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Periodontics > S2 - Perio-systemic relationships 1 > Flashcards

S2 - Perio-systemic relationships 1 Flashcards

1
Q

5 overall types of systemic diseases and disorders affecting the periodontium

A
  1. endocrine disorders
  2. haematological disorders
  3. genetic factors
  4. stress
  5. nutritional influences
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2
Q

Hormonal disturbances may affect periodontal tissues in 3 ways. What are they?

A
  1. directly as periodontal manifestations of endocrine diseases
  2. modify the tissue response to plaque in gingival and periodontal disease
  3. produce anatomic changes in oral cavity that may favour plaque accumulation or trauma from occlusion
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3
Q

3 oral manifestations of diabetes mellitus

A
  1. frequent perio abscesses
  2. diminished salivary flow resulting in mucosal drying, cracking, burning mouth and tongue
  3. increased rate of caries (in poorly controlled diabetes)
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4
Q

Effects of uncontrolled diabetes on periodontium? Both limited to the gingiva (2) and extending to attachment (4)

A

Limited to gingiva:

  1. severe inflammation
  2. sessile or pedunculated gingival enlargements - polyps

Features extending to attachment:

  1. abscesses
  2. mobility
  3. deep pockets
  4. rapid bone loss (rate)
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5
Q

What is the only systemic disease positively associated with attachment loss?

A

diabetes mellitus

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6
Q

Which bacteria have a greater prevalence in the oral cavity in diabetes? (3)

A

candida albicans

hemolytic streptococci

staphylococci

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7
Q

What is poorly controlled diabetes in HbA1c results?

A

>9%

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8
Q

How can poorly controlled diabetes cause severe perio (contributing pathogenic mechanicms)?

A

Change in PMN function and bacterial composition lead to altered collagen metabolism

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9
Q

Which types of cells’ function is affected by poorly controlled diabetes. What does this mean for perio risk?

A
  • impaired function of PMNs, monocytes and macrophages
  • PMN deficiencies → result in impaired chemotaxis, defective phagocytosis or impaired adherence (main function is to adhere then go into area of inflammation through chemotaxis then phagocyte bacteria) therefore lower defence mechanism
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10
Q

How does uncontrolled diabetes affect bacterial pathogens implicated in perio? Give examples of some for type I and II

A

glucose content of GCF and blood higher → bacteria which need glucose will have higher incidence

type I: A.A, P.intermedia, Campylobacter rectus

type II: P.gingivalis, P.intermedia, C. rectus

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11
Q

How are collagen turnover defects implicated in poorly controlled diabetes. (2) What medication might alter this?

A

marked decreased in collagen production and impaired collagen degradation (2 prong)

insulin prevents the onset and correct defective collagen production (but perio is not a reason to start insulin)

AGE-RAGE interaction instrumental

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12
Q

How does collagen changes lead to impaired wound healing in diabetes? (4)

A

increased cross linkage (happens to get to mature stage, usually limited)

when this happens they become resistant to digestion

if not degraded or recycled, there is impaired remodelling

→ impaired wound healing

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13
Q

What are the 4 mechanisms of bone destruction of diabetes? And how do they cause alveolar bone loss? (3)

A
  • increased RANKL/OPG
  • increased AGEs
  • increased ROS
  • increased cytokines/inflammation
  1. enhanced PDL and osteoblast apoptosis
  2. reduced bone formed
  3. enhanced osteoclastogenesis

explanation extra:

  • increased RANKL/OPG (molecules that interact w RANK ligands which are on the activation path of osteoclasts → increased bone destruction)
  • increased AGEs (increase in BG leads to increased bone destruction)
  • increased ROS (active molecuels released by immune cells, mostly neutrophils, directly involved in tissue destruction)
  • increased cytokines/inflammation (cytokines increase inflammation)
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14
Q

What is the AGE-RAGE axis

A

RAGE = receptor that sits on different cell types (monocytes and endothelial cells)

AGE = advanced glycated end products, which are present in patients with diabetes bind to their receptor RAGE → this triggers increase in ROS and inflammation

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15
Q

Inflammatory cytokines involved in diabetes

A

TNF

IL-1B

IL-6

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16
Q

*****Perio and diabetes mechanism/relationship summary*****

A

Perio is the ‘6th’ complication of diabetes, only systemic disease positively associated w attachment loss

PMN function (defective phagocytosis, impaired chemotaxis and adherence → therefore reduced defence mechanism) and change in bacterial composition (due to BG and GCF glucose content) lead to altered collagen metabolism → decrease in collagen production and impaired collagen degradation (why? increased cross-linkage → resistant to digestion → impaired remodelling → impaired wound healing)

Bone destruction mechanisms (4)-

  1. increased RANKL/OPG
  2. increased AGEs
  3. increased ROS
  4. increased cytokines/inflammation

/AGE-RAGE axis: advanced glycated end products present in diabetic pt bind to RAGE receptor triggering increase in ROS and inflammation

How they^ cause enhanced bone loss: increased PDL and osteoblast apoptosis, reduced bone formed, enhanced osteoclastogenesis

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17
Q

What are the 3 general effects of female sex hormones in puberty, pregnancy and menopause

A
  • non specific inflammatory reaction
  • increased vascularity
  • increased bleeding
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18
Q

Effect of menstrual cycle on periodontium. (3 things that can happen and when in cycle, what DOESNT happen)

A
  • transient
  • increased prevalence of gingivitis
  • bleeding gums or bloated, tense feeling in gums in days preceding menstrual flow
  • increased salivary bacteria during menstruation and ovulation
  • NO increase in tooth mobility
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19
Q

What determines if gingival changes will happen during pregnancy?

A
  • NO notable changes in gingiva in absence of local factors
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20
Q

What 3 changes happen to diseased periodontium during pregnancy?

A

tooth mobility

pocket depth

gingival fluid

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21
Q

How does severity of gingivitis vary across pregnancy?

A

peaks around 8m, drastically reduces after 9m when baby born, then takes around 1yr after birth to go down to normal

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22
Q

Clinical presentation of pregnaancy gingivitis (4) Specify the most striking feature.

A
  1. striking feature: pronounced ease of bleeding
  2. edematous, pitting, smooth and shiny, soft and pliable
  3. extreme redness resulting from marked vascularity
  4. usually painless unless complicated by acute infection
23
Q

Microscopic presentation of pregnancy gingivitis

A

newly formed engorged capillaries

24
Q

Hypotheses for pregnancy gingivitis/bleeding (4)

A
  1. P. intermedia increase significantly coincide w peak in gingival bleeding
  2. Depressed maternal T-lymphocyte response alters tissue response to plaque
  3. Elevations in systemic levels of hormones (1st trim - gonadotropins, 3rd trim - estradiol and progesterone)
  4. Gingival mast cells
25
Q

How do progesterone and other sex hormones affect periodontium?

A

increase irritability of tissue

26
Q

Features of pregnancy granuloma (4)

A
  • localised (usually)
  • semi-firm, various degrees of softness, or soft/friable
  • association w food impaction
  • discrete mushroom-like mass that protrudes from interproximal space/gingival margin (unless on labial - flattened by lip)
  • does not invade the underlying bone
  • usually painless
  • appears after 3rd month of pregnancy but may occur earlier
27
Q

When can a pregnancy granuloma become painful?

A
  1. secondary infection
  2. ulceration due to:
  • size and shape leads to accumulation of debris under margin
  • interfere w occlusion
28
Q

What is the histology of pregnancy granuloma and how does this pertain to its other name?

A

angiogranuloma

granulation tissue w lots of blood vessels

29
Q

What is menopausal gingivostomatitis (senile atrophic gingivitis), when does it occur?

A

gingiva and remaining oral mucosa are dry and shiny, vary in colour from abnormal paleness to redness and bleed easily

occurs during menopause or in post-menopausal period

not common

30
Q

3 broad groups of haematological disorders

A
  1. hemostatic disorders
  2. RBC disorders
  3. WBC disorders (most commonly affects periodontium)
31
Q

Classification of WBC disorders and how they affect periodontium

A

quantitative or qualitative, most commonly related to WBC function or number

quantitative PMN defiencies associated w generalised periodontal destruction

functional defects associated with localised destruction (defects in chemotaxis, phagocytosis)

32
Q

What is neutropenia,causes and types?

A

characterised by decrease or absence of circulating PMNs

causes: diseases, medications, chemicals, infections, idiopathic conditions or hereditary disorders
types: chronic or cyclic and severe or benign

cyclic can be cause in itself

33
Q

What is needed for chronic neutropenia diagnosis?

A

low ANC (absolute neutrophil count) for >6m

34
Q

What is cyclic neutropenia? When does it present and how does it affect periodontium?

A

periodic recurring symptoms of fever, malaise, mucosal ulcers and possibly life threatening infections related to cyclic fluctuations

usually presents before age 10 (most of time pt will alr know)

generalised severe periodontitis

a complete blood count, twice weekly for 6 weeks to get accurate picture of cycle

35
Q

What is Leukemia?

A

malignant neoplasia of WBC precursors

36
Q

What is Leukemia characterised by?

A
  1. diffuse replacement of bone marrow with proliferating leukemic cells
  2. abnormal numbers and forms of immature WBCs in circulating blood AND
  3. widespread infiltrates in liver, spleen, lymph nodes and other sites
37
Q

Classification of leukemia according to type and evolution/presentation.

A

type: lymphocytic, myelogenous-monocytic

evolution/presentation: acute (fatal), subacute or chronic

38
Q

Presentation of Leukemic infiltration on skin and gingiva

A

Leukemic Cutis: elevated/flat macules and papules

Leukemic gingival enlargement: most common in acute monocytic leukemia

39
Q

Oral and periodontal manifestations of leukemia (4)

A
  • leukemic infiltration
  • bleeding
  • oral ulcerations
  • infections
40
Q

How does leukemic infiltration cause enlargements?

A
41
Q

Presentation of leukemic gingival enlargment (4) Why is it important to recognise?

A
  • bluish red and cyanotic gingiva
  • rounding and tenseness of gingival margin
  • increase in size, most often in interdental papilla
  • marginal gingiva is usually ulcerated and marginal necrosis w pseudo-membrane formation

might be the only presenting sign of leukemia

42
Q

Microscopic features of leukemic gingival enlargment

A
  • dense infiltration of immature leukocytes
  • ectopic hematopoiesis “mitotic figure”
  • connective tissue components displaced by leukemic cells
  • blood vessels distended: leukemic cells w decreased RBCs

Generally leukocytes don’t divide in peripheral circulation, only forms in bone marrow then flows through, if you can see it forming in blood or CT –> alarm bells

43
Q

What may be an early and presenting sign of leukemia and why?

A

bleeding

thrombocytopenia (low platelet count) due to: replacement of bone marrow cells by leukemic cells + inhibition of normal stem cell function by leukemic cells

44
Q

Why do patients with leukemia have frequent opportunistic infections and ulcerations?

A

granulocytopenia

45
Q

Describe oral ulceration lesions in patients w terminal leukemia?

A

frequent and severe acute lesions

46
Q

What is a side effect of persistent gingival bleeding with leukemia?

A

blood loss and constant pain

47
Q

Name some genetic disorders that can cause perio, which most commonly does?

A

Papillon-Lefèvre Syndrome (most likely to cause perio, but uncommon condition)

Chédiak-Higashi Syndrome

Lazy Leukocyte Syndrome

Leukocyte Adhesion Deficiency

Down Syndrome

48
Q

What type of genetic disease is Papillon-Lefèvre Syndrome?

What is the presentation? What is the treatment?

A

rare autosomal recessive disease

diffuse palmar plantar keratosis (palms, knees, feet) + severe periodontitis affecting perm and prim dentition

appear together between age 2-4, primary teeth lost by 5/6y, perms lost by 15-20y

tx: cant do much other than help prevent tooth loss by managing local factors to some extent

49
Q

What are the defects in PMN in PLS? (3)

A

decreased chemotactic activity

decreased phagocytosis

decreased intracellular killing (of bacteria)

50
Q

Most notable documented relationship between stress and periodontal disease

A

soldiers at war or students during exams and NG

51
Q

What are the pathways between stress and periodontal disease?

A

can directly affect cells (hormone related)

but more often related to habits: poor oral hygiene/compliance, smoking, overeating (high fat diet can lead to cortisol)

52
Q

2 schools of thought on the effect of nutritional deficiencies on oral tissues. What is the starkest documented example?

A
  1. cannot cause gingivitis or perio themselves but they aggravate effects of local factors
  2. can produce periodontal or oral effects

(main link is that if nutritional defs affect immune system, they can cause perio destruction)

Noma in malnourished African children

53
Q

How can vitamin deficiencies disturb the periodontium?

A

Vit A, B complex and C: reduce resistance of tissues to irritation and infection

Vit K: affects permeability of blood vessels or blood clotting mechanism (low Vit K means increased bleeding - rmb Vit K reduces effect of Warfarin -lowering INR)

Vit D: decrease rate of bone formation and cementum and also decrease degree of mineralisation

Periodontics (8 decks)

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