Periodontitis and Systemic Disease 1 Flashcards

1
Q

What is the surface area of the exposed ulcerate periodontal pockets in a patient with generalized deep periodontal pocketing?

A
  • Around 20 - 30 cm2.
  • Equivalent to the surface area of the PALM.
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2
Q

What do the inflamed periodontal tissues next to the periodontal pocket contain? (2)

A
  1. Invading bacteria.
  2. Host INFLAMMATORY cells (secrete pro-inflammatory mediators, ex. IL1, TNFa, PGE2).
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3
Q

How can periodontal disease lead to systemic effects?

A

Periodontal tissues are very VASCULAR and the blood vessels are LEAKY.
1. Bacteremia (periodontal bacteria in systemic blood).
2. Inflammatory mediators into the systemic blood stream.

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4
Q

What accounts for the possible link between periodontal disease and systemic chronic disease?

A

The LEAKING of PRO-INFLAMMATORY MEDIATORS/ PERIODONTAL BACTERIA into the systemic bloodstream by either:
1. Raising systemic inflammation (making systemic chronic disease ex. diabetes worse).
2. Direct effects of the periodontal bacteria (bacteremia).
3. Both of the above.

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5
Q

What is the relationship between periodontal disease and diabetes:

A

STRONG BIDIRECTIONAL RELATIONSHIP:
- Poor periodontal disease can make glycemic control worse. (and vice versa).

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6
Q

8 systemic diseases linked to periodontal disease?

A
  1. Diabetes.
  2. Cardiovascular disease (CVD).
  3. Adverse pregnancy outcomes.
  4. Respiratory disease.
  5. Kidney disease.
  6. Osteoporosis.
  7. Alzheimer’s disease.
  8. IBD.
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7
Q

Why is it difficult to confirm a link between many chronic conditions and periodontal disease?

A

They SHARE THE SAME RISK FACTORS (smoking, poor diet, genetic factors).

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8
Q

How can systemic diseases affect the periodontal tissues?

A
  1. Affect the progression of plaque induced periodontitis (negative effect of the host response to plaque usually by affecting host ability to fight the plaque).
  2. The periodontium independently of dental/plaque induced inflammation.
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9
Q

Do all systemic diseases increase periodontitis risk.

A

No, many systemic diseases can show lesions on the periodontal tissues without causing increased risk of periodontitis (ex. LICHEN PLANUS).

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10
Q

Periodontal Manifestations of Systemic Diseases and Conditions - Classification (3).

A
  1. Systemic diseases that have a MAJOR IMPACT on the loss of periodontal tissues by influencing periodontal inflammation (downregulate the host immune or inflammatory response).
  2. Other systemic disorders that INFLUENCE the pathogenesis of periodontal diseases (ex. risk factors/ disease modifying factors like diabetes).
  3. Systemic disorders that can result in loss of periodontal tissues INDEPENDENT of periodontitis (ex tumors).
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11
Q

What is GROUP 1 of periodontal manifestations of systemic diseases and conditions?

A

Systemic disorder that have a MAJOR IMPACT on the loss of periodontal tissues by influencing periodontal inflammation.

  • Have a negative effect on the HOST RESPONSE to plaque bacteria; lower the IMMUNE/INFLAMMATORY response to the invading bacteria and thus promote periodontal disease progression.
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12
Q

What are the 3 groups of conditions that fall under Group 1 (systemic conditions affecting the periodontium)?

A
  1. Genetic disorders.
  2. Acquired immunodeficiency diseases.
  3. Inflammatory diseases.
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13
Q

Give 4 examples of genetic disorders associated with group 1 (systemic diseases affecting the periodontium).

A
  1. Down syndrome.
  2. Papillon Lefevre.
  3. Chediak- Higashi Syndrome.
  4. Cyclic neutropenia.
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14
Q

What causes down syndrome?

A
  • Trisomy of chromosome 21.
  • Causes learning difficulties, tendency for inadequate OH.
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15
Q

What is the incidence of cardiac abnormalities in patients with trisomy 21?

A

40-50%

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16
Q

What is the relationship between Trisomy 21 and periodontitis? Why?

A

INCREASED PREVALENCE AND SEVERITY of periodontitis with evidence of HIGH RISK OF LoA STARTING IN ADOLESCENCE.

  • Due to immune defects and abnormal collagen biosynthesis
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17
Q

What are two immune defects seen in down syndrome?

A
  • Neutrophil (PMN) defects (chemotaxis, phagocytosis, killing defects).
  • T-cell migration to periodontal tissues & increased release of matrix metalloproteinases leading to tissue damage.
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18
Q

What is the prevalence of Papillon Lefevre? Where is it typically seen? What is its genetic type (dominant, recessive, sex linked etc)?

A
  • Rare (1 in 4 million).
  • Typically seen in ethnic group from India/ Pakistan.
  • Autosomal recessive, defect in chromosome 11.
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19
Q

What is the physiological effect of Papillon Lefevre?

A
  • Defect in chromosome 11.
  • REDUCED FUNCTION OF NEUTROPHILS.
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20
Q

What are the classical signs of Papillon Lefevre? When do they begin?

A
  • begin around 2-4 years old.
  • PALMAR and PLANTAR HYPERKERATOSIS.
  • SEVERE PERIODONTITIS soon after eruption and EARLY LOSS of primary and permanent teeth.
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21
Q

What is the genetic makeup of chediak higashi syndrome?

A

Rare autosomal recessive condition.

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22
Q

What are the physiological effects of chediak-higashi syndrome?

A

Defects in NEUTROPHIL + MONOCYTE chemotaxis, phagocytosis and intracellular killing.

23
Q

What are the oral effects of Chediak-Higashi Syndrome?

A
  • Severe periodontitis associated with a high risk of early loss of primary and permanent teeth.
  • Responds POORLY to perio treatment.
24
Q

What is the genetic makeup of cyclic neutropenia?

A

Rare autosomal dominant condition.

25
Q

What are the physiological effects of cyclic neutropenia?

A

Cyclical depression of neutrophils (PMNs).

26
Q

What are the oral symptoms of cyclic neutropenia?

A
  • Oral ULCERATION, RAPID PERIODONTAL DESTRUCTION, ULCERATION/NECROSIS OF GINGIVAL MARGIN associated with periods of LOW NEUTROPHIL NUMBERS.
27
Q

Name a disease affecting the connective tissue and associated with periodontitis?

A

Ehler danlos syndrome

28
Q

What causes Ehler danlos syndrome?

A

Various GENETIC DEFECTS which result in DEFECTS OF COLLAGEN SYNTHESIS.

29
Q

What is the physical presentation of Ehler Danlos syndrome? (gneral not oral)

A
  • Excessive JOINT MOBILITY.
  • Skin hyper-extensibility.
  • Cardiac valve defects.
30
Q

How many subtypes of Ehler Danlos are present? Which one are important for dentists?

A
  • 10 SUBTYPES.
  • Type 4: associated with BLEEDING TENDENCY.
  • Type 8: associated with agressive-like (grade C) periodontitis.
31
Q

Which Ehler danlos subtype is associated with agressive (grade C) periodontitis?

A

Type 8.

32
Q

Which Ehler danlos subtype is associated with a bleeding tendency?

A

Type 4

33
Q

What is a metabolic and endocrine disorder important in periodontology?

A

Hypophosphatasia.

34
Q

What causes hypophosphatasia? What is its genotype? How common is it?

A
  • RARE (1:100,000).
  • Autosomal RECESSIVE.
  • Deficiency in ENZYME ALKALINE PHOSPHATASE.
35
Q

What are the oral effects of hypophosphatasia?

A
  • Abnormal mineralizaiton of BONES and TEETH (abnormal cementum).
  • Premature loss of DECIDUOUS TEETH.
  • Permanent teeth appear UNAFFECTED.
36
Q

What are 2 periodontal conditions associated with HIV infection?

A
  • Necrotizing gingivitis.
  • Necrotizing periodontitis.
  • (Necrotizing stomatitis - spreads to the face, very rare).

Likely different ends of the spectrum of the SAME DISEASE (NP more severe than NG). NS most severe.

37
Q

3 reasons the study of HIV and periodontal diseases is difficult?

A
  • Variation in terminology and classification.
  • Contradictory research (biased samples - very poorly).
  • HAART may reduced the incidence of HIV related periodontal disease.
38
Q

What is the difference between NPD in HIV and non HIV infected (4)?

A
  • Clinically identical hower HIV-associated have higher RISK OF PROGRESSION TO MORE SEVERE LESIONS (NG –> NP/NS).
  • HIV associated has HIGHER RISK OF RECURRENCE & POORER RESPONSE TO TREATMENT.
  • Often has CANDIDA, CYTOMEGALOVIRUS & unusual bacterial species.
39
Q

What are the 4 main different between HIV associated and non HIV associated NPD? Why?

A
  • HIV associated more at risk of progressing to more severe (NG to NP/NS).
  • HIV associated higher risk of recurrence.
  • HIV associated poorer response to treatment.
  • HIV associated candida, cytomegalovirus, and other unusual bacteria.
  • HIV associated HIV occurs in HIV patients with low CD4 levels (<200 cells) & detectable viral load (aka failing immune system and AIDS).
40
Q

What is the clinical presentation of NECROTIZING GINGIVITIS (8)?

A
  • Painful, red, bleeding, swollen gingivae.
  • Yellowish/greying SLOUGH.
  • Marginal necrosis.
  • LOSS OF INTERDENTAL PAPILLAE (permanent).
  • Halitosis (metallic taste).
  • No LOA (although loss of papillae is permanent).
  • ANTERIOR gingivae most affected.
  • LOCALIZED or GENERALIZED.
41
Q

What is the clinical presentation of NECROTIZING PERIODONTITIS (9)?

A
  • Ulceration/ necrosis leading to SOFT TISSUE LOSS.
  • Exposure/ destruction/ sequestration of BONE (especially in severely immunocompromised).
  • Severe DEEP PAIN LOCALIZED TO THE JAW BONE.
  • Not always associated with deep pockets due to rapid HARD and SOFT TISSUE LOSS.
  • Rapid increase in MOBILITY
  • Widespread BOP (50% of sites bleed spontaneously, nocturnal bleeding).
  • HALITOSIS.
  • Usually SEVERAL INDEPENDENT LOCALIZED LESIONS (can affect entire dentition if severe).
  • Can be chronic with acute phases of ulceration (if left untreated).
42
Q

What is a clinical feature (that the patient will complain of) that may suggest NP?

A

Severe DEEP PAIN IN THE JAW BONE.

43
Q

What is the prevalence (%) of HIV positive patients presenting with NP?

A

Under 5% (although likely even less now due to HAART).

44
Q

3 steps for treatment of NP?

A
  1. Conventional debridement (OHI + PMPR etc).
  2. Remove necrotis tissue/ bone under LA.
  3. FLush is povidone iodine (pain relief).
  4. Antimicrobial treatment (oral metronidazole 200-400mg 3 x a day for 7 days - improves healing + pain relief + chlorhexidine mouth wash 2x daily).
45
Q

What do we flush exposed bone with in NP? Why? What must we be aware of?

A
  • Povidone Iodine.
  • Provides PAIN RELIEF.
  • Watch for IODINE ALLERGY.
46
Q

What antimicrobial treatment do we prescribe for NP (2)? Why? What must we watch out for (2)?

A
  • 2x daily chlorhexidine (both during treatment and maintenance)
  • Metronidazole 200-400mg 3x daily for 7 days.
  • Improves HEALING + PAIN RELIEF.
  • Watch LIVER FUNCTION.
  • Avoid BROAD SPECTRUM due to risk of untreatable fungal infections.
47
Q

What are systemic disease that “influence” the pathogenesis of periodontal diseases? Name 5.

A

Systemic diseases/ conditions which are RISK FACTORS/ DISEASE MODIFIERS for periodontitis (like smoking) aka PRESENCE MAY MAKE PERIODONTITIS WORSE.
Ex. Diabetes mellitus, obesity, osteoporosis, rheumatoid & osteoarthritis, stress/ depression.

48
Q

What are group 2 systemic disorders classfied as in the 2017 guidelines?

A

Under PERIODONTITIS.

49
Q

What are group 3 conditions? Give the 2 main categories and 2 examples of each.

A
  • Systemic disorders that can result in loss of periodontal tissues iNDEPENDENT of periodontitis (aka NOT plaque induced).
  • Neoplasms (squamous cell carcinoma, odontogenic tumors).
  • Other disorders (giant cell granulomas, systemic sclerosis/ scleroderma).
50
Q

What is scleroderma/ what does it affect?

A

AUTOIMMUNE disease affecting the body’s CONNECTIVE TISSUE.

51
Q

What are the physical effects of scleroderma?

A

TIGHT, INFLEXIBLE skin due to FIBROSIS.

  • Mask like fase/ Mona Lisa face.
  • Microstomia (limited mouth opening).
52
Q

What are the oral effects of scleroderma (4)?

A
  • Restricted mouth opening (microstomia).
  • Gingival recession common.
  • Increased prevalence of periodontitis.
  • Increased tooth mobility.
  • Increased width of PDL + gradual obliteration of lamina dura on radiograph.
53
Q

What are the radiographic effects of scleroderma (2)?

A
  • Widening of PDL and gradual obliteration of lamina dura.
54
Q

What is oral squamous cell carcinoma classified as in the 2017 classification?

A

Systemic diseases or conditions affecting the periodontal supporting tissues.