to the vWF activates the platelets; the platelets secrete thromboxane A2 and
Adenosine diphosphate (ADP), which also activate other platelet. -> positive feedback loop.
C. Aggregation
Activated platelets express glycoprotein IIb/IIIa, and the platelets stick to each other.
The fibrinogen also sticks to the platelet by GP IIb/IIIa
② Platelet disorders.
A. Von willebrand disease: vWF deficiency : affects both platelets and coagulation
Most common congenital bleeding disorder(1%)
The vWF also act as a carrier for factor VIII
B. Thrombocytopenia: low platelet count.
a. Can be drug induced (drugs that are toxic to the bone marrow) or immune mediated
disease (leaukemia, HIV), other disease.
b. Normal: 150,000~450,00 platelets/uL
Increased clinical bleeding : <50,000
Spontaneous: <20,000
③ Antiplatelet medications
A. Used in patients who have history of heart attack, coronary artery stent and etc.
B. Aspirin
a. Inhibits Cox-1 enzyme to prevent synthesis of thromboxane A2.
b. Irreversible. *other NSAIDS are reversible.
C. Clopidogrel : competes with ADP
D. Abciximab: bind to the glycoprotein IIb/IIIa complex
④ Platelet testing
A. Quantity Platelet count
B. Both: Ivy bleeding test – used to screen platelet function and platelet number -> unreliable
and no longer used.
C. Quality
a. Peripheral blood smear: cell morphology
b. Platelet aggregation test
c. Platelet function analyzer (PFA-100): measures platelet-dependent coagulation under
flow conditions. Better than bleeding test but unfortunately it’s not sensitive to rule out
mild bleeding disorders. -> not recommended
⑤ Patient considerations: same as vascular wall defects.

4. Coagulation
① Coagulation factors
② Steps
A. Extrinsic
a. Damaged endothelium expresses tissue factoer (III)
b. Quicker than intrinsic pathway
B. Intrinsic
a. Hageman factor: trauma can expose collagen on the inside of blood vessels which
activates factor 12.
b. Memory tip: 9, 8 and 7 are on the same line.
C. Both:
a. Factor 1/ fibrinogen: the most imp. factor and also sticks to GPIIb/IIIa.
b. Factor II activates factor I and XIII (small and biggest number)
Activates V, VII, VIII, XI and XIII
Speed everything up

③ Clotting factor defects


A. Von Willebrand disease : vWF deficiency
B. Hemophilia A
a. Factor 8 deficiency(most common among the hemophilia)
b. Autosomal recessive
c. 80% chance the patient might develop hematoma after IAN block injection without
prior factor 8 infusion. -> can be fatal if it accumulates in mediastinum and compromise
airway. So stick with local infiltration in mandible.
C. Hemophilia B: factor 9 deficiency *call 911, all hemophilia affects
D. Hemophilia C: factor 11 deficiency intrinsic pathway
E. Vitamin K deficiency
a. Most common acquired coagulation disorders.
b. Factors II, VII, IX, and X are all made in liver and require vitamin K for their synthesis.
F. Liver disease : except for III and IV (calcium), all coagulation factors are made in liver.
(fibrinogen, prothrombin, factor V, VII, IX, X, XI, XII, as well as protein C and S)
*Protein C and S: are 2 anticoagulation proteins that inactivate coagulation factors Va and VIIIa in the
coagulation cascade.

④ Anticoagulants
A. Used in patients such as Reducing the risk of heart attack, patients with atrial fibrillation,
prosthetic heart valves, history of Deep venous thrombosis blood clots
B. Different from anti-platelet, as it affects coagulation not platelet pathway.
* both anticoagulants and anti-platelets are blood thinners.
C. Medications
Anticoagulants drug name Mechanism of action
Warfarin Blocks reduction recycling of vitamin K (blocking factors II, VII, IX and X)
Heparin Pulls thrombin and anti-thrombin together (blocking factor II)
Apixaban (ellquis) Inhibits factor Xa
Dabigatrin Directly binds to thrombin (factor IIa) – direct thrombin inhibitors
⑤ Coagulation testing
A. Activated partial thromboplastin time (aPTT)
a. Measures no. of seconds a clot to form in a sample of blood after certain reagents are
added to it.
b. Test for intrinsic system and common pathway.
c. Best single screening test -> vonWillebrand disease, hemophilia’
d. Normal range: 25~35s.
e. Shorter time: clotting spectrum, longer time: bleeding spectrum.
B. Prothrombin time (PT/INR)
a. Used almost exclusively for patients on WARFARIN.
b. INR
⑥ Patient considerations for INR
A. For all patients taking warfarin:
a. Avoid NSAIDS, so acetaminophen with or without codeine is suggested instead.
b. Avoid metronidazole, erythromycin and broad spectrum antibiotics that can potentiate
the anticoagulation effect of warfarin.
c. Avoid herbal supplement can potentiate the anticoagulant effects and enhance the
bleeding.
d. Barbiturates and steroids antagonize the action of warfarin.
e. Local hemostatic measures.
- Compressive packing
- Extra sutures
- Topical thrombin
- 4.8% tranexamic acid mouthwash
* Clinically, it is better to stay on the medications, thus it is benefit for the patient to bleed rather than
to clot, as it can be life-threatening.
However if a major oral surgery is planned, where significant bleeding is likely, only then would
modification of warfarin therapy with medical consultation be potentially necessary.
B. Patients INR 2.0~3.0
a. Great therapeutic range for atrial fibrillation, DVT
b. Proceed with any dental tx and no bleeding concerns for patients in this range.
C. Bet. 3.0~3.5
a. Desired for prosthetic heart valve
b. Simple surgery -> continue with tx.
c. Bit high for major complex surgery -> defer tx and refer to medical doctor.
Changing warfarin dose temporarily, and retesting INR before proceeding with dental
care.
D. >3.5: refer to medical doctor.
After an adjustment is done, it will take 3~5 days for the desired reduction to occur, which should be
confirmed by a new INR. The dental procedures should be scheduled within 2 days after that new INR,
and after the procedure is done, and there are no complications -> resume the warfarin dose.

5. Oral manifestations of bleeding disorders.


① Spontaneous gingival bleeding
② Petechiae and ecchymoses (sometimes can also see jaundice, pallor and uclers)
③ Hemarthrosis of TMJ -> bleeding into jaw joint, linked specifically to hemophilia.
SUBSTANCE ABUSE

1. Substance abuse
① Diagnosis of substance abuse: recurrent use of a substance over the past 12moth with
subsequent adverse consequences.
② Dependence: uncontrollable need for use of a substance despite adverse consequences.
Requires tolerance and withdrawal as its diagnosis.
A. Tolerance: need for increased amount of a substance to achieve the desired effect or
B. Withdrawal: group of symptoms that emerge upon abstinence of a habitually used
substance.
Symptoms: irritability, insomnia, difficulty concentrating, etc.

*Almost all the drug disrupts the reward systems in the brain primarily dopamine circuits in the brain.

2. Marijuana
① Manufactured from cannabis plant
② Most commonly used illicit drug.
③ Delta-9-tetrahydrocannabinol (THC) is the major psychoactive ingredient.
④ Can be inhalation (20~30mins peak),oral (2~3 hours)
⑤ Primary effects are pain reduction, seizure alleviation and altered perception
⑥ Overdose can cause anxiety, paranoia and delusions.
⑦ Can destabilize schizophrenia and may cause psychosis in some people.
⑧ Abuse or chronic use can lead to chronic bronchitis, airway obstruction via smokoing,
orthostatic hypotension
* Memory tip: THC (Tachycardia, Hallucination and Chronic bronchitis)

3. Opioids – narcotics (↓CNS) -> hard on brain and lungs.


① Come from poppy plant
② Natural opioid analgesics include morphine and codeine
③ Can be administered orally or IV (associated with contaminated needles that can spread
diseases like Hepa B, Hepa C and HIV)
④ Inhibits the ascending pathways of the CNS, via mu opioid receptors
⑤ Primary effect: pain reduction, modest sedation and euphoria.
⑥ Abuse can lead to pupil constriction and respiratory depression.
⑦ Naloxone (Narcan) is an reversal agent. (no overdose effect, it can be safely administered to all
people, No effect on those who do not have opioids overdose)
⑧ Prescription drug monitoring program (PDMP) is recommended and DEA number required to
prescribe.
Percocet: combination of oxycodone and acetaminophen
Vicodin: combination of hydrocodone and acetaminophen

4. Cocaine (↑CNS)
① Manufactured from coca leaf. Act as an stimulant
② Local anesthetics and potent vasoconstrictor. (-caine )
③ After alcohol it is the leading drug of abuse, in terms of frequency of hospital admissions, and
domestic violence.
④ Oral, intranasal, topical (on mucous membranes), I administration or inhalation.
⑤ Blocks the reuptake of dopamine, serotonin and norepinephrine. -> euphoria.
⑥ Side effect : tough on heart (tachycardia, arrhythmias, hypertension, heart attack or stroke. ),
pupil dilation,
 If the cocaine is taken together with opioids, it can mask the appearance of the overdose.

5. Amphetamines (↑CNS)
① Manufactured synthetically in the lab.
② Oral, intranasal, IV administration or inhalation.
③ Cause release of dopamine stores into the synapse. (more intense and long lasting than
cocaine)
④ Used clinically for attention deficit hyperactivity disorder(ADHD) , narcolepsy, weight loss, and
depression.
⑤ Abuse or overdose can lead to tachycardia, hyperactivity, dysphonia(difficulty speaking),
headache, confusion and acute schizophrenia.
 Adderall is one of the amphetamine drug that is used for ADHD, narcolepsy
 Narcolepsy is a chronic sleep disorder characterized by overwhelming daytime drowsiness and sudden
attacks of sleep.

6. Sedative-hypnotics (↓CNS)
① Used to treat anxiety and seizures.
② Benzodiazepines are most frequently abused sedative hypnotics, followed by barbiturates are
the 2nd most.
③ Longer use or higher dosage is more likely to lead to dependence.
④ Withdrawal symptoms include nausea and vomiting, weakness, tachycardia, sweating. Anxiety,
tremor, loss of appetite, tinnitus, and delirium (mental state in which you are confused,
disoriented, and not able to think or remember clearly)

7. Alcohol (↓CNS)
① CNS depressant but has temporarily stimulatory effect.(such as tachycardia)
② Chronic use can lead to cognitive impairment, distress, liver cirrhosis, hepatic encephalopathy,
GI bleeding, cardiac arrhythmia and ascites
③ Withdrawal includes loss of appetite, tachycardia, anxiety, insomnia, delirium tremens,
impaired attention and memory.
④ Withdrawal can be managed by adequate nutrition and rest and benzodiazepine/beta blocker
in gradually decreasing doses.
 Hepatic encephalopathy or portal-systemic encephalopathy represents a reversible impairment of
neuropsychiatric function associated with impaired hepatic function
 Delirium tremens (DTs) is a rapid onset of confusion usually caused by withdrawal from alcohol.
(shaking tremors and hallucination)

8. DEA scheduling (schedule 1: highest abuse and dependence potential)


Schedule Definition Drug example Rx
I No currently accepted Heroin, LSD, cannabis, ecstasy Cant prescribe
medical use, illegal, high (Marijuana are still in schedule I and
potential for abuse doctors can’t prescribe it but can
recommend it for medicinal use in
states that are legalized.)
II High potential for Vicodin (<15mg hydrocodone per Written Px, no refills
abuse/ dependence dosage unit), cocaine, without written script.
methamphetamine, methadone,
Hydromorphone, Meperidine,
oxycodone, fentanyl, Adderall, Ritalin
III Moderate to low Tylenol #3 (<90mg codeine per dosage Does not need written
potential for unit), ketamine, anabolic steroids, and can have refills
abuse/dependence testosterone
IV Low potential for Benzodiazepines (Xanax, Valium, Does not need writte
abuse/dependence Ativan), Ambien, Tramadol and can have refills.
V Very low potential for Robitussin (<200mg codeine per dosage Mostly on the
abuse/dependence, unit), Lomotil, Motoren, lyrica, counter.
limited quantities of Parepectolin.
certain narcotics

9. Patient considerations for substance abuse.


① Marijuana abusers have higher risk of squamous metaplasia, and in general oral cancers.
② Cocaine and methamphetamine.
A. Waiting period: at least 6~8 hours after their last dose of illicit drug before having any
dental tx.
B. Local anesthetics with epinephrine MUST NOT be used for 24 hours. -> because both of
these drugs increase the power of epinephrine leading to hypertensive crisis, stroke or
heart attack.
C. Avoid epinephrine retraction cords.
D. Monitor the BP and Pulse.
③ Alcohol
A. Brief advice or discussion are recommended by dentist
B. Beware excessive bleeding.
C. Oral cancer screening. -> Alcohol, marijuana, tobacco are strong risk factors for the dev. of
OSCC.
D. Avoid acetaminophen. Both can affect the liver alone but will exponentially affect the liver
when combined.
10. Oral manifestations
① General abuser
A. Oral neglect -> poor oral hygiene
B. Missing dental appointments
C. Increased risk of bloodborne infections due to IV (Hep B, Hep C, HIV)
② Marijuana
A. Xerostomia -> caries, periodontal disease, candidiasis.
B. Leukoplakia
C. THC, principal psychoactive constituent of cannabis, is an appetite stimulant, high sugar
diet.
D. Immunosuppressant, chronic inflammation of the oral mucosa with hyperkeratosis->
leukoplakia -> OSCC.
E. Leukoenema: non-malignant bluish, grey or white appearance of mucosae, particularly the
buccal mucosa. -> more common in marijuana abusers.
③ Opioids
A. Dental phobia
B. Caries
C. Periodontal disease
D. Candidiasis
E. Bruxism.
 Intraoral cocaine can cause gingival recession and facial erosion may be due to rubbing of the
powder over those surfaces.
④ Methamphetamine
A. Xerostomia
B. High sugar diet
C. Bruxism
D. Vomiting and gastric regurgitation -> lead to rampant caries, tooth wear and periodontal
disease.
⑤ Alcohol
A. SCC
B. Glossitis – nutritional deficiency
C. Candidiasis
D. Spontaneous gingival bleeding, petechiae, and ecchymoses. -> vitamin K deficiency
E. Sialadenitis - > bilateral painless enlargement of the parotid gland -> frequent finding in the
liver cirrhosis.

Example questions
Q1: what to do if a patient has severe pain and an opioid is indicated.
- 10mg of hydrocodone every 6 hours for 24`48 hours (somewhere bet. 4~8 capsules)

Q2: best pain medication for a patient with history of opioid abuse
- Combination of NSAIDS and acetaminophen
Q3: what to do if a dental staff member is revealed to be a substance abuser.
- consult and ask for the help of the consultant, suspend the work if not controllable. For dentist, license
suspension, and jail.

THYROID DISEASE

1. Thyroid gland produces 3 hormones


① Follicular cells: produce thyroid hormone -> influence metabolism, temp, heart rate, growth
and maturation.
A. T3 : trilodothyronine
B. T4: thyroxine
② Parafolicular/C-cells: produce calcitonin which decreases serum calcium

2. Epidemiology
① 12% of population
② More common in females
③ Most common in late teens to 40s
④ Thyroid nodules are found in 5% of adult populations and have 1~5% incidence of cancer
⑤ 5 y survival rate is 97%

3. Hyperthyroidism/ thyrotoxicosis
① Endogenous: due to benign tumor, immune-mediated stimulation (Graves disease), etc.
A. Primary : ↑T3,T4 at thyroid gland
B. Secondary: ↑TSH at ant. pituitary
C. Tertiary: ↑TRH at hypothalamus
② Dental related: adverse interaction with epinephrine, cardiac arrhythmias, congestive heart
failure, and thyrotoxic crisis or thyroid storm.
③ Graves disease
A. Most common
B. Autoantibodies are produces that target the TSH receptor and stimulate the release of
thyroid hormone.
C. Sy/S: fatigue, nervousness, heat intolerance, weight loss, tachycardia, exophthalmos,
goiter.
D. Epinephrine can trigger thyrotoxic crisis.
④ Thyrotoxic Crisis/ thyroid storm
A.Associated with untreated hyperthyroidism.
B.T3,T4 are critically high, and any amount of stress can trigger a severe reaction with
symptoms such as tachycardia, atrial fibrillation, sudden fever, sweating, and loss of
consciousness and coma.
C. Management
a. Activate EMS, monitor vital signs, apply wet or ice packs -> IV hydrocortisone/ oral
dexamethasone (inhibit release of thyroid hormone) -> give IV glucose, and administer
prophylthiouracil (anti-thyroid medications)
b. CPR is sometimes needed depending on the severity
*Having a sudden fever can help distinguish thyrotoxic crisis and hyperthyroidism.
⑤ Oral manifestations
A. Accelerated tooth eruption.
B. Lingual thyroid
C. Osteoporosis
D. Caries
E. Periodontal disease
F. Propylthiouracil can lead to oral ulcerations, sialoliths, and necrotizing gingivostomatitis.

4. Hypothyroidism
① Cause
A. Most common cause in underdeveloped countries is iodine deficiency
B. Most common cause in developed countries is Hashimoto’s thyroiditis where
antithyroglobulin antibodies attack the thyroid gland.
② S/Sy: weight gain, cold intolerance, bradycardia, goiter, Wormian bones.
③ Cretinism: hypothyroidism in children.
Severely stunted physical and metal growth
④ Myxedematous coma
A. Critically low T3 &T4
B. Stress leads to bradycardia, severe hypotension, low body temp. (more common in winter)
C. Management
a. Activate EMS, monitor vital signs, cover with blankets, administer IV levothyroxine and
hydrocortisone, and give IV glucose.
b. CPR when needed
⑤ Oral manifestations
A. Delayed eruption of teeth
B. Macroglossia
C. Xerostomia
D. Radiating pain -> if hashimoto thyroiditis is the cause

5. Thyroid cancer
① Men 2 involves multiple neuromas, medullary thyroid carcinoma and pleochromocytoma of the
adrenal gland.
② Kidney is the most common site of origin for metastasis to the thyroid gland.

③ Oral manifestations (thyroid cancer)


A. Multiple neuromas (MEN 2B)
B. Radiation related complications
a. Xerostomia
b. Sialadenitis
c. Loss of taste
d. Mouth pain
e. Caries

6. Thyroid medications
① For hyperthyroidism
A. Thyroid peroxidase inhibitors : thyroid peroxidase is a key enzyme in thyroid hormone
biosynthesis.
a. Propylthiouracil
b. Methimazole
c. Carbimazole (prodrug which will be converted to methimazole)
B. Radioactive iodide (RAI): kill thyroid cells via raidaiton -> for thyroid cancer and
hyperthyroidism.
② For hypothyroidism
A. Lyrothyronine: T3 hormone replacement
B. Levothyroxine: T4 hormone replacement longer half-life and less expensive – go to drug for
treating hypothyroidism.

7. Patient considerations for thyroid disorders.


① For all patients: palpation of thyroid gland should be done as basic head and neck evaluation.
② Hyperthyroid
A. Avoid epinephrine (limit to 2 carpules) and gingival retraction cord for poorly controlled
and untreated thyrotoxic patients -> can trigger cardiac issues.
B. Limit NSAIDS : increase the amount of thyroid hormone (esp. T4) making it harder to
control.
③ Hypothyroid
Avoid narcotics, barbiturates and sedatives

PARATHYROID DISEASES

1. Parathyroid glands
① Located on the posterior surface of the thyroid gland. (2 on one side)
② Made up of 2 types of cells
A. Chief cells: produce parathyroid hormone -> regulating amount of calcium
a. Bone: Binds to the osteoblasts ↑RANKL↓OPG(osteoprotegeran) which activates
osteoclasts.
b. Kidney: ↑calcium reabsorption at the distal tubule and collecting duct and
↓phosphate reabsorption
c. Intestines: ↑vitamin D
B. Oxyphil cells

2. Calcium
① Calcitonin secreted by the thyroid gland, puts the calcium back into the bone. (*tones down the
calcium level in the blood)
② FGF23(fibroblast growth factor 23)
Produced in bone cells which reduce serum phosphate level and calcium. (opposite of vitamin
D)
 FGF23 acts on the receptor complex in the parathyroid glands to decrease parathyroid hormone
(PTH) gene expression and PTH secretion through activation of the MAPK pathway.

3. Hyperparathyroidism
① Classification
A. Primary: most common, parathyroid gland tumor -> Leading to hypercalcemia
Treated by surgical removal of the tumor
B. Secondary: insufficient vitamin D or chronic renal failure -> initial hypocalcemia
Treated by supplementation of vitamin D and treating the chronic renal failure.
C. Tertiary: chronic secondary hyperparathyroidism. -> leading to hyperplastic gland, even if
the secondary is treated, the baseline parathyroid hormone is higher than it should be.
Treated by removal of hyperplastic tissue.
② Manifestation of hyperparathyroidism in dental patients -> hypercalcemic patient
A. Kidney stones, painful bones (osteoporosis), abdominal groans(constipation, nausea and
vomiting), and psychiatric moans(fatigue, depression, psychosis)
B. Brown tumors: giant cell lesions, broken down bones with blood accumulated.
C. Generalized loss of lamina dura
D. Salt and pepper -> decreased in trabecular pattern.
E. Elevated alkaline phosphatase levels in the blood.

4. Hypoparathyroidism: over accumulation of calcium in the bone.


① Most commonly due to damage to or removal of parathyroid glands during thyroidectomy
② Manifestation -> hypocalcemia
A. Paresthesia and tetany
B. Radiopacity in skull by basal ganglia
C. Pitted enamel hypoplasia
D. Late eruption
E. Dlaceration
F. Increased radiopacity in the jaws.

 Downcoding: means the adjudication of claims in a manner that reduces dental procedure codes to
a less complex or lower-cost code.
 "Bundling" means the adjudication of claims in a manner that denies payment for one or more of
multiple dental procedure codes unless expressly provided for in the CDT Code on Dental
Procedures and Nomenclature.
Q: A dentist does treatment for 2 crowns but the insurance company pays the money for one crown what is
it? -> bundling
Q: A dentist does 2surface composites and insurance made it 1 surface what is it? -> downcoding
 Congenital granular cell epulis : a mesenchymal tumor with marked female predilection (10:1,F:M)
 It develops in utero with rapid growth during 3rd trimester
 Diagnosis is confirmed by observing @-100 negative sheets of granular cells on microscopy (as a
distinction, the conventional granular cell tumor (Abrikossoff’s tumor) is positive for S-100)

PREGNANCY

1. Trimester
① 1st trimester: 0~3w.
② 2nd trimester: 14~26w.
③ 3rd trimester: 27~40w.
*chances of malformation is lower in 2nd~3rd trimester but more susceptible to discoloration by the
administration of tetracycline
 Preterm born before 37w.
 Viable pregnancy should be minimum of 25 w and above.
 1st is the worst(constipation, extreme tiredness, most at risk), best (safest period for dental tx),
burning chest (heartburn, shortness of breath, contraction and generalized swelling)

2. Effects of pregnancy
① ↓Iron
② ↓Plateles :
③ ↓Lung capacity : decrease about 5%
④ ↑Coagulation factors: clotting factors 1,7,8,9 and 10 are increased during pregnancy -> hyper-
coagulable state
⑤ ↑WBCs: increase in neutrophil

3. Complications of pregnancy
① Acid reflux
② Urinary frequency
③ Gestational diabetes mellitus
④ Preeclampsia: high blood pressure, proteinuria, edema, and blurred vision.
A. Hypertension can lead to preeclampsia
B. Can progress to eclampsia
⑤ Miscarriage

4. FDA pregnancy categories


 NSAIDS should not be used on 3rd trimester as they promote premature closure on ductus arteriosus
leading to fetal pulmonary hypertension.
 Prilocaine and lidocaine are in the B categories and are considered to be safest local anesthetics.
 Benzodiazepine should be avoided

5. Supine hypotensive syndrome


① It is not advised to place pregnant patient in a fully supine position esp. during late pregnancy.
② Gravid uterus compresses aorta and inferior vena cava.
③ Hypotension, pallor sweating, nausea, weakness, air hunger and dizziness.
④ Turn on their left side (left lateral decubitus position)

6. Patient considerations
① Recline rather than supine
② Monitor BP -> if >140/90, call their gynecologist, maybe a sign of preeclampsia.
③ Take only necessary Rx
④ Elective dental care should be avoided during 1st trimester and 2nd half of the 3rd trimester, but
urgent care, plaque control and oral hygiene should be provided.
⑤ Avoid NO2 in 1st trimester and for other trimester, limit to 30mins and deliver at least 50%
oxygen.
⑥ Tetracycline and excessive fluoride should be avoided from 2nd trimester all the way to the 8y of
age.
⑦ Avoid NSAIDS in 3rd trimester
⑧ Avoid benzodiazepine : associated with preterm delivery and low birth weight.

7. Oral manifestations
① Pregnancy gingivitis : most common complications.
A. Hormone mediated but plaque induced, no plaque no disease.
B. Increases the risk of pre-term labor
② Increased caries risk: decreased pH in the oral cavity and towards more sugary food
③ Pyogenic granuloma
A. Pregnancy tumor, mass of gingival granulation tissue with fibroblasts, macrophages, and
vasculature.
B. Found at the labial surface of interdental papilla.
④ Sinus congestion : Extra estrogen causes swelling of the mucosa in the nose and upper
respiratory tract. -> rhinitis -> sinus congestion.
⑤ Dental erosion : secondary to nausea and vomiting.
⑥ Hypersensitive gag reflex: exaggerated during pregnancy.

PAIN AND INFECTION MANAGEMENT

1. Pain levels (acute pain)

2. Analgesics use

 Ibuprofen has been found to be the most effective medications and is the 1 st line therapy. Except,
 Pregnant
 Asthma -> nsaids can induce bronchospasm and opiods have respiratory depressants ->
acetaminophen .
 Liver disease: low-dose acetaminophen not exceeding 2g/day
 Heart disease
 Ibuprofen can interfere with anti-hypertensive medications (beta blockers, diuretics.)
 Nsaids with ace inhibitors can increase the risk of acute renal failure.
 Kidney disease
 Stomach disease -> increased risk of gastric ulcers.
 Allergy
 Regular tablet Tylenol is 325mg and extra strength is 500mg.
 Opioid like hydrocodone should be very low and only for 1~2 days.
 Salt water and cold compresses can also be used together.

3. Antibiotic use

 If there is no infection, antibiotics are not recommended


 Always remove the source
 Clindamycin is no longer used for the next choice if the patient is allergic to penicillin due to
clostridium difficile, replaced by azithromycin.

HIGH CHOLESTEROL/ hyperlipidemia

1. Cholesterol: is the precursor for all the steroid hormone, and also for the integrity of cell membrane.
Triglycerides are converted to phospholipids also for the cell membrane.

2. Lipoproteins
① Substances that are made of protein and fat that carry cholesterol and triglycerol through blood
② Classified by the density (protein are more dense
A. HDL (high density lipoprotein: less lipid, more protein)
a. Transports cholesterol to the liver, help body to remove the excess cholesterol that it doesn’t
need
b. >50mg/dL is ideal for most people.
B. LDL (low density lipoprotein)
a. Transports cholesterol to the walls of arteries
b. <130mg/dL is desirable

3. Atherosclerosis: Fatty deposits build up on the inner wall of arteries, which impacts the body in 2 ways
① Constricts the diameter of artery
② Separate endothelial cells from smooth muscle cells blocking nitric oxide (vasodilator)

4. High cholesterol medications


Statin drug name Mechanism of action
Atorvastatin (Lipitor) Inhibits HMS-CoA reductase (responsible for the synthesis of cholesterol in the liver,
Lovastatin (Altoprev) no effect on the diet-attained cholesterol) -> decrease serum level of LDL
Pitastatin(Pravachol)
Rosuvastatin (Crestor)
Simavastatin (Zocor)

5.Patient considerations for high cholesterol


① High cholesterol with statin drugs -> avoid macrolide antibiotics(erythromycin, clorithromycin) and
antifungals (metabolized by the cytochrome P450, which lead to increased plasma concentration of statin
drug which may lead to undesirable side effects like muscle myalgia, pain, rhabdomyolysis, and even
kidney failure.)
② May also have diabetes and hypertension, follow the guidelines of it accordingly
 Rhabdomyolysis (often called rhabdo) is a serious medical condition that can be fatal or result in permanent
disability. Rhabdo occurs when damaged muscle tissue releases its proteins and electrolytes into the blood.
These substances can damage the heart and kidneys and cause permanent disability or even death.

6. Oral manifestations
① Increased risk of calcification in pulp chamber -> pulp stones
② Side effect of statin results in muscle pain and soreness or weakness, that can affect the daily life like
chewing and breathing
③ High cholesterol maybe associated with periodontal disease.

CANCER, CHEMOTHERAPY and RADIATION

1. Epidemiology of cancer in hong kong


Male: lung > colorectum > prostate > liver > stomach > non-Hodgkin lymphoma
Female: breast > lung> colorectal> uterine> thyroid
The highest leading cause of death in hong kong is malignant neoplasia

2. Head and neck cancer


① Visual inspection and digital palpation on intraorally and lymph nodes on the head and neck region.
(looking for fixed or matted lymph nodes)
② SCC is the most common cancer of the head and neck
③ Most common to least common head and neck are oral cavity> oropharynx> larynx>nasopharynx>
hypopharynx>> salivary glands and sinuses.
*Matted lymph nodes: there’s a bunch of lymph nodes that are kind of stuck together and move together as one
single unit.
*Palpating the lymph nodes: occipital -> preauricular area -> parotid gland and the TMJ (asking the patient to open
and close the jaw), submandibular area (bend their chin down and put the tongue on the palate) -> palpate front
and behind the SCM for the ant. and post cervical chains. (turn the head to the side and down) -> thyroid gland.

3. Oral cancer
① Risk factor: Tobacco> alcohol> HPV > immunocompromised.
Alcohol and tobacco are synergistic.
② Tongue (posterior-latero aspect)> lip (lower lip – basal cell carcinoma) > floor of mouth
A. Inspection of the color of the mucosa: pink is normal, redness – erosion, bv near the surface. White –
surface thickening and less vascular structures.
B. For palpation of mucosa: smooth is normal except for the rugae

4. Patient considerations for cancer patients (for radiotherapy/chemotherapy not applicable for surgical excision)
① Before chemo/radio
A. Comprehensive examination (pano xray, edentulous area should be surveyed for impacted teeth and
retained root tips and any latent osseous disease)
B. Maintain excellent oral hygiene
C. Eliminate all sources of irritation and infection.
a. Abscesses, gum disease, sharp bony edges, active caries, chronic inflammatory lesions, gingival
opercula excision should be done if there’s frequent food impaction, remove orthodontic bands
etc
b. Symptomatic non-vital teeth should be endodontically treated
Dental treatment with asymptomatic teeth even with periapical involvement can be delayed
until later
D. Remove all nonrestorable and questionable teeth -> can lead to sepsis, osteoradionecrosis,
② During chemo/radio
A. Removable prosthodontics appliances should be removed during the cancer tx, to prevent the
irritation of the mucosa.
B. Manage salivary flow such as pilocarpine.
C. Mange complications
③ After chemo/radio
A. Call physician for outcome.
B. Oral recall program -> recall pts for every 1~3 months for the first 2 years, and after 3 years, it can be
adjusted to the 3~6 month.
-> Recurring lesions, manage complications.
C. Avoid extraction if possible -> osteonecrosis, delayed healing, prolonged alveolar bone exposure
infections.
D. Manage complications

5. Oral complications (C: chemotherapy, R: radiotherapy)


① Xerostomia (C&R) -> 2nd week of the tx
② Mucositis (C&R)
A. Painful inflammation and ulceration of the oral mucosa.
B. 2nd week and occurs about 40% of patients undergoing C&R
C. Non-keratinized tissues -> buccal mucosa, labial mucosa, ventral tongue, and more common metallic
radiation (radiation beams accumulate)
D. Younger patients exp. more mucosities (due to active mitosis)
E. Salt water rinses, supplemental zinc, oral chlorhexidine rinse, oral cryotherapy, soft diet, humidified
air and topical anesthetics and analgesics
③ Taste alteration (C&R)
A. Radiation damages microvilli of taste cells leading to generalized diminished taste.
B. Chemotherapy agents: bitter taste, unpleasant odors, and even aversions to certain foods.
④ Secondary infections (C&R)
Naturally prone to secondary infections such as fungal or viral (most common candidiasis)
⑤ Bleeding (C) -> suppress bone marrow leading to thrombocytopenia -> petechiae and pupura can result
from minor trauma like biting tongue or brushing.
Management: careful be gentle on brushing, use anti-fibrinolytic rinse, topical thrombin.
⑥ Radiation caries (R) -> labial surface of the teeth near the gum line (decrease salivary and increased
acidity)
⑦ Hypersensitive teeth (R)
⑧ Trismus (R) -> spasms of jaw muscles
Radiation can damage to the muscles of the jaw (perform daily stretching exercise and use warm
compresses to help with this)
⑨ Carotid atheroma (R): More likely to develop carotid artery atheromas (calcified atherosclerotic plaques)
⑩ Osteoradionecrosis: just like MRONJ, more impacts on posterior and mandible.
 Can you extract teeth on someone who had radiation therapy 10yrs ago? The osteoradionecrosis risk DOES
NOT DIMINISH WITH TIME (PERMANENT) unlike MRONJ. -> if deemed necessary after consultation, extract 1
tooth at a time atraumatic as possible, get primary soft tissue closure, use antibiotic coverage, hyperbaric
oxygen.
 When to provide routine dental care for a patient undergoing chemotherapy? -> when patient is comfortable
(usually 17~20 days after their most recent chemotherapy session)
 How much time should you wait after an extraction before starting chemotherapy or head and neck radiations
-> 7 days for chemotherapy and 14 days after radiations.

HIV &AIDS

1. Epidemiology
① More common in males and most common bet. 25~29years old.
② Black> Hispanic> Asian> White

2. Etiology
① HIV is enveloped RNA retrovirus (belong to lentivirus)
② Glycoprotein such as GP 41 and GP 120, and allow binding to the human host cells.
③ Capsid surrounds the genetic materials and viral enzymes (protease, integrase, reverse transcriptase)
④ Infects cells with CD4 receptors
A. T helper cells
B. Macrophages.

3. Transmission
① HIV is found in most bodily fluids (every secretion except for saliva and sweat)
② Sexual transmission: most common
③ Shared needles
④ Vertical transmission
⑤ Occupational exposure. (0.3% for needle stick injury)

4. Staging
① Stage 1: HIV begins (lasts for years)
A. T helper/ CD4 cells ≥ 500cells/uL (cells/uL is the same as cubic ml of blood)
B. Antibody positive
C. Asymptomatic
② Stage 2: HIV gets worse
A. T helper/CD4 cells 200~499cells/uL
B. Symptomatic (lymphadenopathy, weight loss, thrush, fever,malaise, diarrhea)
③ Stage 3: AIDS begins (10~11 yrs after HIV begins)
A. T helper/.CD4 cells <200cells/uL
B. Symptomatic (malignancy, wasting, dementia, opportunistic infections)

5. Diagnosis – Elisa and western blot does not tell what stage.
① ELISA = Enzyme-linked immunosorbent assay -1st phase
Main screening test for identification of antibodies to HIV.
② WESTERN blot
A. When Elisa test tested twice positive, then go for western blot.
B. Detects specific protein molecules from mixtures of proteins
③ PCR (polymerase chain reaction)
A. Used to amplify DNA
B. Can be performed in the HIV positive patients to determine the viral load of HIV in the blood.
C. Can help with identification of staging.

6. Medications :goal is to inhibit HIV replications.


Antiretroviral drug names Mechanism of action
Ritonavir Protease inhibitor, inhibits HIV replications
Zidovudine Nucleoside reverse transcriptase inhibitor, inhibits HIV replication
Efavirenz Non-nucleoside reverse transcriptase inhibitor, inhibits HIV replication
Tenofovir Nucleotide, inhibits HIV replication
Enfuviritide Entry inhibitor, inihibits HIV replication
ART: antiretroviral therapy, when initiated early after infection and taken everyday can lengthen their lives and
limiting the risk of transmitting.
HAART: highly active antiretroviral therapy, using at least 3 antiretroviral medications

7. Patient considerations for HIV/AIDS


① Patients diagnosed with HIV
A. Treat identically as other patients

B.
With standard precautions (gloves, masks, eyewear, gowns), post-exposure prophylaxis may be
prescribed with the healthcare workers are exposed to HIV patient within the first 72 hours.
(contains 2~3 antiretroviral drugs for about 4 weeks)
C. Be aware of drug interactions with antiretroviral medications
a. Avoid acetaminophen with zidovudine -> granulocytopenia and anemia
b. Avoid meperidine (narcotics) with ritonavir -> lethargy, agitation and seizures.
② AIDS
A. Noninvasive/ elective -> same as above.
B. Invasive surgical
a. If CD4 <200/ml3 or if neutrophil count is less than 500 cells -> neutropenia -> may require using
prophylactic antibiotics.
b. Consult with physician
c. Patients with severe thrombocytopenia may need platelet replacement and NSAIDS.

8. Oral manifestations: one of the earliest sign


① Xerostomia : up to 40%
② Increased caries risk
③ Increased periodontal disease risk including NUG/NUP
④ Candidiasis: Linear gingival erythema
A. Linear gingival erythema is a Candida-associated lesion that has been described in HIV patients.
B. Pseudomonas candidiasis
⑤ Herpes simplex: HHV1 and 2 (genital)
⑥ Herpes zoster (HHV3) cause shingles
⑦ HPV -> causing oral warts
⑧ Oral hairy leukoplakia -> sign of advanced AIDS
Caused by Epstein virus (also known as HHV4)
⑨ Cytomegalovirus (CMV) also known as HHV5 -> oral ulcer.
⑩ Kaposi sarcoma -> caused by HHV 8
A. Malignant cancer that affects blood and lymph vessels
B. Brown or purple macule on palate, gingiva or tongue
⑪ Non-Hodgkin lymphoma

Example questions
1. Does a patient have to disclose their HIV status -> better so but not legally.
2. Does a dentist have to disclose their HIV status -> SHOULD INFORM
3. Patient has HIV and accidently stick yourself with a needle after using it on the patient
Start post-exposure prophylaxis ASAP.
4. Patient has HIV and accidentally stick with a needle before using it on the patient
Washing the area and reporting the incident but will not need the post-exposure prophylaxis

GERD and peptic ulcer


1. Peptic ulcer disease
① Peptic ulcer is break in the lining of the stomach, esophagus or duodenum
② Most common cause is infection with Helicobacter pylori
③ 2nd most common cause is chronic NSAID use
④ Other risk factors include old age, smoking alcohol, stress, bisphosphonates, anticoagulants.
Normally gastric acid is pH 1.5~3.5

2. Medications
Drug Mechanism of action Comments
Antibiotics Eradicates H pylori
Antacids Counteracts low pH and Quick relief, only fix the symptoms.
neutralizes gastric acid Antacids and daily products will chelate or bind and
interfere antibiotics and limit their effectiveness.
(tetracycline and erythromycin)
Ranitidine H2 receptor antagonist Selective for the parietal cells in the stomach,
stopping it from responding to histamine, thus
stopping them to secrete so much acid.
Over the counter
Not much drug interactions
Omeprazole PPI Much stronger than ranitidine.
As it completely blocks the acid into the lumen of the
stomach.
Much more drug interactions.
Reduce the absorption of ampicillin, ketoconazole
and itraconazole.
Increase the concentration of benzodiazepine,
warfarin and phenytoin

3. Patient considerations for GERD/ PUD


GERD -> ask about acidic diet and test salivary function.
PUD -> avoid NSAIDS, encourage good oral hygiene (H. pylori can habour in the dental plaque),
reconsider antibiotic regimen (patients having antibiotics for H. pylori, should select a different class
of antibiotic for tooth issue).

4. Oral manifestations
① Candidiasis: due to side effects of broad systemic antibiotics -> median rhomboid glossitis
(central papillary atrophy of the tongue and generally no tx, if symptomatic go for nystatin
suspension or clotrimazole troches)
② Taste alteration
PPI can alter taste perception.
③ Erythema multiforme
Reported in some people who take H2 blockers or PPI.
④ Erosion: regurgitation of acids
⑤ Xerostomia: associated with PPI.

5. Tooth erosion
① Different age groups to be at risk for erosion
A. Teenagers: eating disorders (bullemia), sugary drinks
B. Middle- aged: GERD, Obstructive sleep apnea.
C. Elderly: polypharmacy causes xerostomia.(buffering capacity of the saliva is lost)
② Perimolysis: acid erosion facilitated by gastric acid -> 3 signs of dental erosion
A. Cupping: smooth bowl-shaped dots on cusp tips.
B. Standing proud : restorations sticking up from surrounding tooth structure.
C. Whipped clay: loss of anatomic detail. (ridges and grooves)

③ Sleep acid triad/ bruxism triad:


A. Increased negative pressure in the chest during an apneic episode causes this acid to move
up into the esophagus. This alone can also trigger arousal in sleep which can lead to tooth
grinding. (strong correlation between these 3 things)
B. GERD is more common in patients who have asthma and asthma medications such as
theophylline/ abuterol can worsen acid reflux.
 Inhaled beta agonist bronchodilators not only increase the thoracic pressure but also lead to
an increased abdominal pressure favoring GERD by affecting the esophagogastric barrier.
 The blood pressure medications known as calcium channel blockers and beta blockers can provoke
heartburn by relaxing the lower esophageal sphincter, which can allow stomach acid to seep up into
the esophagus.

SLEEP APNEA

1. Obstructive sleep apnea falls under sleep disorders (F>M but OSA specifically is M>F)

2. Types of sleep disorders


① Insomnia: difficulty falling and /or staying asleep.
② Parasomnia: sleepwalking, night terrors (a person quickly awakens from sleep in a terrified
state)
③ Sleep-related breathing disorders: snoring, CSA, OSA.
④ Sleep related movement disorders: restless leg syndrome, nocturnal bruxism.
⑤ Narcolepsy: overwhelming daytime drowsiness and fall asleep suddenly
⑥ Circadian rhythm sleep-wake disorders : different time zone, shifted work.

3. Snoring
① Male >Female.
② Results from the vibration of loose soft tissues as air passes
③ Snoring in children is usually due to enlarged tonsils or adenoids.

4. Sleep apnea
① Types
A. Central sleep apnea: airflow stops as a result of a temporary lack of inspiration
Occur with poliomyelitis, spinal cord injury, encephalitis
B. Obstructive sleep apnea: airflow stops as a result of a physical obstruction
Nasopharyngeal/ oropharyngeal/hypopharyngeal obstruction
② Episodes
A. Apnea: total cessation of airflow for at least 10s.
B. Hypopnea: reduced airflow for at least 10s.
C. Respiratory effort-related arousal (RERA): increased respiratory effort for at least 10s
leading to an arousal.

③ Apnea-hypopnea index
A. AHI = (# apnea +# hypopneas)/sleep hours.
B. Adults
a. Mild: 5~15 episodes/ hour
b. Moderate: 15~30 episodes/ hour
c. Severe: 30 or more episodes/hour.
C. Children
a. Mild: 1~5 episodes per hour
b. Moderate: 5~10 episodes per hour
c. Severe: 10 or more episodes per hour.
Obstructive events in children occur primarily during REM sleep cycle.
④ Signs and symptoms.
A. Intermittent snoring
B. Somnolence : excessive daytime sleep.
C. Fragmented light sleep
D. Nocturnal sweating
E. Nocturia : frequent urination.
F. Poor memory
G. Morning headaches
H. GERD
I. Nocturnal bruxism : tooth grinding or clenching during sleep.
J. Cardiovascular symptoms: hypertension, arrhythmia, and stroke
⑤ RISK factors
A. Obesity (BMI = kg/m^2
B. Older age
C. Male gender
D. Family history
E. Alcohol or sedative use
F. Supine sleeping position
G. Smoking
H. Breathing disorders such as asthma, COPD
I. Menopause.
J. Anatomic abnormalities
a. High and narrow palate-> high nasal resistance)
b. Narrow dental arches -> limited tongue space and the tongue goes back.
c. Increased ant. face height and overjet -> with lip incompetence, signals of mouth
breathing
d. Retrognathia/ mandibular hypoplasia -> Pierre robin sequence, Treacher Collins
e. Elongated soft palate
f. Large tongue -> can be seen in beckwith-wiedemann syndrome, amyloidosis,
acromegaly, MEN type 2, hypothyroid
g. Enlarged uvula
h. Tonsillar hypertrophy.(esp. children)
 Beckwith-Wiedemann syndrome: overgrowth syndrome, which means that affected infants are
larger than normal (macrosomia), and some may be taller than their peers during childhood.
K. Sickle cell anemia -> sickle cell related adenotonsillar hypertrophy.
L. Mucopolysaccharidosis: accumulation of glucosaminoglycans -> manifest as macroglossia,
adenotonsillar hypertrophy, narrowing of the trachea and bronchi due to the accumulation
of GAG.
M. Down syndrome -> small midface and cranium, relative macroglossia, nasopharynx and
obesity.
N. Cleft palate -> cleft palate repair surgery generally lengthens and or thickens the palate.
⑥ Screening
A. Mallampati score : size of tongue when not protruded and in a relaxed position.
a. A large tongue can block posterior pharyngeal space
b. Modified version involves sticking tongue out as far as possible.
c. Correlates with OSA and severity
d. Classifications

B. Scalloped tongue
a. When tongue presses up against teeth constantly or regularly creating half-ciurcle,
wavy indentations.
b. Scalloping of the tongue is 70% diagnostic for OSA.
C. Brondsky score
a. Size of tonsils, the bigger the score the bigger the tonisls.
b. Correlates with OSA and severity

D. STOP BANG questionnaire. -> indicating of higher risks.


a. Snoring
b. Tired
c. Observed apnea
d. Pressure of blood
e. BMI elevated
f. Age >50
g. Neck has increased circumference
h. Gender is male.
⑦ Diagnosis -> polysomnogram is the gold standard
Polysomnography, also called a sleep study, is a comprehensive test used to diagnose sleep disorders.
Polysomnography records your brain waves, the oxygen level in your blood, heart rate and breathing, as
well as eye and leg movements during the study.
⑧ Treatment
A. Behavioral modification: weight loss, lateral sleeping position,etc.
B. Positive airway pressure
a. CPAP (Continuous positive airway pressure)-> gold standard for tx of OSA, it is effective for both
moderate and severe obstructive sleep apnea.
- Continuous positive airway pressure (CPAP) is a form of positive airway pressure (PAP)
ventilation in which a constant level of pressure greater than atmospheric pressure is
continuously applied to the upper respiratory tract of a person.
- Very effective, but low compliance as it can cause laceration of the bridge of the nose,
rawness of the throat and dry mouth, uncomfortable, reduced cardiac output and renal
function.
b. Bipap (bilevel positive airway pressure) -> for more severe cases, that delivers both inhale and
exhale pressure.
C.Oral appliances -> for mild to moderate sleep apnea.
a. Maintain the mandible and tongue anteriorly, increasing the upper airway volume.
b. Successful rate and compliance rate is fairly good
c. Can lead to occlusal changes -> as it is basically a class II functional appliance
D. Orthodontic tx -> if the patient is children and have narrow palate
E. Surgery
F. Hypoglossal nerve stimulation-> stimulates the tongue to push itself out rhythmically to help open
the airway during sleep.
 With OSA and UARS, probably retrognathia is more common and physiologically associated than high and
narrow arched palate. For kids definitely something to look out for since it can be expanded MUCH easier and
effectively than in adulthood.
 Mallampati score can sometimes be used be used to gauge candidacy for maxillomandibular advancement.
When the jaws are advanced the mallampati score can often be lowered, especially in those with severe
hypoplasia. Can also place fingers underneath the chin like when testing for intubation to see how many will
fit.
 Obesity also can result in fat depositing into the tongue, enlarging the tongue, whereas MMA(maxilla-
mandibular advancement surgery) can move the jaws forward or rotate counterclockwise away from the
airway.

HEPATITIS

1. Cause
① Most commonly caused by hepatitis virus -> major cause of cirrhosis(scarring) and liver carcinoma.
② Alcohols and use of certain chemicals. (hepatotoxins such as phosphorus, carbon tetrachloride,
acetaminiophen in large doses)
③ Autoimmune

2. Immunology
① B lymphocyte: mediate humoral immunity, first cell to recognize antigen and becomes a plasma cells
which produces antibodies.
② T lymphocyte: cellular immunity.
③ Antibodies
A. IgA -> main antibody found in saliva.
B. IgE: bind to receptors on mast cells and basophils, and is involved in the allergic response and
anaphylaxis.
C. IgG: principal antibody, most common
D. IgM: first responder, most abundant in neonates is maternal IgG but principal antibodies synthesized
by the newborn are IgM.

3. Hepatitis A
① Transmission: fecal-oral (Hepatitis E -> Transmission: fecal-oral)
② Incubation period: 2~6w.
③ Acute rapid onset, but does not lead to chronic disease or carrier state.
④ Acute S/Sy: jaundice, fever, malaise, loss of appetite, nausea.
⑤ Vaccine available.

4. Hepatitis B
① Transmission: contaminated blood and bodily fluids.
② Considered to be a major risk of infection in dental office -> high risk of transmission (30% by
percutaneous injury -> break in skin with an infected needles)
③ Incubation period: 1~6month.
④ S/Sy: jaundice, fever, malaise, loss of appetite, nausea.
⑤ All other hepatitis virus are RNA virus except hepatitis B which is DNA virus. (Dane particle: a spherical
particle found in the serum in hepatitis B that is the virion of the causative double-stranded DNA
virus.)
⑥ Greatest concentration in the oral is at gingival sulcus.
⑦ Vaccination is available and very effective -> administered in 2~3 injections over the course of 6months.
Vaccine should be freely available to employees occupationally exposed to blood.
⑧ Post-exposure prophylaxis with vaccine
⑨ Hepa B serologic test results
A. Surface antigen (HBsAg): diagnostic, a positive lab test result indicates the pts is infectious.
B. Surface antibody (anti-HBs): recovery and immunity -> Vaccinated
C. Core antibody (anti-HBc): history, persistent. -> Onset of symptoms in acute or chronic heap B cases,
indicates a past or current hepatitis B infection.
D. IgM antibody(IgM anti-HBc): history, temporary. -> acute or recent, present for only about 6 months.

5. Hepatitis C
① Transmission: contaminated blood and bodily fluids.
② Most common bloodborne pathogen in US. (but only 1.8% risk of transmission after percutaneous injury)
③ Incubation period: 2~6w.
④ Usually asymptomatic, if present it is usually mild.
⑤ No vaccine, but tx is available (weekly interferon alpha, and daily ribavirin)
⑥ Along with Hepa B can cause liver cirrhosis.

6. Hepatitis D
① Transmission: contaminated blood and bodily fluids, but cannot occur in the absence of hepatitis B virus.
② HDV-HBV co-infection is considered the most severe form of chronic viral hepatitis due to more rapid
progression towards hepatocellular carcinoma and liver-related death. Vaccination against hepatitis B is
the only method to prevent HDV infection.

7. Patient considerations for hepatitis


① Active hepatitis
A. Elective: defer and refer.
B. Urgent: isolated operatory, standard precautions, minimal aerosols, avoid drugs metabolized in the
liver (amide local anesthetic like lidocaine, analgesics like aspirin, acetaminophen, ibuprofen,
sedatives like diazepam and barbiturates and antibiotics such as ampicillin and metronidazole.)
② Recovered from hepatitis (including the carriers): no tx modifications, universal precautions always.
 CDC recommends that dentist who are acutely infected with hepatitis should stay home from work for a week
after the onset of jaundice.

8. Oral manifestations of liver dysfunctions


① Jaundice of skin and oral mucosa.
② Petechiae -> clotting factors made by liver -> vitamin K therapy, clotting factor and/or platelet
replacement
③ Fetor hepaticus: distinctive bad breadth associated with liver disease
④ Atrophic glossitis : smooth tongue with no papilla on dorsal surface
⑤ Xerostomia
⑥ Lichen planus : increased incidence of hepa B and C
⑦ Increased risk of Hepatocellular carcinoma -> rarely manifest but can be as hemorrhagic expanding mass
located in the premolar or ramus region of the mandible.

SMOKING
1. Nicotine
① Primary addicting component of tobacco products
② Peaks within 10s of inhalation
③ Activates the dopamine circuits and stimulates adrenal gland to release epinephrine.
④ Nicotine withdrawal
A. Symptoms: irritability, depression, anxiety, craving, cognitive and attention deficits, disturbed sleep,
increased appetite.
B. Begins: hours
C. Peaks: days
D. Subsides: weeks

2. Cigarettes
① Finely chopped tobacco leaves wrapped in paper.
② Contains menthol (for masking the smell, but FDA are trying to ban it), tar, carbon monoxide, and
formaldehyde.
③ 2nd hand smoke has same adverse health effects.
④ Cigar: larger wrapped in tobacco
⑤ Cigarillo: smaller, wrapped in tobacco.

3. Pipes
① Conventional pipe: bowl containing loose leaf tobacco
② Hookah: water pipe containing shredded tobacco leaves with fruit, spice or candy flavors.

4. Smokeless tobacco
① Snuff: finely ground tobacco -> buccal mucosa
② Chaw: coarsely shredded tobacco
③ Snus: moist powder tobacco pouch, hold it in the lip.
5. Electronic nicotine delivery system
① E-cigarretes: electronic cigarettes
② Vape pen: pen shaped device that produces vapor.
③ Contains nicotine, prophhlene glycol, glycerin and diacetyl (very harmful substance that can cause
popcorn lung, scarring of lung tissues)
④ Not recommended as a method to prevent relapse to cigarette smoking. (increased risk of not able to
quit)
6. Tobacco cessation
① Behavioral: counseling
② Pharmacologic: medication indicated except for pregnant woman, light smokers or with epilepsy.
A. Nicotine-replacement therapy: nicotinic receptor agonist
B. Bupropion: norepinephrine-dopamine reuptake inhibitor (NDRI)-> antidepressant that blocks the
reuptake of norepinephrine and dopamine. Should be taken while smoking and set a quit day.
C. Varenicline: nicotinic receptor partial agonist, taken while smoking and set a quit day.

7. Patient considerations for smoking -> 5As

8. Oral manifestations of tobacco smokers


① Leukoplakia
② SCC: most common cancer found in smokers. (nicotine by itself is not a carcinogen)
③ Nicotinic stomatitis: inflamed salivary gland -> reverse smokers and pipe users.
④ Smoker’s melanosis : The amount of pigmentation increases with greater tobacco use, tissues typically
return to normal color in six to 36 months after quitting smoking.
⑤ Hairy tongue
⑥ Halitosis
⑦ Smokeless tobacco keratosis -> where chewing tobacco are held in the buccal mucosa.
⑧ Periodontal disease
Smokers have less gingival bleeding than non-smokers.
TUBERCULOSIS

1. Caused by macobacterium tuberculosis (acid fast bacillus)


① Transmitted via droplet nuclei.
② Tuberculosis is the leading cause of death in AIDS patient
③ BCG vaccine is available but not required in dental professionals.

2. Latent and active


Latent TB TB disease
Tb lives but doesn’t grow in the TB is active and grows in the body
body
Do not have symptoms Have symptoms
Can’t spread from person to Can spread
person
Can advance to TB disease Can cause death if not treated
Isoniazid to prevent advancing to Isoniazid, + additional drugs like rifampin,
TB disease. pyrazinamide, Ethambutol

3. Infection control
① Administrative: most imp. cutting the source
A. Having written TB infection plan and instruction.
B. Screening of the TB disease
② Environmental : reducing the spread and concentration of droplets such as isolated room
③ Protective: N95 masks

4. TB screening: Test at beginning of employment, but routine testing no longer recommended unless there is
known exposure.
① TB skin test : Mantoux tuberculin skin test
A. How is it tested
a. First day: inject tuberculin purified protein derivative (PPD)
b. 2nd day: observe 2~3 days later, and measure the size of the induration (a delayed type IV
hypersensitivity)
B. BCG vaccinated individuals might lead to false positive
② TB blood test/ interferon gamma release assay (IGRA)/ quantifier and gold test
Preferred as it is single visit and does not have the false positive result for BCG vaccine.

5. Considerations for TB
① Latent TB -> no tx modifications
② Active TB
A. Elective: defer and refer
B. Urgent: isolated operatory, standard precautions and N95, minimal aerosols.
6. Oral manifestations: manifests infrequently in oral cavity
① Ulcer : on the tongue, palate buccal mucosa.
② Tuberculous osteomyelitis -> most affects the femur but can also affect the jaw
③ Scrofula: TB infection outside the lungs, inflamed and irritated lymph nodes in the neck.
MULTIPLE MYELOMA

1. Multiple myeloma
① Cancer of plasma cells
A. Abnormal plasma cells secrete the same antibodies, and multiple myeloma can be classified by the
type of immunoglobulin produced.
B. Common: IgG> IgA> IgD
② Median age is 70 years old
③ Bone resorption -> causing bone pain, and bone marrow replacement -> leads to Anemia, leukopenia,
thrombocytopenia.
④ Death by infection (most common cause of death) or renal failure.

2. Diagnosis
Bence-Jones protein urine test is used most often to diagnose and check for multiple myeloma.
Bence jones is a normal antibody called a light chain, however not found in normal urine.

3. Medications
Multiple myeloma drug name Mechanism of action
Thalidomide Inhibits secretion of TNF-a and IL-6
Bortezomib Proteasome inhibitor -> proteasome are required for the accumulation of
regulatory proteins imp. in cell cycle control. -> anti-chemotherapeutic drugs
Bisphosphonates Induces osteoclasts to undergo apoptosis.

4. Patient considerations
-> If taking bisphosphonates/ chemotherapeutic agents, follow the pts considerations accordingly
-> WBC < 2000 -> antibiotic prophylaxis may be indicated, to prevent endocariditis
-> Platelet count < 50,000 -> platelet transfusion is indicated before certain invasive and surgical procedures
are indicated.

5. Oral manifestations
① Multiple Punched out radiolucencies or mottled areas on dental Rx. (common in cranium and posterior
mandible)
② Amyloidosis of the tongue -> enlargement
③ Oral manifestations of bisphosphonates/ chemotherapeutic if the patients are undergoing those.

BETEL NUT

1. Betel nut is CNS stimulant


① Seed of areca palm fruit
② Quid: betel leaf package (with tobacco or so on) for chewing
2. Oral manifestations
① Oral submucous fibrosis -> betel nut intakers are of high risk in oral submucous fibrosis, it is incurable.
A. Affects lips, cheek, soft palate, and pharynx.
B. Gets progressively worse as more collagen is deposited into soft tissues -> cause of stiffness and
eventual the loss of movement of the mouth -> wont be able to open and close the mouth anymore
and have to be fed in a tube.
C. Pre-malignant -> leading to OSCC.
② SCC
③ Attrition
④ Gingival recession: betel nut is a risk factor for periodontal disease.
⑤ Extrinsic staining of teeth and gums: reddish-brown staining.
⑥ Does not cause xerostomia.

9 dental specialties
① Public health
② Endodontics
③ OMS
④ Oral and maxillofacial pathology
⑤ Radiology
⑥ Orthodontics
⑦ Pediatrics
⑧ Periodontics
⑨ Prosthodontics

7. Dental public health


① Is defined as the science and art of preventing and controlling disease and promoting oral health through
organized community efforts.
② 3 core competencies
A. Assessment
B. Policy development
C. Assurance.
 Air abrasion: used to treat small cavities with a blast of air and aluminum oxide pellets to remove decay. Can
be done mostly without anesthesia
 Bone replacement
 Autograft
 Allograft
 Alloplast: synthetic bone replacement material such as platelet derivative growth factor (PDGF: used in
conjunction with bone grafts to achieve maximum results.
 Lasers
 Diodide: absorbed by pigmented tissues such as the hemoglobin and melanin and it is particularly good
for tx of soft tissue.
 Nd-YAG and CO2 laser good for hemostasis
 Erbium lase: good for hard tissues.
 Argon laser: cure resins and improve bonding

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