Periodontics Flashcards

1
Q

Reasons for taking a medical history

A
  1. To identify systemic factors which may account for the periodontal condition
  2. To identify systemic conditions that require more caution during periodontal treatment
  3. To identify transmissible disease which may present a hazard to the clinician, staff and other patients
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2
Q

Bacteraemias

A

Patients with periodontitis are more at risk of bacteraemias after full-mouth probing than those with gingivitis.
Flossing and SRP cause the same amount of bacteraemia in patients with chronic periodontitis.

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3
Q

Bacteraemias and prophylaxis

A

There is no evidence about whether penicillin prophylaxis is effective against bacterial endocarditis in at-risk patients who are about to undergo dental procedures.
Lack of evidence

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4
Q

Antibiotic prophylaxis for infective endocarditis TGA guidelines

A

Endocarditis prophylaxis is recommended for people with the following heart conditions;

  1. Prosthetic cardiac valve
  2. Prosthetic material used for cardiac valve repair
  3. Previous history of infective endocarditis
  4. Congenital heart disease only if it involved unrepaired cyanotic defects or repaired defects with residual defects.
  5. Risk of rheumatic heart disease
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5
Q

Systematic factors which influence periodontium

A
  1. Hormonal
  2. Haematological
  3. Genetic
  4. Smoking
  5. Stress
  6. Nutritional deficiency
  7. Drug-induced gingival overgrowth
  8. Psychosomatic
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6
Q

Hormonal and endocrine factors that affect the periodontium

A
  1. Diabetes mellitus
  2. Pregnancy
  3. Puberty
    - Pregnancy and puberty induce an exaggerated response to plaque and calculus. Gingiva becomes irritated and inflamed (overgrowth as well)
  4. Contraceptive pill
  5. Thyroid/pituitary/parathyroid glands
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7
Q

Pregnancy and periodontal health

A

Pregnancy gingivitis - plaque induced gingivitis is exacerbated by hormonal fluctuations in the 2nd and 3rd trimesters (35-100% prevalence)

  • Together oestrogen and progesterone increase gingival capillary permeability and dilation.
  • Oestrogen and progesterone are used as a nutritional source by Prevotella intermedia
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8
Q

Menopause and periodontal health

A

Cessation of oestradiol and progesterone production by the ovaries.
- Results in increased erythema of the gingival tissues, which may be alleviated by hormone replacement therapy

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9
Q

HIV and periodontal health

A

HIV is associated with increased risk of periodontal conditions such as linear gingival erythema, NUG, NUP, NUS.
- LGE is characterised by a 2-3mm band of erythema and oedema at the gingival margin. Increased tendency to progress into NUP. Prevalence of 5-49%.

Gingival recession and loss of CAL appears more frequently in adult HIV patients.

As the disease progresses and immune competence decreases, periodontal diseases increase.

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10
Q

Neutropenia and periodontal manifestations

A
  1. Oral ulceration
  2. Gingival inflammation
  3. Rapid periodontal breakdown
  4. Alveolar bone loss
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11
Q

Leukemia and periodontal manifestations

A
  1. Gingival enlargement
  2. Gingival bleeding
  3. Infection
  4. Oral mucosal erosions and ulcers
  5. Bone pain
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12
Q

Down syndrome and periodontal health

A

High incidence of periodontal disease. Especially as this population has small conical roots, with an increased rate of destruction with age.

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13
Q

Hereditary gingival fibromatosis

A

Gingival tissue keeps growing - as fibrous tissue.

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14
Q

Stress and periodontitis

A

There is a relationship between:

  • Acute stress and NUGA
  • Accumulation of stress events and past periodontal breakdown

Corticosteroids released while under stress depress the immune response and reduce phagocytic cell function.

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15
Q

Physiology of stress

A

Stress -> stimulates the anterior hypothalamus -> corticotropin releasing factor CRF and arginine vasopressin -> stimulates pituitary gland -> adrenocorticotrophic hormone is released -> stimulates adrenal cortex -> glucocorticoid hormones (cortisol) -> which stimulates the immune response.

CRF and ACTH mediate the immune response. These together release adrenaline from the adrenal medulla.

Constant increased levels of CRF and ACT can disrupts homeostasis and lead to increased susceptibility to disease.

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16
Q

Nutritional deficiencies and gingivitis

A
  1. Vitamin B complex - gingivitis, glossitis and angular chelitis
  2. Vitamin C - bleeding, swollen gingiva and loose teeth (scurvy)
  3. Protein - accentuates the destructive effects of local irritants
  4. Serum antioxidant levels - Oxidative stress is reported in periodontal disease both locally and systemically.
17
Q

Osteoporosis and periodontal disease

A

Reduced bone mineral density is a shared risk factor for periodontitis.

18
Q

Desquamtive gingivitis

A

Gingival desquamation is a clinical sign in which the gingiva appears reddish, glazed and friable with destruction of the epithelium. Gingival desquamation may be the result of various disease processes in gingiva.

19
Q

Psychosomatic habits that result in periodontal disease

A

Injuring the oral cavity through development of habits.

20
Q

Drug induced gingival overgrowthB

A

Phenytoin (anticonvulsant)

  • used in epilepsy, neuralgia and ventricular arrhythmias
  • 50% patients taking phenytoin get gingival overgrowth
  • good OH cannot prevent hyperplasia but can reduce incidence and severity
  • Serum level of phenytonin is associated with incidence and severity
  • Proliferation of connective tissue: increased fibroblasts and collagen production

Cyclosporin (immunosuppressant)

  • Selectively inhibits T-lymphocyte immune response
  • Used to prevent graft rejection and suppress auto-immune disease
  • Cells/tissues similar to phenytoin overgrowth
  • Relationship between dosage, plasma levels and hyperplasia not proven

Calcium channel blockers (reduce BP)

  • Used to manage angina, hypertension and cardiac arrhythmia
  • Most common CC blockers (Nifedpine and Verapamil)n
21
Q

Bisphosphonates and periodontal disease

A

Bisphosphonates reduce bone turnover by preferentially binding to calcium in bone and causing apoptosis of osteoclasts when ingested.

Risk is increased for IV bisphosphonates.

All patients on oral bisphosphonates are at risk of ONJ if they have extractions.
- There is not difference in risk between a single and multiple extractions

22
Q

Periodontitis and artherosclerosis

A

They share common risk factors (age, male gender, smoking, fibrinogen levels, white cell counts, diabetes)
Periodontitis is also associated with changes in blood cells and biochemical markers, which are also markers for CVD (clotting factors, fibrinogen, white cells, C-reactive protein)

23
Q

Perio-artherosclerosis mechanisms

A
  1. Chronic infection (gram-negative bacteria in periodontitis instigates inflammation)
    - activated cells infiltrate into the blood vessels
    - smooth muscle proliferates
    - fatty degeneration and intravascular coagulation occur
  2. LPS can increase the expression of adhesion molecules
    LPS from gram negative bacteria in periodontitis:
    - can cause leukocytes to infiltrate into artery walls (through and under the tunica intima).
    - affects lipid metabolism when in the blood stream leading to atherosclerosis (plaque builds up in the vessel)
  3. Hyper-inflammatory trait of macrophages
    - genetic or induced from smoking or infection
    - activated macrophages produce excessive amounts of pro-inflammatory molecules
    - activated cells excited other cell, furthering inflammation
    - patient becomes more likely to have atherosclerosis
24
Q

Obesity and periodontal disease

A

There is a 2x increase in getting periodontitis when obese or overweight

25
Q

Metabolic syndrome and periodontitis

A

Low grade systemic inflammation is associated with an increase in metabolic syndrome.
Metabolic syndrome components were associated with periodontal status (specifically pocket depths)

26
Q

Maternal infection and inflammation

A

Maternal infection is linked with pre-term delivery

  • alterations in levels of inflammatory mediators may be crucial (increased prostaglandins results in increased oxytocin and early birth)
  • Fn and Pg have been found in amniotic fluid
  • Offenbacher et al showed that perio disease to be a significant risk factor for preterm birth
27
Q

Systematic reviews - PD and systemic disease

A
  1. Two systematic reviews concluded that there is a modest evidence or no evidence that periodontal therapy may result in a reduction of serum CRP levels
  2. Plaque removal by local periodontal therapy reduces circulating CRP
  3. PD treatment reduces CRP levels but not serum lipoprotein cholesterol
  4. Non-surgical treatment reduced CRP levels but not lipid parameters
28
Q

Physiology of PD affecting systemic disease

A

Increase in serum lipid in systemic diseases induces a pro-inflammatory state. This increases oxidative stress, resulting in imbalance between the production of highly reactive molecules and antioxidants, which increases risk of periodontal disease.

Increase in systemic inflammation response to periodontitis might increase the metabolic changes in someone with metabolic syndrome promoting both insulin resistance, dyslipidaemia and CVD risk.

29
Q

Physiology of PD affecting systemic disease

A

Increase in serum lipid in systemic diseases induces a pro-inflammatory state. This increases oxidative stress, resulting in imbalance between the production of highly reactive molecules and antioxidants, which increases risk of periodontal disease.

AND/OR (bi-directional interaction)

Increase in systemic inflammation response to periodontitis might increase the metabolic changes in someone with metabolic syndrome promoting both insulin resistance, dyslipidaemia and CVD risk.