Intro to gingival and periodontal diseases Flashcards

1
Q

Periodontology definition

A

the study of the periodontal tissues in health and disease; including the causes, prevention and treatment of diseases of the periodontal tissue

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2
Q

What makes up the periodontium (periodontal tissues)?

A

gingivae, periodontal ligament, root cementum, alveolar bone

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3
Q

What is the border between the enamel and cementum known as?

A

Amelocemental junction (ACJ) / cementoenamel junction (CEJ)

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4
Q

What are the two types of gingiva?

A

free gingiva and attached gingiva

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5
Q

What forms the seal between the enamel and gingiva at the bottom of the sulcus?

A

Junctional epithelium

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6
Q

What is the difference between a sulcus and pocket?

A

A sulcus is the healthy 1-3mm gap between the free gingiva and the tooth. An inflamed sulcus is known as a pocket.

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7
Q

Size of healthy sulcus

A

1-3mm

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8
Q

What determines an individuals periodontal health?

A

The balance between bacteria of the dental plaque and the host immune system

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9
Q

Periodontal disease definition

A

a group of diseases affecting the periodontal tissues, representing an immune reaction (innate and adaptive) to adjacent microbial plaque.

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10
Q

How can periodontitis be prevented?

A

By catching it at the gingivitis stage and doing screening BPE twice a year

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11
Q

Difference between gingivitis and periodontitis

A

gingivitis is reversible whereas periodontitis is life-long. Gingivitis only involves soft tissues whereas periodontitis involves bone loss too (which can lead to tooth loss)

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12
Q

What percentage of the entire world population is estimated to have periodontal disease?

A

~70%

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13
Q

Why is periodontitis a significant disease?

A

Periodontitis is a risk factor for systemic disease e.g. rheumatoid arthritis, CVD

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14
Q

Inflammation definition

A

Biological response to remove harmful stimuli (e.g. pathogens, damaged cells, irritants) and to initiate healing.

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15
Q

Cardinal signs of inflammation

A

Pain, heat, swelling, redness, loss of function (e.g. bone loss)

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16
Q

Why is it a problem that periodontitis does not cause patients much pain? (as it’s a small tissue)

A

Patients can ignore blood (but not pain like in pulpitis). Dentists can’t detect periodontitis early to put it into a stable stage. Patients may only come to dentist when teeth become mobile which is too late (only 10-20% bone left)

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17
Q

Effects of inflammation

A

vasodilation, increased permeability of vessel walls, inflammatory exudate, emigration of WBCs from blood vessels into connective tissue (diapedesis)

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18
Q

Why is periodontitis chronic inflammation?

A

There is no resolution of inflammation

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19
Q

Etiopathogenesis definition

A

cause and development of a disease

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20
Q

Factors that can contribute to the development of periodontal disease

A

general health, immune system function, genetics, other pathological conditions

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21
Q

Aspects of general health that can contribute to periodontal disease

A

stress, fatigue, smoking, diet, hygiene habits, medications

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22
Q

Examples of pathological conditions that can contribute to the development of periodontal disease

A

viral infections, bacterial infections, diabetes mellitus, hypoxia, liver disease

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23
Q

Example of acquired local risk factors for periodontal disease

A

plaque, calculus, overhanging, poorly contoured restorations

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24
Q

Examples of anatomical local risk factors for periodontitis

A

malpositioned teeth, root grooves, concavities and furcations, enamel pearls (ortho-perio synergy)

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25
Q

How can local risk factors contribute to periodontal disease development?

A

intensify plaque accumulation

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26
Q

non-modifiable systemic risk factors for periodontal disease

A

ageing, genetic factors

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27
Q

modifiable systemic risk factors for periodontal disease

A

smoking, poorly controlled diabetes, stress, medications, hormonal changes, poor nutrition, socioeconomic status

28
Q

What was the non-specific plaque theory of the 19th century?

A

accumulation of dental plaque was responsible for oral disease without discriminating between bacterial virulence

29
Q

What was the specific plaque theory of the 20th century?

A

few species of the total microflora are actively involved in disease

30
Q

What was the ecological plaque theory of the 20th century?

A

changes in the environment (e.g. pH, redox) can favour the growth of certain bacterial species (composition of plaque depends on environment)

31
Q

What has been the most recent theory about periodontal disease?

A

Polymicrobial dysbiosis theory and Keystone-pathogen hypothesis

32
Q

What is the polymicrobial dysbiosis theory and the keystone-pathogen hypothesis of the 21st century?

A

certain low-abundance microbial pathogens can cause inflammatory disease by interfering with the host immune system and remodelling the microbiota into a dysbiotic one.

33
Q

Example of a keystone-pathogen

A

Porphyromonas gingivalis

34
Q

Biofilm definition

A

an aggregate of microorganisms that adhere to each other on a (living/non-living) surface. The adherent cells are embedded within a self-produced matrix of EPS

35
Q

What is EPS?

A

Extracellular Polymeric Substance - a matrix made of DNA, proteins, polysaccharide

36
Q

Why is biofilm advantageous to bacteria?

A

Resistance to antibiotics, antibacterial agents and mouthwash (cannot penetrate), hidden from immune system of host

37
Q

Where can biofilm form?

A

Living or non-living surfaces in natural, industrial and hospital settings. Can form in water and sewage pipes.

38
Q

Difference between biofilm and planktonic bacterial growth?

A

Planktonic bacteria are free-living so are not protected by biofilm and can be treated with antibiotics.

39
Q

What is dental plaque?

A

A type of biofilm found subgingival and supragingival tooth surface

40
Q

Why can the concept of commensal and pathogenic bacteria be twisted?

A

Because some ‘commensal’ bacteria can assist pathogens - infections are polymicrobial not monomicrobial. Porphyromonas gingivalis is unable to trigger disease without presence of other bacterial species.

41
Q

How can you visualise dental plaque?

A

using disclosing agent

42
Q

What is the dental pellicle?

A

A protein film formed by proteins and glycoproteins in saliva a few minutes after brushing. Protects against acidity and is important in remineralisation.

43
Q

How does biofilm form?

A
  1. dental pellicle forms in a few minutes
  2. Trailblazing bacteria (Streptococcus, Actinomyces) can adhere to pellicle
  3. growth of microcolonies and production of polysaccharide matrix (EPS)
  4. transition of mature biofilm colonies into metabolic complexes
44
Q

How do bacteria cooperate?

A

Bacteria have different enzymes so can form a chain of metabolism so each species has access to nutrients. Range of virulence factors protects whole colony.

45
Q

How have pathogens been categorised based on their association with the severity of periodontitis?

A

Socransky’s complex

46
Q

What are keystone bacteria?

A

certain low-abundance microbial pathogens that can cause inflammatory disease by changing the composition of normal microbiota and interfering with the host immune system

47
Q

In which of Socransky’s complexes is Porphyromonas gingivalis located?

A

red complex

48
Q

Why does Porphyromonas gingivalis manipulate the host immune system?

A

P. gingivalis needs iron from hemin in GCF so bleeding due to inflammation will aid survival. However, P. gingivalis needs to avoid the immune system.

49
Q

How does Porphyromonas gingivalis cause inflammation?

A

By manipulating toll-like receptor response. P.gingivalis has LPS type 1 which is a TLR4 agonist (activates immune response), and LPS type 2 which is a TLR4 antagonist (blocks receptor once there is enough bleeding/inflammation)

50
Q

How does Porphyromonas gingivalis escape the host immune system?

A
  1. local chemokine paralysis (innate)
  2. corrupts complement system (adaptive)
  3. invade keratinocytes to hide
51
Q

How does Porphyromonas gingivalis cause local chemokine paralysis?

A

P. gingivalis secretes serine phosphatase which inhibits the synthesis of IL-8 so there is a low chemokine concentration near the pathogen.

52
Q

Why does periodontitis cause damage to the periodontium?

A

Immune cells (e.g. neutrophils) enter the invaded tissue via diapedesis. However, as P. gingivalis breaks down IL-8, immune cells do not phagocytose P. gingivalis and instead break down the surrounding periodontium.

53
Q

How does Porphyromonas gingivalis corrupt the complement system?

A

Gingipains arginine-specific cysteine proteinases cleave complement factors C3 and C5. P. gingivalis therefore avoids complement-mediated detection and destruction.

54
Q

How could someone’s immune system make them more susceptible to periodontitis?

A

An overly active immune system can launch inflammation against own biofilm (healthy, aerobic bacteria) leading to destruction of periodontium. Or an impaired immune system that has a lack of protection (leads to acute periodontitis)

55
Q

Why may an individual’s immune system be impaired?

A

genetic condition or disease

56
Q

Examples of genetic conditions associated with impaired immune system

A

Papillon-Lefevre syndrome, Chediak-Higashi syndrome, LAS syndrome, Down’s syndrome, chronic granulomatous disease

57
Q

Examples of diseases leading to impaired immune system

A

Leukaemia, agranulocytosis, neutropenia, HIV

58
Q

How is calculus formed?

A

By calcification of dental plaque

59
Q

Why can a small amount of calculus lead to faster formation of more calculus?

A

Calculus is a plaque retention factor

60
Q

Clinical signs of gingivitis

A

erythema (redness), swelling, bleeding on gentle probing, (no deep pockets unlike periodontitis)

61
Q

Patient complaints from periodontitis

A

bleeding on brushing, halitosis, bad taste, sensitivity, drifting teeth, mobility, discomfort

62
Q

Why can periodontitis cause teeth sensitivity?

A

Bone recession can expose root surface. Cementum is worn down quickly so dentine is exposed which contains nerve endings

63
Q

When can periodontitis be painful?

A

rarely - mostly in necrotising periodontal disease

64
Q

Clinical signs of periodontitis

A

bleeding on gentle probing, erythema, loss of knife edge margin, halitosis, swelling (false pocket), bone loss, true pocket, recession, mobility, purulence

65
Q

Difference between a false and true pocket

A

false pocket is due to gingival swelling whereas a true pocket is due to loss of attachment (exposed root surface)

66
Q

Furcation definition

A

bone loss in between roots

67
Q

What will you need to warn the patient might happen when inflammation decreases?

A

During inflammation, gingival swelling will cover root surface despite bone loss. However, when inflammation decreases, swelling will decrease so gingival recession will be more prominent, root exposed, sensitivity. Sign of success (can block dentinal tubules)