Pathogenesis and Aetiology of Periodontal Disease

Question 1

what is gingivitis

Answer 1

inflammation localised to gingival tissues, acute inflammation, normal physiological response to infection or injury

Question 2

what is periodontitis

Answer 2

inflammation of the gingival tissues and supporting periodontal structures, chronic inflammation, pathological inflammatory response associated with tissue destruction

Question 3

what type of plaque has saliva as a major immune defence strategy?

Answer 3

supragingival

Question 4

what contents of saliva target and inhibit microbial growth?

Answer 4

antimicrobials, peptides and antibodies

Question 5

what is the most successful intervention for preventing caries and periodontal disease?

Answer 5

mechanical intervention (brushing)

Question 6

what types of barriers do the oral mucosa provide?

Answer 6

physical and functional

Question 7

how does the oral mucosa provide a physical barrier?

Answer 7

prevents microbes accessing underlying tissues

Question 8

how does the oral mucosa provide a functional barrier

Answer 8

by detecting and responding to microbial challenge through activation of TLR which activates inflammatory pathways

Question 9

where does gingival crevicular fluid have a predominant effect?

Answer 9

subgingival portion of tooth

Question 10

what is the primary aetiological factor for periodontal diseases?

Answer 10

poor oral hygiene

Question 11

what is the unique biofilm profile determined by?

Answer 11

interactions by microbiomes and host factors and interactions amongst bacteria

Question 12

what are the first species to colonise the tooth surface?

Answer 12

gram+ streptococcal

Question 13

what do gram+ streptococcal species do on the tooth surfaces?

Answer 13

modify the environment and create new attachment sites for different species and bind directly or provide metabolites to support other species

Question 14

what are the early colonisers of the oral biofilm?

Answer 14

aerobic gram+ species

Question 15

what are the late colonisers of the oral biofilm?

Answer 15

gram- anaerobic species

Question 16

what is the red complex?

Answer 16

triad of periodontal pathogens

Question 17

what species are in the red complex?

Answer 17

porphyromonas gingivalis, tannerlla forsythia, treponema denticola

Question 18

do all periodontal patients have the red complex?

Answer 18

no

Question 19

what does periodontitis need to occur?

Answer 19

bacteria

Question 20

comment on the presence of periodontal pathogens?

Answer 20

present at low numbers in healthy sites, increased numbers in diseased sites or can be absent from diseased sites

Question 21

what is polymicrobial dysbiosis?

Answer 21

periodontitis associated with community of microorganisms which work together to disrupt the homeostasis of health

Question 22

how does gingivitis occur?

Answer 22

the homeostatic relationship is disrupted through the accumulation of plaque or transition of periodontal pathogens leading to modest inflammation

Question 23

what is the effect of persisting inflammatory reactions in the oral biofilm?

Answer 23

it exerts an ecological pressure on species present in biofilm and gives some species a competitive advantage allowing them to exist while others succumb to inflammation

Question 24

what type of species succumb to inflammation and are eliminated

Answer 24

commensal species

Question 25

what type of species can persist and adapt in inflammatory environments

Answer 25

accessory pathogens and periodontal pathogens

Question 26

what is periodontitis associated with?

Answer 26

a shift to dysbiotic biofilm which actively disrupts homeostasis for its own benefit which damages host tissues

Question 27

what are the virulence factors of P gingivalis?

Answer 27

asaccharolytic, gingipains, atypical LPS, inflammophilic, drives dysbiosis

Question 28

what does asaccharolytic mean?

Answer 28

it takes nutrients from the breakdown or proteins and peptides

Question 29

what are gingipains

Answer 29

proteases with broad specificity

Question 30

what does the atypical LPS of p. gingivalis do?

Answer 30

it is a TLR4 antagonist so it blocks inflammatory signalling

Question 31

what does inflammophilic mean?

Answer 31

inflammatory environment favours expression of virulence

Question 32

what do virulence factors do?

Answer 32

give immune system something to attack and alerts the immune system to the presence of microbes

Question 33

how are virulence factors regulated

Answer 33

in response to environmental conditions

Question 34

how does p. gingivalis persist in the oral environment

Answer 34

atypical LPS is used to hide from the immune system and persist in oral health, plaque accumulation stimulates inflammation and then P. gingivalis can express full virulence factors

Question 35

name some factors which cause dysbiosis in the oral environment

Answer 35

smoking, salivary flow rates, diet, oral hygiene, innate/adaptive immune factors

Question 36

what is the aetiology of periodontitis associated with?

Answer 36

accumulated plaque bacteria, presence of periodontal pathogens, polymicrobial dysbiosis, in susceptible hosts, host-pathogen interactions

Question 37

what is the false pocket in gingivitis due to?

Answer 37

inflammation and swelling, no attachment loss

Question 38

how does periodontitis have attachment loss?

Answer 38

PDL has came away from tooth surface so larger pocket, exposes more tooth surface available for biofilm accumulation deeper into the pocket and degradation of alveolar bone

Question 39

what are the 2 hallmark signs of periodontitis

Answer 39

attachment loss and alveolar bone loss

Question 40

what is the pathogenesis of gingivitis?

Answer 40

1 - increased TLR stimulation 2 - increased pro-inflammatory mediators (cytokines, peptides, chemokines) 3 - acute inflammatory response 4 - neutrophils remain predominant cell type 5 - monocytes recruited and differentiate to macrophages 6 - lymphocytes recruited to fine-tune the immune response (T cells coordinate and B cells release antibodies)

Question 41

what do neutrophils do in the pathogenesis of gingivitis?

Answer 41

phagocytose, degranulate and release enzymes into GCF which bathes the attachment surface

Question 42

how does increased vasodilation help immune cell defence?

Answer 42

it allows immune cells to migrate and control infection

Question 43

what can you see histologically with periodontitis in the PDL?

Answer 43

large aggregates of granular cells which overwhelm and destruct the integrity of the tissue

Question 44

what is the role of neutrophils in periodontal destruction?

Answer 44

they are crucial for maintaining healthy periodontium so when gingivitis occurs there is excessive infiltration which is associated with chronic inflammation (microbial subversion, degradative enzymes, inflammatory cytokines and oxygen radicals make a hypoxic environment, connective tissue destruction)

Question 45

what does a loss of neutrophil function present like at a young age?

Answer 45

aggressive periodontitis as neutrophils are not available to control bacterial growth in a healthy gingivae

Question 46

what is excessive infiltration of neutrophils associated with?

Answer 46

inflammation but is ineffective at controlling periodontal pathogens so it starts to contribute to periodontal tissue destruction

Question 47

what is the role of adaptive immunity in periodontal destruction?

Answer 47

T and B lymphocytes present , aggregates rich in CD4 T cells and B cells evident as lesion progresses, unable to regulate dysbiotic biofilm, B cells predominant in advanced lesions, IgG fails to regulate dysbiotic biofilm, inflammation induced alveolar bone loss

Question 48

what is the protective role of the adaptive immunity in periodontal destruction?

Answer 48

it prevents systemic infection by creating a barrier between pathogens and blood vessels

Question 49

what do osteoblasts do?

Answer 49

synthesis and secrete bone tissue and contribute to bone formation

Question 50

what do osteoclasts do?

Answer 50

resorbs bone, derived from monocyte/macrophage lineage

Question 51

what is bone formation and resorption regulated by?

Answer 51

RANK/RANKL/OPG triad

Question 52

how does inflammation lead to bone loss?

Answer 52

1. T and B cells in gingival tissues are activated 2. Lymphocytes release cytokines with RANKL and secrete into periodontal lesion 3. RANKL binds to RANK on pre-osteoclast e.g., monocyte 4. monocyte turns into osteoclasts 5. OPG binds to RANKL to prevent RANKL binding to RANK and further osteoclast production - HEATH 6. high levels of RANKL due to lots of T and B cells, low levels of OPG so it cannot inhibit RANKL binding 7. large numbers of monocytes recruited 8. osteoclast differentiating 9. resorbed bone, alveolar bone resorption, tooth loss

Question 53

on a cellular level how does bacterial induced inflammation and pathologic tissue destruction occur?

Answer 53

1 - bacterial products bind TLR on epithelium which stimulates cytokines, chemokines and AMPs 2 - vasodilation and recruitment of leukocytes (neutrophils) 3 - bacterial products activate neutrophils and further release of pro-inflammatory mediators 4 - activated lymphocytes express RANKL so RANKL/OPG balance disrupted 5 - RANKL binds RANK on osteoclast precursors (monocytes) so osteoclastogenesis activated and alveolar bone resorption occurs 6 - pro-inflammatory cytokines contribute to bone resorption by inhibiting bone formation 7 - elevated and dysregulated MMP activation contributes to connective tissue destruction

Question 54

what is the outcome of the initial infection determined by?

Answer 54

host/biofilm interactions

Question 55

what is the nature of interactions between host and biofilm modified by?

Answer 55

environmental and genetic risk factors