aetiology of Periodontal disease P2

Question 1

Describe the Nonspecific Plaque Hypothesis.

Answer 1

The Nonspecific Plaque Hypothesis, proposed by Theilade in 1986, suggests that periodontal diseases result from the accumulation of plaque over time, combined with a diminished host response and increased susceptibility with age. It posits that periodontal disease arises from the noxious products produced by the entire plaque flora.

Question 2

Define the Specific Plaque Hypothesis.

Answer 2

The Specific Plaque Hypothesis, introduced by Loesche in 1979, emphasizes the importance of the qualitative composition of the microbiota in dental plaque. It states that the pathogenicity of dental plaque is dependent on the presence or increase of specific microorganisms, with certain bacteria being associated with specific types of periodontal disease.

Question 3

How do mixed infections influence microbial interactions in dental biofilm?

Answer 3

Mixed infections can lead to both favorable and antagonistic bacterial interactions within dental biofilm. Some bacteria may provide growth factors or enhance the attachment of others, while others may compete for nutrients and binding sites, potentially affecting the pathogenicity of one another.

Question 4

What are some examples of bacterial co-existence in periodontal conditions?

Answer 4

Examples of bacterial co-existence include: ANUG with spirochetes and fusobacteria, active lesions with P. intermedia and Pg, implant failure with Tanerella forsythia and Pg, diabetes with P. intermedia, Pg, and Campylobacter, and preterm labor with A. actinomycetemcomitans, Pg, Tanerella forsythia, and Treponema denticola.

Question 5

Describe the classification of bacteria in dental biofilm according to Socransky et al.

Answer 5

Socransky et al. (1998) classified bacteria in dental biofilm into color clusters based on their nutritional and atmospheric requirements. These clusters include the yellow cluster (Streptococcus species), purple cluster (Actinomyces odontolyticus and Veillonella parvula), green cluster (Capnocytophaga and A. actinomycetemcomitans), and orange cluster (Fusobacterium and Prevotella species).

Question 6

How does the yellow cluster of bacteria contribute to dental biofilm?

Answer 6

The yellow cluster, composed of species like Streptococcus sanguis, is thought to consist of early colonizers that express receptors for host proteins, enabling rapid and firm attachment to the host surface.

Question 7

What role do bridging species play in dental biofilm?

Answer 7

Bridging species, such as those in the orange cluster (Fusobacterium spp and Prevotella spp), are important in dental biofilm as they have physiological capabilities to utilize and release nutrient substances, facilitating the binding of early colonizers to other members of the biofilm.

Question 8

Define the ecological plaque hypothesis.

Answer 8

The ecological plaque hypothesis, proposed by Marsh et al. in 1999, suggests that the interactions among bacteria in dental biofilm can be both beneficial and harmful, influencing the overall pathogenicity of the biofilm based on the presence of various microbial species.

Question 9

How does the presence of specific microorganisms affect periodontal disease?

Answer 9

The presence of specific microorganisms, as highlighted in the Specific Plaque Hypothesis, is crucial for the pathogenicity of dental plaque. Certain bacteria are linked to specific forms of periodontal disease, indicating that not all plaque is equally harmful.

Question 10

Describe the characteristics of P. gingivalis and T. denticola in relation to periodontal disease.

Answer 10

P. gingivalis and T. denticola are specific bacterial species that are prime candidates as pathogens involved in the clinical destruction of periodontal tissues, occurring alongside clinical signs of periodontal destruction.

Question 11

Define pathogenicity in the context of periodontal bacteria.

Answer 11

Pathogenicity is the ability of a microbe to produce disease and cause damage in the host, distinguishing pathogenic oral bacteria from non-pathogenic ones based on their virulence factors.

Question 12

How do virulence factors contribute to the pathogenicity of periodontal bacteria?

Answer 12

Virulence factors are bacterial products, including proteins and polysaccharides, that help bacteria avoid or destroy normal human immune defenses, leading to tissue damage.

Question 13

What are the key components of bacterial virulence?

Answer 13

Bacterial virulence includes the capacity to colonize, the ability to evade host defense mechanisms, and the ability to produce substances that initiate tissue destruction.

Question 14

Explain the significance of virulence in periodontal pathogens.

Answer 14

Virulence determines the strength of a pathogen’s potential to cause damage in the host and its ability to overcome host defenses, including invasiveness and tissue-destructive capacity.

Question 15

List some virulent periodontal pathogens.

Answer 15

Virulent periodontal pathogens include Actinobacillus actinomycetemcomitans, Prophyromonas gingivalis, Bacteroides forsythus, Prevotella intermedia, Fusobacterium nucleatum, Campylobacter rectus, Eikenella corrodens, and spirochetes.

Question 16

Describe Actinobacillus actinomycetemcomitans (A.a) and its role in periodontitis.

Answer 16

A.a is a nonmotile, gram-negative, coccobacillus that is a typical cause of periodontitis and may also be associated with systemic infections, fulfilling the criteria of an etiological agent of periodontitis.

Question 17

How is Actinobacillus actinomycetemcomitans detected in periodontitis cases?

Answer 17

A.a is highly detected in localized aggressive periodontitis (90%) and to a lesser extent in chronic periodontitis (50%), with high serum antibody levels indicating its presence.

Question 18

What happens to Actinobacillus actinomycetemcomitans when periodontal disease is successfully treated?

Answer 18

The organism is eliminated when the periodontal disease is successfully treated, indicating its role in the disease process.

Question 19

Describe the role of lipopolysaccharide (LPS) in the virulence of A. actinomycetemcomitans.

Answer 19

LPS has a broad spectrum of immunological and endotoxic activities, including stimulating B lymphocytes, activating macrophages, producing IL1, and releasing prostaglandin E2, which contributes to bone resorption.

Question 20

How do adhesins contribute to bacterial virulence?

Answer 20

Adhesins mediate bacterial cell adherence and attachment to epithelial cells, other bacteria, and extracellular matrix proteins, facilitating colonization and infection.

Question 21

Define leukotoxin and its impact on immune cells.

Answer 21

Leukotoxin is a protein antigen that is cytotoxic to human polymorphonuclear leukocytes, monocytes, and T-lymphocytes, leading to loss of immune cell function and contributing to the severity of aggressive periodontitis.

Question 22

Explain the function of the capsular polysaccharide in Porphyromonas gingivalis.

Answer 22

The capsular polysaccharide provides protection against phagocytosis by PMNs and prevents the activation of the alternative complement pathway, shielding Pg LPS.

Question 23

How does Pg lipopolysaccharide (LPS) differ from that of other gram-negative bacteria?

Answer 23

Pg LPS does not directly stimulate the production of E-selectin by endothelial cells, preventing leukocyte binding and migration, thus blocking a key step in the inflammatory response.

Question 24

Describe the role of enzymes produced by Porphyromonas gingivalis.

Answer 24

Pg produces enzymes that degrade serum proteins, including immunoglobulins and complement components, which helps it evade the host immune response.

Question 25

What is the significance of extracellular membranous vesicles in bacterial virulence?

Answer 25

Extracellular membranous vesicles mediate endotoxic, leukotoxic, and bone resorption activities, enhancing the pathogenicity of the bacteria.

Question 26

How do fimbriae contribute to the virulence of A. actinomycetemcomitans?

Answer 26

Fimbriae facilitate adherence to host tissues and may trigger an immune response, with antibodies against them potentially providing protection against Aa infection.

Question 27

Explain the role of epitheliotoxin in bacterial infection.

Answer 27

Epitheliotoxin aids in penetrating the sulcular epithelium, allowing bacteria to invade deeper tissues and evade the immune response.

Question 28

Describe the role of collagenase in bacterial activity.

Answer 28

Collagenase is a protease enzyme that degrades collagen, facilitating bacterial invasion and tissue damage.

Question 29

How do black pigmented strains protect themselves from immune responses?

Answer 29

They elaborate superoxide dismutase, which splits PMN derived hydrogen peroxide and superoxide anions, helping them resist oxygen-dependent intra-leukocytic killing.

Question 30

Define gingipain and its significance in bacterial virulence.

Answer 30

Gingipain is a cysteine protease virulence factor of Porphyromonas gingivalis (Pg), responsible for 85% of its proteolytic activities and targeting various host proteins.

Question 31

Explain the function of fimbriae in bacterial adhesion.

Answer 31

Fimbriae are hair-like protein structures on the bacterial surface that enable binding to human gingival tissues, triggering cellular responses that facilitate bacterial uptake.

Question 32

What are membrane vesicles and their role in bacterial infection?

Answer 32

Membrane vesicles are shed by bacteria and carry secreted proteases that help permeate host tissues, aiding in infection.

Question 33

How does Pg hemagglutinin and hemolysin activity contribute to its colonization?

Answer 33

Pg can utilize hemin-containing compounds, lysing red blood cells to release hemin, which promotes colonization by providing necessary iron and maintaining an anaerobic environment.

Question 34

Describe the direct effects of dental plaque biofilm on host cells.

Answer 34

Direct effects include bacterial adherence and invasion, cytotoxic products, bacterial metabolites, and evasion of the immune system.

Question 35

What is the importance of bacterial adherence in the oral cavity?

Answer 35

Bacterial adherence is crucial for persistence in the oral cavity, as organisms that cannot adhere are quickly removed by host defenses.

Question 36

How do bacteria invade epithelial tissue?

Answer 36

Bacteria such as Pg, Aa, spirochetes, and Bacteroides forsythus can invade epithelial tissue, contributing to periodontal disease.

Question 37

Describe the advantage of pathogens surviving within host tissue.

Answer 37

Pathogens that survive within host tissue are protected from host defense mechanisms, allowing them to evade the immune response.

Question 38

Define exotoxins and their general characteristics.

Answer 38

Exotoxins are proteins or polypeptides secreted by living bacteria, which can act enzymatically or directly on host cells, stimulating various host responses.

Question 39

How do endotoxins affect tissue cells?

Answer 39

Endotoxins, specifically lipopolysaccharides from Gram-negative bacteria, have a direct toxic effect on tissue cells such as fibroblasts, osteoblasts, and epithelial cells.

Question 40

What role do bacterial proteolytic enzymes play in periodontal disease?

Answer 40

Bacterial proteolytic enzymes degrade components of periodontal connective tissue and can also degrade elements of the host defense system, contributing to periodontal disease.

Question 41

Explain the interaction between exotoxins and the immune system.

Answer 41

Exotoxins can stimulate T cell proliferation, leading to the production of interleukins and tumor necrosis factor, which are principal mediators of periodontal destruction.

Question 42

How do endotoxins activate the complement system?

Answer 42

Endotoxins activate the complement system via the alternative pathway, which can contribute to the pathology of Gram-negative bacterial infections.

Question 43

Describe the effects of proteolytic enzymes on host defense mechanisms.

Answer 43

Proteolytic enzymes can degrade immunoglobulins and complement proteins, weakening the host’s immune response.

Question 44

What is the significance of fibrinolytic activity in certain bacteria?

Answer 44

Fibrinolytic activity in bacteria prolongs clotting time, providing a nutritional advantage to bacteria like Pg that utilize heme for sustenance.

Question 45

Define the role of collagenase in bacterial infections.

Answer 45

Collagenase, produced by certain bacteria, can activate latent host collagenases, contributing to tissue degradation and the progression of infections.

Question 46

Describe the role of hydrolytic enzymes produced by certain bacteria in periodontal disease.

Answer 46

Hydrolytic enzymes produced by bacteria like Pg, capnocytophaga, and fusobacterium nucleatum degrade non-proteinaceous elements of the periodontal connective tissue, such as glycosaminoglycans in the extracellular matrix, increasing tissue permeability to bacterial products.

Question 47

How do bacterial metabolites affect host cells?

Answer 47

Bacterial metabolites like butyric acid, propionic acid, indole, and ammonia are metabolic end products of anaerobic bacteria and spirochetes that have toxic effects on host cells, being diffusible and lipid-soluble, allowing them to penetrate intact epithelium.

Question 48

Define the function of the bacterial capsule in pathogens like Aa and Pg.

Answer 48

The bacterial capsule in pathogens like Aa and Pg helps resist phagocytosis and opsonization, stimulates antibody production and release of IL-1, may cause bone resorption by stimulating osteoclasts, and aids in bacterial attachment.

Question 49

How do bacterial extracellular substances facilitate invasion of host tissues?

Answer 49

Bacterial extracellular substances, known as invasins, help pathogens invade host tissues by breaking down primary or secondary defenses of the body, such as through the action of exotoxins and enzymes.

Question 50

Describe the impact of exotoxins on the immune response.

Answer 50

Exotoxins, such as leukotoxins, damage polymorphonuclear leukocytes (PMNs) and monocytes, and may kill mature T and B lymphocytes, thereby impairing the immune response.