Oral Diagnosis I Third Year

1. Review of pulmonary
diseases
Dr. Hassan M. Abouelkheir
BDS, MSC, PhD

2. 1- Chronic Obstructive
Pulmonary Disease.
• COPD is a group of
conditions in which
there is persistent
difficulty in expelling (or
exhaling) air from the
lungs. It includes two
diseases:
• A- Chronic bronchitis
• B- Emphysema.

3. A- Chronic bronchitis
• bronchitis is defined as
coughing and overproduction of
mucus for at least 3 months of
the year for more than 2
consecutive years.
• Characterized by:
• Irritation of the bronchial tubes
(from smoking, air
pollution, etc.)
• Constant coughing causes
damage to the bronchial tubes.
• Reduced airflow to the lung
(shortness of breath).

4. Chronic bronchitis (cont.)
• The pathologic change consists of thickened
bronchial walls with inflammatory cell
infilterate, increase of the size of mucous
glands & global cell hyperplasia.
• Inflammation also causes the glands that line
the bronchi to produce excessive amounts of
mucus, further narrowing the airways and
blocking airflow.
• This leads to chronic productive cough with
shortness of breath.

5. B- Emphysema
• Is distention of the air spaces distal
to the terminal bronchioles because
of destruction of alveolar walls
(septa).
• It causes an overproduction of the
enzyme elastase; one of the
immune system's infection-fighting
biochemicals. This results in
irreversible destruction of a protein
in the lung called elastin which is
important for maintaining the
structure of the walls of the alveoli.
Obstruction occur by collapse of
these unsupported and enlarged air
spaces on expiration.

6. Emphysema (cont.)
• Causes and symptoms:
• Cigarette smoking is by far the most important risk
factor.
• Age: Chronic bronchitis is more common in people
over 40 years old; emphysema occurs more often in
people 65 years of age and older.
• Socioeconomic class. COPD-related deaths are
about twice as high among unskilled and semi-skilled
laborers as among professionals.

7. Emphysema (cont.)
• Family clustering. It is thought that heredity
predisposes people in certain families to the
development of COPD when other
causes, such as smoking and air
pollution, are present.
• Lung infections. Lung infections make all
forms of COPD worse.
• In emphysema, shortness of breath on
exertion is the predominant early symptom.
Coughing is usually minor and there is little
sputum.

8. COPD (cont.)
• The first step in diagnosing COPD is a
good medical evaluation, including a
medical history and a physical
examination of the chest using a
stethoscope.
• Additional tests can be ordered;
Pulmonary function test by using
spirometer

9. Additional diagnostic tests:
• Using a spirometer, an instrument that
measures the air taken into and exhaled
from the lungs, the doctor will determine two
important values:
• (1) vital capacity (VC), the largest amount of
air expelled after the deepest inhalation.
• 2) forced expiratory volume (FEV1), the
maximum amount of air expired in one
second. The pulmonary function test can be
performed in the doctor's office, but is
expensive.
• Chest x rays can detect only about half
of the cases of emphysema. Chest x
rays are rarely useful for diagnosing
chronic bronchitis.

10. 2- Asthma
• Is a chronic inflammatory
respiratory disease
consisting of recurrent
episodes of dyspnea,
coughing, and wheezing.
• Characterized by:
• Constriction of the airways
in the lungs.
• Swelling of the lining of the
bronchial tubes in the lungs.
• Secretion of excessive
amounts of thick mucus.

11. Etiology:
Types:
1- Extrinsic(allergic or atopic).
2- intrinsic (idiosyncratic).
3- drug induced.
4- exercise induced.
5- infectious.
Allergic asthma is the most common 35% of adult
cases is triggered by inhaled seasonal
allergens such as polens, dust, house mites.

12. 1- Extrinsic(allergic or atopic):
• Most common 35% of cases.
• Triggered by inhaled allergen such as
pollens, dust, house mites & animal danders.
• It affects young adults and childern.
• The complex of antigens with antibody
causes degranulation of mast cells to secret
bradykinins , histamine & prostaglandins.
• These compounds causes
bronchoconstriction increased vascular
permeability.

13. 2- intrinsic (idiosyncratic).
• It is associated with family history of
allergy or with known causes.
• Non response to skin tests with normal
IgE .
• Middle aged adults due to endogenous
causes; emotional stress or vagal
mediated response.

14. 3- drug induced:
• Drugs such as aspirin, NSAIDs, Beta-
blockers, angiotensin-converting
enzyme inhibitors .
• Food substances such as nuts,
shellfish, strawberries, milk & food dye
can trigger asthma.

15. 4- Exercise Induced:
• It is stimulated by exertional activity.
• The pathogenesis of this form is
unknown.
• Childern and young adults are more
commenly affected.
5- infectious asthma: respiratory
infection can develop bronchial
constriction due to inflammatory
response to infection.

16. Signs & symptomes:
• Wheezing.
• Shortness of breath, perhaps only with
exercise .
• Feeling a tightness in the chest.
• Coughing, which may occur only at
night .
• Chronic asthma can be classified into;
mild, moderate and sever according to
the frequency of acute attacks and lung
function.

17. Triggers of Attacks can be dentistry-related.
Documented Cases include:
• Tooth enamel dust (OOO 75:599,1993)
• Methyl methacrylate (Thorax 39:712, 1984;
Tubercle & Lung Dis 75:99,1994)
• Menthol (J Investig Allergol Clin Immunol. 2001;11(1):56)
• Aspirin-induced (Chest. 1994 Aug;106(2):654)
• Toothpaste (J Aller Clin Immunol. 1992; N Engl J
Med. 1990 323(26):1845)
• Foreign bodies: Lego (N Engl J Med. 1996
334(6):406)11

18. Mediators of Asthma
• Released from bronchial mast
cells, alveolar macrophages, T
lymphocytes and epithelial cells
• Histamine, tryptase,
leukotrienes and prostglandins
• Early-phase response: injury from
eosino- and neutrophils
Bronchoconstriction
• Late-phase: epithelial damage,
airway edema, mucous
hypersecretion,
hyperresponsiveness of bronchial
smooth muscle

19. Warning Signs of an Asthma Attack
Irregular breathing: wheezing, labored
breathing, cough
Dyspnea, chest tightness
Drop in FEV (<50% of optimum)
Tachypnea, tachycardia
Diaphoresis – sweating and paleness
Pulsus paradoxus (decline of pulse magnitude,
i.e. > 10 mm Hg in blood pressure, during inspiration
compared to expiration)

20. Additional Features of Asthma Attack
• Anxious or scared look
• Flared nostrils during inhalation
• Pursed lips breathing, Fast breathing
• Hunched-over body posture; patient can't
stand or sit straight and can't relax
• Intercostal (between ribs or
supraclavicular) depressions during
inhalation
Poor oxygenation (pulse oximeter, blue lips, nails, struggle to breathe)
Emergency

21. Oral Manifestations -Asthma
• Altered nasorespiratory function (mouth breathing)
• Increased prevalence of caries with moderate to
severe asthma.
• B2 agonist decrease salivary flow by 20-35%,
associated with increased # of lactobacilli
• Misuse of inhaled corticosteroids increases the risk
of oral candidiasis

22. Asthma -Complications
• Most patients can expect reasonably good
prognosis; however small % of patients
progress to emphysema and respiratory failure
or develop status asthmaticus
• Status asthmaticus
is the most serious complication associated with
asthma
• consists of a severe and prolonged asthmatic
attack (lasts > 24 hours) and is refractory to usual
therapy.

23. Asthma –Complications(cont.)
• Signs include increased dyspnea, jugular
venous pulsation, cyanosis and pulsus
paradoxus (a fall in pulse magnitude as
measured by ↓ systolic pressure with
inspiration). It is often associated with
infection.
• Can lead to exhaustion, severe
dehydration, peripheral vascular collapse
and death.

24. •Chest x-rays (for
hyperinflation)
• Skin testing (for specific
allergens)
• Histamine or methacholine
chloride challenge testing,
• Sputum smears & blood
counts (for eosinophilia)
• Arterial blood gases,
• Antibody-based enzyme-
linked immunosorbent assay
(ELISA) for measurement of
environmental allergen
exposure,
and SPIROMETRY (a peak
expiratory flow meter that
measures pulmonary function
Commonly ordered tests

25. Managing Asthma
• Classification
• Goal: limit exposure to triggering agents,
allow normal activities, restore and maintain
pulmonary function.
• Choice of medication
based on type & severity;
and lifestyle change
• Written action plan

26. Drugs used by Asthmatics
• Anti-Inflammatory Agents (1st agents of
choice)
• Secondary Agents
– Bronchodilators (can be faster acting – use in
emergency)
– Methylxanthines
– Anticholinergic drugs

27. Additional Treatment approaches
Systemic steroids +/- cyclosporine or
methotrexate – for severe asthma
NEW: Recombinant injectable humanized
monoclonal antibody that binds IgE (Omalizumab
[Xolair]; SubQ; Genetech/Novartis) prevents IgE
from binding mast cell/basophil receptors
It is effective in treating adults and children with
asthma; allowed for withdrawal of inhaled steroids
successfully in 55% of asthmatics (ADES HA,
fever, urticaria and pruritis)

28. Dental Management of Asthmatic Patient
Pretreatment Assessment: STABILITY
– History (duration, severity, recent hospitalizations, respiration
rate, eosinophil count, triggers)
– Taking medicines (type, how much, today?), bring inhaler
– Avoid triggers: cold air, dust, feathers or molds, animal
dander, cigarette smoking, pollution, fragrances
– Prophylax with inhaler
– Being Stressed is a trigger
• Use Anxiolytic: nitrous oxide, hydroxyzine (antihistamine
+ sedative.

29. Dental Management of Asthmatic Patient
Treatment: avoid/reduce irritating odorants,
sulfites, rotary-derived particulate matter,
continue anxiolytic therapy,
– Avoid barbiturates and narcotics, particularly
meperidine. They are histamine-releasing drugs
and can provoke an attack. Aspirin use can
trigger an attack. . .
– special needs for pt on systemic steroids

30. Dental Management of Asthmatic Patient
Post treatment: avoid macrolide antibiotics with
Theophylline (drug interaction).
Asthma attack: act immediately; stop procedure,
remove RD, administer SA-bronchodilator
and O2, if no relief subQ epinephrine (1:1000)
0.3-0.5 mL, repeat inhaler and epinephrine q5
min as needed

31. 3-Tuberculosis
Tuberculosis is a chronic, infectious disease
that primarily attacks the lungs.
• Mycobacterium tuberclosis is a bacterial
causative organism. It is transmitted by
salivary droplets.
• An infectious disease of humans and animals
caused by the tubercle bacillus and
characterized by the formation of tubercles on
the lungs and other tissues of the body, often
developing long after the initial infection

32. Tuberculosis(cont.)
• Tuberculosis (TB) is caused by a
bacteria that primarily attacks the
lungs.
• An individual may be "TB infected,"
meaning the bacteria are in the
body but are in an inactive state,
walled off behind scab-like
structures that are the body's
defense mechanism.
• Or have "TB disease," when the
bacteria actively spread throughout
the body and can cause damage to
the lungs or other organs
Scanning electron
micrograph of
Mycobacterium
tuberculosis

33. Tuberculosis(cont.)
Mode of transmission:
1- Air borne droplets of mucous or saliva
by cough sneezing or talking.
2- ingestion (contaminated milk) rarely
occur due to using pasteurized milk.
Interval from infection to active TB ranges
from few weeks to decades.
• Active TB can be triggered when
a person's immune system is
weakened, such as from human
immunodeficiency virus (HIV),
malnutrition, or alcohol abuse.
Mycobacterium tuberculosis
(stained red) in sputum

34. Tuberculosis(cont.)
• Pathogenesis:
• TB infection begins when the
mycobacteria reach the pulmonary
alveoli, where they invade and
replicate within alveolar
macrophages.[19] The primary site
of infection in the lungs is called
the Ghon focus.
• Bacteria are picked up by dendritic
cells, which do not allow
replication, although these cells
can transport the bacilli to local
(mediastinal) lymph nodes

35. Tuberculosis(cont.)
• Further spread is through the bloodstream to the
more distant tissues and organs where secondary
TB lesions can develop in lung apices, peripheral
lymph nodes, kidneys, brain, and bone.
• Tuberculosis is one of granulomatous
inflammatory conditions as a group of epithelioid
macrophages surrounded by a lymphocyte cuff.
• TB granuloma develops caseous necrosis at the
center of tubercle. Tissue destruction and necrosis
are balanced by healing and fibrosis.
• Affected tissue is replaced by scarring and cavities
filled with cheese-like white necrotic material

36. Tuberculosis(cont.)
• Diagnosis:
• 1- Tuberclin skin test:
subcutaneous skin injection of
purified protein derivatives of M.
tuberculosis.
• If the bacteria are present,
whether active or inactive, the
patch of skin will swell.

37. Tuberculosis(cont.)
2- Chest x-ray:
Presence of cavitation in
the lung of AP view of
chest x-ray can help in
TB diagnosis.
3- sputum culturing for
detection of bacillus
bacteria .
X-ray of a patient with
tuberculosis. A cavity-
like lesion is visible on
the upper-right lobe of
the lung.

38. Interpretation of TST
• > 5 mm: considered
positive if close contact
with infected person,
abnormal chest x-ray,
or HIV positive
• >10 mm: considered
positive if other medical
risk factors present,
foreigner, medically
underserved, alcoholic,
long-term care resident
• > 15 mm: positive

39. Tuberculosis(cont.)
• Signs & Symptoms:
• A cough lasting three or more weeks that may
produce discolored or bloody sputum
• Unintended weight loss
• Fatigue
• Slight fever
• Night sweats
• Chills
• Loss of appetite
• Pain with breathing or coughing (pleurisy)

40. Tuberculosis(cont.)
• Other sites of TB infections:
• Scrofula:form of tuberculosis affecting the
the neck lymph nodes, most common in
children and is usually spread by
unpasteurized milk from infected cows. Also
called struma.
• Milliary TB : spread of TB through the
blood.
• wasting disease; white plague: TB of the
skin, because sufferers appear markedly
pale.

41. Tuberculosis(cont.)
Medical treatment:
I) medical regimen:
1-- Patient education and compliance.
2- Appropriate selection of drugs.
3- Multiple drug use.
4- Drug administration continuance For a sufficient time.
• It is treated with a regimen of strong antibiotics
such as Rifampin and Isoniazid for six months
to two years.

42. Tuberculosis(cont.)
Dental management:
• 1- active sputum- positive tuberculosis should not
be treated on an outpatient basis.
• 2- patient with a past history of TB: dentist should
obtain medical history of treatment duration if less
than 18 months or 9 months with physician
consultation.
• 3- patient with positive tuberculin test and give a
history of active TB , prophylactic ionized may be
started for 6 months to a year to prevent clinical
disease. Normal treatment can be done without
special precautions.

43. Tuberculosis(cont.)
4- patients with signs or symptoms
suggestive of TB:
If any symptoms of suggested TB such as non
productive cough, pleuritic chest pain, fatigue,
fever, dyspnea, hemoptysis, weight loss →
dental care should not be provided and pt
referred to physician.

44. Tuberculosis(cont.)
• High-risk populations:
• 1-THE ELDERLY:Many elderly patients developed the
infection some years ago when the disease was more
widespread.
• 2-RACIAL AND ETHNIC GROUPS:
• It is more common in blacks, who are more likely to live
under conditions that promote infection.
• two-thirds of all cases of TB in the United States affect
African Americans, Hispanics, Asians, and persons
from the Pacific Islands.
• 3- LIFESTYLE FACTORS:HIV pts who have not yet
developed clinical signs of AIDS. Alcoholics and
intravenous drug abusers are also at increased risk of
contracting tuberculosis.

45. THE END