This document discusses periodontal management considerations for patients with respiratory diseases. It begins with introductions to periodontal diseases, respiratory system anatomy, and pathogenesis. Key points are that periodontitis results from bacterial infection and inflammation in the tissues surrounding teeth. The lungs have defenses against inhaled microbes but can be compromised. The document then discusses specific respiratory conditions like pneumonia, asthma, COPD, and tuberculosis, noting oral bacteria that may cause infections. Dental management for these patients includes reducing aerosols, avoiding triggers, using preventive treatments, and considering medical conditions and medications.

2. PERIODONTAL MANAGEMENT IN PATIENTS
WITH RESPIRATORY DISEASES

3. CONTENTS:
Introduction
Anatomy of respiratory system
Pathogenisis
Cause for the disease
Dental management of respiratory diseases

4. INTRODUCTION

5. Periodontal diseases are bacterial infections associated with bacteraemia,
inflammation, and a strong immune response
Periodontitis is an inflammatory reaction to bacterial infections that results in the
destruction of the tooth-supporting structure I.e periodontium
The periodontium comprises:
Gingiva
Periodontal ligament
Root cementum
Alveolar bone

6. ANATOMY OF RESPIRATORY SYSTEM

7. –Johnny Appleseed
• The lung is composed of numerous units formed by the progressive branching of the
airways
• The airway of each terminal respiratory unit is lined by epithelial cells in close
proximity on their basal aspect to capillaries, which permits the efficient exchange
of gases.
• The lower airways are normally sterile, despite the fact that the secretions of the
upper airways are heavily contaminated with microorganisms seeded from the oral
and nasal surfaces.

8. • Sterility of the lower airway is maintained by intact cough reflexes, the action
of tracheobronchial secretions and mucociliary transport of inhaled
microorganisms and particular material from the lower respiratory tract to the
oropharynx, and immune and non immune defense factors
• The defense factors are contained within a secretion that coats the pulmonary
epithelium. The secretion contains surfactant, other proteins such as
fibronectin, complement and immunoglobulins.

9. PATHOGENESIS

10. In lungs
Accumulation of respiratory pathogens
|
Relase of bacterial toxins such as Protease
|
Activation of complement system
|
Recruitment and activation of neutrophils
|
phagocytosis
|
Relase of neutrophil proteinases
|
Abnormal Connection tissue destruction

11. In Periodontal tissues
Accumulation of pathogenic periodontal microflora
|
Release of bacterial toxins such as Protease
|
Activation of complement system
|
Recruitment and activation of neutrophils
|
phagocytosis
|
Release of neutrophil proteinases
|
Abnormal Connection tissue destruction
|
Periodontitis

12. CAUSE?
The oral bacterial species implicated in causing pneumonia and lung abscesses are
Actinobacillus actinomycetemcomitans, Actinomyces israelii, Capnocytophaga
species, Eikenella corrodens, Prevotella intermedia, Porphyromonas gingivalis and
Streptococcus constellatus
Scannapieco has proposed several mechanisms to explain the potential role of oral
bacteria in the pathogenesis of respiratory infection:
Aspiration of oral pathogens (such as Porphyromonas gingivalis, Actinobacillus
actinomycetemcomitans, etc.) into the lung to cause infection

13. Periodontal disease-associated enzymes in saliva may modify mucosal surfaces to
promote adhesion and colonization by respiratory pathogens, which are then
aspirated into the lung,
Periodontal disease-associated enzymes in saliva may destroy salivary pellicles on
pathogenic bacteria to hinder their clearance from the mucosal surface
Cytokines originating from periodontal tissues may alter respiratory epithelium to
promote infection by respiratory pathogens.

14. RESPIRATORY INFECTIONS INCLUDES:
Pneumonia
Chronic obstructive pulmonary disease
Asthma
Tuberculosis

15. DENTAL MANAGEMENT

16. IN PNEUMONIA PATIENTS :
Use 0.12% chlorhexidine gluconate rinse prior to beginning
treatment to reduce the bacterial load
Avoid use of ultrasonic scalers due to the production of
aerosols

17. IN ASTHMA PATIENTS
During treatment
Prevent triggering a hypersensitive airway by properly placing cotton rolls, fluoride trays,
and suction tip.
Use local anesthetic without sulfites.
Fluoride treatment for all patients with asthma, especially those using beta-2 agonists.
If asthma attack occurs, stop treatment, rule out foreign-body obstruction, initiate
emergency procedures

18. After treatment:
Home care instructions: advise patient to rinse mouth with water after using inhaler
to decrease oral candidiasis. Analgesic drug of choice is acetaminophen (aspirin or
non steroidal anti-inflammatory drugs may trigger attack).

19. IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE:
THINGS TO AVOID
Rubber dam use
Nitrous oxide sedation(in severe cases)
Barbiturates and narcotics
Antihistamines and anticholinergics
Macrolide and ciprofloxacin(if patient is on theophylline)

20. THINGS TO DO
Treat in upright chair position
Use inhalers prior to treatment
Use pulse oximeter
Use low flow oxygen when oxygen saturation is less than95% unless baseline is
lower
Use low dose oral diazepam
Supplement steroids maybe required

21. IN TUBERCULOSIS PATIENTS:
After 2 to 3 weeks of treatment for tuberculosis treat the
patient normally
History of tuberculosis :treat normally if no active disease
If the test is positive,treat normally if no active disease
New,active tb:treat only in emergency conditions with proper
isolation
If any clinical signs of tuberculosis,do not treat

22. REFERENCES
Wilkins clinical practice of the dental hygienist

23. THANK YOU