Melinda Basics 3

8/13/2019 Melinda Basics 3

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Medical History&

Periodontal MedicineDr Melinda NewnhamDr Melinda NewnhamDr Melinda NewnhamDr Melinda Newnham

BDSc(WA) FRACDS DCD (Perio) FRACDS (Perio)BDSc(WA) FRACDS DCD (Perio) FRACDS (Perio)BDSc(WA) FRACDS DCD (Perio) FRACDS (Perio)BDSc(WA) FRACDS DCD (Perio) FRACDS (Perio)


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Medical Conditions&

The Periodontium


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Systems Check

1. CNS & special senses

2. CVS

3. Respiratory

4. Endocrine5. Haematological

6. Dermatological

7. Musculoskeletal

8. GIT

9. Genitourinary

10. Immune system

11. Past hospitalisations and cancer history


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Special Precautions for SystemicConditions

1. Cardiovascular Diseases & Infective Endocarditis

watch BP/ adrenaline, may need antibiotic (AB) cover

2. Coagulation Disorders: managing bleeding

3. Renal Diseases

usually on immunosuppressants and may also need AB cover

4. Blood Dyscrasias: infection, ulceration & bleeding


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Transmissible Diseases

Hepatitis A,B,C,D

HIV Infection

Tuberculosis

CJD


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Systemic Factors which can influencePeriodontium

1. Hormonal

2. Haematological

3. Genetic

4. Smoking

5. Stress

6. Nutritional Deficiency

7. Drug-induced Gingival Overgrowth

8. Psychosomatic


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Hormonal/ Endocrine

Diabetes Mellitus

Pregnancy

Puberty

Contraceptive Pill

Thyroid/ Pituitary/ Parathyroid Glands


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Diabetes Mellitus

Metabolic disorder of glucose intolerance,

causing prolonged hyperglycaemia

Type 1 - decreased circulating insulin, suddenonset, young patients (


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Diabetes Mellitus - Major Symptoms

1.1.1.1. PolydipsiaPolydipsiaPolydipsiaPolydipsia

2.2.2.2. PolyuriaPolyuriaPolyuriaPolyuria

3.3.3.3. PolyphagiaPolyphagiaPolyphagiaPolyphagia

4.4.4.4. Fatigue/ weaknessFatigue/ weaknessFatigue/ weaknessFatigue/ weakness


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Diabetes - Systemic complications

Affects small vesselssmall vesselssmall vesselssmall vessels (vascular disease).

Increased susceptibility to infection.susceptibility to infection.susceptibility to infection.susceptibility to infection.

Causes poor wound healing.poor wound healing.poor wound healing.poor wound healing.


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Common Complications ofChronic Hyperglycaemia

Retinopathy

Renal disease/ failure

Neuropathy

Cardiovascular disease

Diabetic gangrene Increased risk & severity of

periodontal disease


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Assessing Diabetic Control

Blood glucose: fasting or casual tests.

Glucose tolerance test, HbA1c.

< 6 Normal

6-8 good

8-10 mod

> 10 poor


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Poorly Controlled Diabetes & Perio

1. Expect more periodontal abscesses and a poorresponse to periodontal treatment.

2. Prone to infection & poor wound healing (>frequentpost-operative infection).

3. Antibiotic cover for extractionsand surgery.

4. Encourage patient to monitor/ controltheir blood sugar levels.


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Pregnancy, Puberty &Contraception

Induces an exaggerated response to

plaque/ calculus.

Gingiva becomes irritated and inflamed,

often with overgrowth.


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Periodontal Effects of Pregnancy

Pregnancy gingivitis:

plaque-induced gingivitis exacerbated by hormonal fluctuations in the2nd & 3rd trimesters

Prevalence 35%-100%

Progesterone increases gingival capillary permeability & dilation Oestrogen + progesterone change CT ground substance and

reduce keratinisation of oral epithelium

Reduces effectiveness of barrier to bacterial attack

Increased permeability of blood vessels increases exposure to andresponse to plaque bacteria

Oestrogen & progesterone are used as a nutrient source forPrevotella intermedia (Bacteroides) (Kornman & Loesche 1979)

Some subgingival plaque bacteria can use these sex steroid

hormones as growth factors


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HIV

Associated with increased risk of certain periodontal

conditions such as Linear gingival erythema, NUG, NUP,

NUS.

There appears to be an increased incidence with

diminishing immune competence .

Linear gingival erythema Necrotizing ulcerative periodontitis


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HIV & Chronic Periodontitis

Periodontitis:

Gingival recession and loss of clinical attachment appearsto occur more frequently in adult HIV patients.

But most patients with HIV can maintain periodontal health.

Highly active antiretroviral therapy (HAART):

Reduces viral loads & increases CD4+ counts (T cells). Oral manifestations of HIV infection appear to diminish

when HAART is successful.


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LGE & HIV

Prevalence 5- 49%.

2-3mm band of erythema and

oedema at gingival margin.

Gingiva bleed easily but rarelypainful.

Not associated with white cell count

(CD4+ cells).

Increased tendency to progress to

NUP.

Bacteria similar to periodontitis

but Candida albicansin 50% of cases


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NUP & HIV

Prevalence 17-50%.

Rapid onset with severe pain.

Soft tissue necrosis, gingival ulceration &cratering with bone exposure.

Gingiva bleed easily and spontaneously.

More often incisors and molars.

Hypothesised that change from LGE to NUPassociated with rapid decrease in CD4+ cellnumbers.


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Haematological - Neutropenia

Varied disease group with decrease/absence

of circulating neutrophils.

Causes: Idiopathic

Familial

Following viral, bacterial, protozoal infection andsystemic disease

Drug-induced


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Periodontal manifestations ofNeutropenia:

1. Oral ulceration.

2. Gingival inflammation.

3. Rapid periodontal breakdown.

4. Alveolar bone loss.


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Haematological - Leukaemia

Malignant disease involving proliferation of

leukocyte-forming tissues (especially bone marrow).

Infiltrates tissues.

May be acute or chronic.

Involves granulocytes, lymphocytes or monocytes.


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Periodontal manifestations ofLeukaemia:

1. Gingival enlargement.

2. Gingival bleeding.

3. Infection.

4. Oral mucosal erosions and ulcers.

5. Bone pain.


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Genetic - Downs Syndrome

Chromosomal disorder (Trisomy 21).

Incidence 1:700 (1:100 in mothers >45 years of age).

Periodontally - high incidence of disease, small conicalroots, increased in rate of destruction with age.

Aetiology - local factors:

Plaque.

Occlusal problems, habits.

Saliva and systemic factors: immune system, vascular

and nutritional factors.


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Genetic - Other

Hypophosphatasia

Chediak-Higashi Syndrome

Leukocyte Adhesion Deficiency

Ehlers-Danlos Syndrome

Papillon-Lefvre Syndrome

Hereditary Gingival Fibromatosis


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SMOKING

Increased bone loss, tooth loss, furcation

exposures and prevalence of periodontitis.

Severity of periodontal disease is related to

number of cigarettes smoked per day and for how

long - DOSE RESPONSE RELATIONSHIP.

Strong associations between smoking and both

aggressive and refractory periodontitis.


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Smoking Clinical

1. Fibrotic gingiva with thickened, rolled margins

2. Minimal gingival redness or swelling given the disease severity

3. Relatively severe and widespread disease compared to same-

age never smokers

4. Rapid disease progression with an early onset (@ 20-30 yrs).

5. Greater pocket depths + recession in anterior and palatal sites

local effects of nicotine.

6. More bone loss especially interproximally.

7. No association between periodontal status and plaque/calculus

scores.


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Smoking Mechanisms

Early studies say: no difference between smokers &non-smokers.

Recent studies say: more pathogens in shallower sites ->anaerobic conditions in pockets.

Microbial

Flora

Impaired neutrophil function.

Impaired fibroblast function.

Increased production & release of pro-inflammatory

cytokines.

Reduced antibody production.

Host

Response

Impairs revascularisation.

Vasoconstriction of blood vessels.Vascular


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Smoking - Outcomes

Smoking Causes Poorer Treatment Outcomes

1. Refractory Periodontitis: Up to 90% of non-

responding patients were smokers.2. Non-surgical treatment.

3. Surgical treatment.

4. Regenerative and grafting procedures.

5. In furcations during maintenance.


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Smoking Cessation

Cessation does not reverse the damage of past smoking.

However:

The rate of bone and attachment loss slows afterpatients quit smoking (Bergstrom et al 2000).

Former smokers respond to non-surgical andsurgical therapy in a manner similar to non-smokers (Kaldahl et al 1996, Grossi et al 1997).


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Stress & Periodontitis

Mechanism not understood.

There is a relationship between:

Acute stress and ANUG. Accumulation of stress events and past

periodontal breakdown.

Corticosteriods released while under stress

depress immune responses and reduce

phagocytic cell function.


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Nutritional Deficiencies

Vitamin B Complex = gingivitis, glossitis

and angular cheilitis.

Vitamin C (Scurvy) = bleeding, swollen

gingiva and loose teeth.

Protein = accentuates the destructiveeffects of local irritants.


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Psychosomatic

Injuring the oral cavity through

development of habits

e.g. chewing pens, finger nails, smoking

pipes, or self-inflicted injuries


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Drugs

&the Periodontium


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Revise: Drugs & Dentistry

1. Drugs for systemic conditions.

2. Drugs prescribed by dentists: Local anaesthetics

Antibiotics Analgesics

Antifungals

Calmatives/ sedatives

3. Emergency drug kit. 4. Drugs causing gingival overgrowth.

5. Bisphosphonates.


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Drug-Induced Gingival Overgrowth -1Phenytoin (Anticonvulsant)

Used in epilepsy, neuralgia and ventricular arrhythmias.

50% patients talking phenytoin get gingival overgrowth.

Overgrowth closely related to plaque control- good OHcannot prevent hyperplasia but may reduce incidence andseverity.

Serum level closely associated with incidence and severity dose dependent.

Proliferation of CT: both fibroblasts + collagen production.


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Drug-Induced G.O. IICyclosporin (Immunosuppressant)

Selectively inhibits T-lymphocyte immune response.

Used to prevent graft rejection and suppress auto-immune disease (e.g. Type 1 Diabetes, rheumatoid

arthritis, psoriasis).

Cell/ tissues similar to Phenytoin overgrowth.

Relationship between dosage, plasma levels andhyperplasia not proven. Equivocal relationship withplaque control.


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Drug-Induced G.O. IIICalcium Channel Blockers (BP)

Used to manage angina, hypertension and

cardiac arrhythmia.

Most common - Nifedpine and Verapamil.Nifedpine and Verapamil.Nifedpine and Verapamil.Nifedpine and Verapamil.

Nifedipine can cause hyperplasia in 15-21% of

patients:Similar to Phenytoin hyperplasia.

Few cases described for Verapamil.


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Bisphosphonates & Dentistry

Read the Dental Update 2006 review!

Basic information:

No change in protocols for NON-SURGICAL Rx.

Avoid exposing bone:

Avoid extractions promote prevention & RCT instead.

Avoid periodontal surgery including crown lengthening.

The half life of BPs is 8-10 years therefore stoppingthe medication is of limited benefit.

Warn patient of potential risks if extraction

unavoidable.


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Periodontal Medicine:

Perio-systemic interactions


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Periodontal Disease & Systemic Disease

The effect of periodontitis is not confined to the

mouth i.e. the infection has systemic effects.

Studies in the last 10 years have shown anassociation between periodontal disease and:

1. Atherosclerosis.

2. Coronary Heart Disease.3. Stroke.

4. Pre-term low birth weight babies.


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Periodontitis & Atherosclerosis

Share common risk factors:

E.g. age, male gender, smoking, fibrinogen levels,white cell counts, haematocrit and diabetes mellitus.

Periodontitis is also associated with changes inblood cell and biochemical markers, which arealso markers for cardiovascular disease:

E.g. clotting factors, fibrinogen, white cell counts andC-reactive protein (CRP).


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Perio-Atherosclerosis Mechanisms

1. Chronic infectionChronic infectionChronic infectionChronic infection (gram-negative bacteria in periodontitis)causes inflammationcauses inflammationcauses inflammationcauses inflammation:

Activated cells infiltrate into blood vessels.

Smooth muscle proliferates.

Fatty degeneration and intravascular coagulation occur.

2. LPS can increase the expression of adhesion molecules.LPS can increase the expression of adhesion molecules.LPS can increase the expression of adhesion molecules.LPS can increase the expression of adhesion molecules.

LPS from gram-negative bacteria in periodontitis can:

Cause leukocytes to infiltrate into artery walls (through& under the tunica intima).

Affect lipid metabolism when in the blood stream

leading to atherosclerosis.


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Perio-Atherosclerosis Mechanisms

3. HyperHyperHyperHyper----inflammatory traitinflammatory traitinflammatory traitinflammatory trait ---- macrophagesmacrophagesmacrophagesmacrophages:

Genetic or induced as a result of smoking/ infection (e.g.

periodontitis).

Activated macrophages produce excessive amounts of

pro-inflammatory molecules e.g. cytokines.

Activated cells excite other cells driving inflammation.

Patient becomes more likely to have atherosclerosis.

Influenced by periodontal disease, diet, lifestyle and

environmental factors.


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Low birth weight babies

Less than 2.5kg at birth.

6-7% of all births.

Increased medical problems including:

needing neonatal intensive care.

cardiovascular, diabetes and lung disease in

adulthood.


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Risk Factors for Low birth weight babies

Genetic.

Demographic:

very young or older mothers.

poor socioeconomic status.

maternal education.

Obstetric risk previous LBW babies.

Nutritional risk.

Infection - can affect gestational period.

Toxins: Smoking & Alcohol.


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Revision for Exams

Be able to identify patients who require antibiotic cover.

Know the common drugs e.g. hypertension, asthma,

antibiotics, analgesics, anti-inflammatory medications.

Diabetes & smoking are very important risk factors for

periodontitis.

Know the 3 classes of drugs that can induce gingival

overgrowth.

Remember periodontitis has a role in CVD and pre-term low

birth weight babies by driving both inflammation & infection.


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Q u e s t i o n sQ u e s t i o n sQ u e s t i o n sQ u e s t i o n s? ? ?? ? ?? ? ?? ? ?

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Melinda Basics 3

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