Respiratory Disorder& Periodontal Disease.pptx

Respiratory Disorder& Periodontal Disease relationship

1. Respiratory Disorder And Periodontal Disease 1

2. Recently, there has been a resurgence of interest in the interaction b/w periodontal disease & respiratory disease . Respiratory diseases are responsible for significant morbidity & mortality in human populations. Oral periodontopathic bacteria can be aspirated into the lung to cause aspiration pneumonia. 2

3. The teeth may also serve as a reservoir for respiratory pathogen colonization & subsequent nosocomial pneumonia . Typical respiratory pathogens have been shown to colonize the dental plaque of hospitalized intensive care & nursing home patients. 3

4. Human Respiratory System 4

5. Defence Mechanism Of Respiratory System The dust particles, which enter the nostrils are prevented from entering lungs by filtration action of the hairs in nasal mucous membrane . The small particles, which escapes the nasal hairs , are held by the mucous secreted by the nasal mucous membrane. 5

6. Those dust particles , which escapes the nasal hairs & nasal mucous membrane , are destroyed by the phagocytic action of the macrophages in the alveoli . The particles which escape the protective mechanisms in nose & alevoli are thrown out by cough reflex & sneezing reflex . 6

7. Role of lungs in defence mechanism : Once a bolus of material has been aspirated into the lung instead of being swallowed, it encounters many respiratory defenses . First, the lung is protected from aspirated material by the cough. In order to expel the unwanted material, intact diaphragm is required. The ability of the lung to move the unwanted material, which is referred to as lung clearance, is a key factor in the lung's ability to protect itself from infection. 7

8. Lungs play important role in the immunological defenses system of the body. The defense functions of the lungs are performed by the presence of various types of cells in the mucous membrane lining the alveoli of lungs. 8

9. Respiratory Diseases 9

10. Bacterial pneumonia Pneumonia is the inflammation of lung tissues followed by the accumulation of blood cells, fibrin & exudates in the alveoli. It is caused by a wide variety of infectious agents, including bacteria, mycoplasma, fungi, parasites, & viruses, resulting in the infection of the pulmonary parenchyma. 10

11. Bacterial Pneumonia can be classified as : Community acquired Hospital acquired (nosocomial ) Community acquired bacterial pneumonia is caused by : Streptococcus pnuemoniae Haemophilus influenzae Mycoplasma pnuemoniae Chylamydia pnuemoniae Legionella pnuemophila Staphylococcus aureus Candida albicans Anaerobic species 11

12. Nosocomial pneumonia is caused by : Gram negative bacilli (including enterics such as Escheria coli, Klebsiella pnuemoniae , & Enterbacter spp. as well as Pseudomonas aeruginosa ) Staphylococcus aureus - most prevalent 12

13. Clinical features: - High grade fever, chills , rigors & vomiting. Convulsions may occur in children. - Loss of appetite, headache , aching pains in the body & limbs. - Localized pleuritic chest pain. - Sputum is rust colored. - Breathing is rapid , & shallow. - Tachycardia, hot & dry skin, flushed face & occasionally central cyanosis. 13

14. Chronic Obstructive Pulmonary Disease (COPD) COPD is characterized by chronic obstruction to airflow with excess production of sputum resulting from chronic bronchitis (CB) and or emphysema. Chronic bronchitis is defined as a condition associated with excessive tracheobronchial mucous production , to cause cough with expectoration for at least 3 months of the year, for more than 2 consecutive years. 14

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16. It is the result of irritation to the bronchial airway causing an expansion of the proportion of mucous-secreting cells within the airway epithelium. Incidence Middle and late adult life. More in males. More in smokers. More in urban than in rural areas. 16

17. Etiology: Cigarette smoking. Air pollution with dust, smoke & fumes , sulphur dioxide & particulate matter. Occupational hazards as with exposure to dust, smoke & fumes, toluene di- isocyanate in plastic industry & in cotton mills. Familial & genetic factors Genetic predisposition. Children of smoking parents Passive smoking. Natural gas used for cooking. Infections with rhinovirus , Strep. Pneumoniae & Haemophilus influenzae . Exposure to dampness , fog & sudden changes in temperature 17

18. Clinical features : History of cough with sputum production for many years & a relatively late onset of breathlessness . Fever during mucopurulent relapses, wheezing & tightness in chest. 18

19. Emphysema is defined as the distention of the air spaces distal to the terminal bronchiole with destruction of the alveolar septa. Etiology: Smoking. occupational causes- furnace blowers , goldsmiths, exposure to cadmium. Clinical features: Progressive exertional breathlessness with minimum cough & expectoration. Weakness ,anorexia , lethargy & weight loss can occur with advanced disease. 19

20. Basis Of Relating Periodontal Disease With Respiratory Disorders It has become apparent in recent years that the oral cavity may be an important reservoir for bacterial pathogen that cause lung disease . The incidences of respiratory pathogen oropharyngeal colonization by respiratory pathogens appear to be more common in patients with teeth or dentures than in edentulous(Without teeth) patients . 20

21. Diminished salivary & salivary pH may promote colonization by respiratory pathogens; these conditions occur in ill patients & those receiving various medications. Oral colonization by respiratory pathogens is common in institutionalized patients, especially those admitted to hospital ICUs & in the elderly who are debilitated, hospitalized, or in a nursing home. 21

22. Poor oral hygiene & periodontal disease may foster respiratory pathogen oropharyngeal colonization, & patients who have poorer oral hygiene than community-dwelling individuals. Several oral interventions that improve oral hygiene result in a reduction in the rate of pneumonia in high risk subjects. 22

23. Oral Bacterial As Etiologic Agents Of Respiratory Infection Teeth and periodontium can serve as a reservoir for respiratory infection. Oral bacteria can be released from the dental plaque into the salivary secretions which are then aspirated into the lower respiratory tract to cause pneumonia . Severe anaerobic lung infections can occur following aspiration of salivary secretions especially in patients with periodontal disease. 23

24. 30 to 40% of all cases of aspiration pneumonia, necrotizing pneumonia, or lung abscess involve anaerobic bacteria. A variety of oral anaerobes and facultative species have been cultured from infected lung fluids, including Porphyromonas gingivalis , Bacteroides gracilus , Bacteriodies oralis , Bacteroies buccae , Eikenella corrodens , Fusobacterium nucleatum , Fusobacterium necrophourm , Actinobacillus actinomycetemocomitans , Paptostreptococci , Clostridum , & Actinomyces . 24

25. Most of these organisms have been associated with periodontal disease . Viridans streptococci may participate in the initiation and/or progression of pneumonia . 25

26. Bacteria that colonize the supra- or subgingival dental plaque are shed into the saliva . Bacteria can either be associated with P . gingivalis , F nucleatum etc or respiratory pathogens (P. aeruginosa, Klebsiella pneumonia etc ) 26

27. The saliva is aspirated into the lower respiratory tract where an infection can occur . Cytokines from periodontically diseased tissues that enter the saliva may be aspirated to stimulate local inflammatory processes – initiation and/or progression of infection in the lung 27

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29. Dental Plaque as a Reservoir of Respiratory Pathogens Lack of attention to oral hygiene results in an increase in the mass & complexity of dental plaque, which may foster interbacterial interactions b/w indigenous plaque bacteria & respiratory pathogens such as P. aeruginosa & enteric bacilli . These interactions may result in colonization of the dental plaque by respiratory pathogens. Dental plaque may therefore provide a reservoir for respiratory pathogen colonization that can be shed into saliva. 29

30. Contamination of the distal portions of the respiratory tree by saliva containing such organisms may result in pulmonary infections . Respiratory pathogens that establish in dental plaque may be difficult to eradicate as bacteria in biofilms are much more resistant to antibiotics . Scannapieco FA et al.(1996,1998) found that patients admitted to medical intensive care units (MICU) have poorer oral hygiene than non-hospitalized patients & have a higher prevalence of respiratory pathogen colonization on the teeth & oral mucosa than age & gender-matched outpatients 30

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32. These results strongly suggest that patients admitted to ICUs have a significant risk for oral colonization by respiratory pathogens . Thus the oral cavity may serve as an important factor of infection for respiratory disease in high risk subjects, such as hospitalized or COPD patients. 32

33. Oral status and COPD To evaluate the relationship b/w COPD & oral health status Scannapieco FA et al.(1998) analyzed data from National Health & Nutrition Examination Survey I (NHANES I ) This data base contains information on the general health status of 23,808 individuals. Of these, 464 reported respiratory conditions. 33

34. These subjects were further categorized as having a confirmed chronic respiratory disease (chronic bronchitis & emphysema) , acute respiratory disease ( influenza, pneumonia, acute bronchitis ), or not to have a respiratory disease . Individuals with a confirmed chronic respiratory disease had a significantly greater oral hygiene index than subjects without a respiratory disease. Subjects with acute disease tended to have more decayed teeth than those without disease . 34

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37. Aspiration of oral pathogens 37

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39. Periodontal Disease-Associated Enzymes in Saliva May Modify Mucosal Surfaces Dental pathogens such as P.gingivalis produce enzymes (such as proteases) that alter mucosal surface adhesion receptors for respiratory pathogens such as H.influenzae ,( Haemophilus influenzae ) which adhere , colonize & can subsequently be aspirated into the lung to cause infection. 39

40. Destruction of Protective Salivary Pellicles by Oral Bacteria P.gingivalis produce enzymes that degrade the salivary molecules that normally form pellicle on the pathogens which prevents them from adhering to mucosal surfaces . 40

41. Salivary Cytokines May Alter Respiratory Epithelium In periodontal disease, oral pathogens continuously stimulate cells of the oral tissues periodontium to release a wide variety of cytokines & other biologically active molecules . Cytokines produced by epithelial cells in response to these bacteria including IL-l  , IL-1  , IL-6, IL-8, and TNF . 41

42. Epithelial cells alter expression of various cell adhesion molecules on their surface in response to cytokine stimulation, Variation in expression of such adhesion molecules may alter the interaction of bacterial pathogens with the mucosal surface. Cytokines entering the saliva From inflamed periodontal tissues Up regulate the expression of adhesion receptors on the mucosal surfaces to promote respiratory pathogen colonization. 42

43. Mechanism proposed for the gross airway epithelial damage observed in COPD involves release of pro-inflammatory cytokines (i.e., IL-8) from the respiratory epithelium, resulting in the recruitment and infiltration by neutrophils which subsequently release proteolytic enzymes & toxic oxygen radicals. The release of cytokines from the respiratory epithelium may be the result of the binding of respiratory pathogens or their products to the respiratory epithelial cells. 43

44. This mechanism has been demonstrated for pathogens such as Strepto -coccus pneumoiae & H. influenzae , which are also known to attach to mucosal receptors & to stimulate cytokine production by the underlying cells. Oral bacteria in secretions in contact with respiratory epithelial surfaces may adhere to the mucosal surface. These bound oral bacteria may stimulate cytokine production by mucosal epithelium. 44

45. Cytokines originating from the oral tissues may contaminate the distal respiratory epithelium to stimulate respiratory epithelial cells. The stimulated respiratory cells may then release other cytokines that recruit inflammatory cells (e.g., neutrophils) to the site which may release hydrolytic enzymes & other modifying molecules resulting in damaged colonization respiratory pathogens. 45

46. PREVENTION OF ORAL COLONIZATION BY POTENTIAL RESPIRATORY PATHOGENS 46

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48. Chlorhexidine Inhibit dental plaque formation, gingivitis, & oral mucosal ulcerations . It also inhibits the production of proteases by subgingival bacteria, by inhibiting protease activity, chlorhexidine may diminish the potential of these enzymes to process oral surfaces to expose “ cryptitopes ” that may act as receptors for bacterial adhesions. 48

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54. CONCLUSION Evidence demonstrating that periodontitis poses a significant risk for respiratory diseases. Oral secretions and/or oral bacteria may contain hydrolytic enzymes or cytokines that alter epithelial surfaces in ways that increase susceptibility to adhesion & colonization by respiratory pathogens. Thus , poor oral health may increase the risk for serious lower respiratory tract infection in susceptible subjects, including pneumonia in hospitalized subjects or exacerbation & progression of COPD. 54

55. References 55