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How to assess patient risk at all levels, the patient, individual teeth and individual sites -risk factors

general and local

A RISK PATIENT IS ONE WHO HAS A HIGH PROBABILITY OF DEVELOPING A DISEASE OVER A SPECIFIC PERIOD OF TIME

Dental biofilm is a contributor to the etiology of most periodontal diseases Immunological and inflammatory responses to biofilm components are manifested by signs and symptoms of periodontal disease The outcome of such interaction is modulated by risk factors (modifiers), either inherent (genetic) or acquired (environmental) Definitive genetic determinants responsible for either susceptibility or resistance to periodontal disease have yet to be identified smoking, diabetes, obesity, medications, and nutrition are thought to be related factors

Recent studies have implied relationships between periodontal diseases and systemic conditions Answering critical questions regarding hostparasite interactions in periodontal diseases may provide new insight in the pathogenesis of other biomedical disorders Some risk factors can be modified or eliminated by the patient, e.g. smoking habit or level of diabetic control Dentists have a duty of care to counsel patients about their role in the management of their periodontal disease

A factor that increases the probability that a disease may develop in an individual If a patient possesses a risk factor, it does not mean that they will definitely develop the disease

Equally, absence of a risk factor does not mean that the disease will not develop

The patient must posses genetic risk factors for a disease, and then acquire environmental risk factors capable of exploiting the patients inherent susceptibility to the disease

Systemic risk factors (subject-based) factors that affect the host-response to the plaque biofilm, upsetting the host-microbial balance
Local risk factors (site-based) Factors local to the oral cavity, which may influence plaque accumulation or occlusal forces

A consequence of the disease being present, therefore imply the presence of disease Often used to detect early stages of disease before clinical signs become apparent

Bleeding on Probing (BOP) Tooth mobility Recession Suppuration Past disease experience

because periodontal disease is multifactorial!


1. 2. 3. 4.

Patient level perform at initial examination after


BPE

Whole mouth level perform at initial

examination after BPE Tooth level perform at initial examination after BPE Site-level perform following hygiene and scaling but before root-surface debridement of the sites that require it

Family history gum disease? Early tooth loss?


Medical history - systemic diseases e.g. diabetes? Dental history assess oral hygiene motivation etc Social history smoking (current/former?) Habits bruxism?

(To be carried out at initial examination)

Attachment loss relative to age


future rate of progression

gives idea of

Occlusal examination in static relationship

Occlusal class? (Class 2 division II malocclusion with retroclined lower incisors can create hygiene problems for lingual surfaces of those teeth) Tooth wear? may find secondary occlusal trauma to a tooth that is already periodontally diseased. This can accelerate the disease process but does not initiate it

Occlusal examination in dynamic relationship

Oral hygiene levels periodontitis with good oral

hygiene means greater risk of disease progression than periodontitis with poor oral hygiene

Plaque retentive factors heavily restored mouth?


Restoration quality? Calculus levels?

Presence of removable prosthesis Well

designed bridge is less plaque retentive than a RPD

Recession levels More recession = more surface


area to clean = greater risk of missing plaque

Gingival tissue quality and extent of pocketing relative to levels of plaque in the mouth some patients seem to be resistant to
periodontitis (carried out at initial examination after BPE, which identifies if the patient requires further periodontal examination)

Individual tooth mobility (mobility index)

excessive mobility may compromise function / make a tooth susceptible to sub-luxation

Tooth movement / drifting often seen with

periodontally compromised maxillary anterior teeth

Residual tooth support (radiographically)

helps determine long-term prognosis. Chronically infected teeth with minimal bone support extract to reduce potential pathogen reservoir which could reinfect treated, stable sites

Presence, location and extent of furcation lesions teeth should be vitality tested as furcations
are harder to maintain

Individual tooth anatomy talon cusps? Bulbous


crowns?

Contact points food packing? Cleansability? Ledges / deficiencies on restorations plaque


retentive factors at / below gingival margin?

Individual occlusal contacts Prematurities?


Excessive loading? Non-working-side contacts?

Soft tissue contours Subgingival calculus

Bleeding on probing 20-30% BOP sites are active.


Close to 100% sites that repeatedly fail to BOP are inactive. Smoking may affect these statistics.

Suppuration if the pocket has been treated,

suppuration indicates that the site is unstable, and either re-treatment is indicated or an infected root canal may be present.

Local root grooves or root caoncavities if a


site fails to respond to initial treatment, it should be carefully examined for root grooves or cracks

Individual probing pocket depths represent

HISTORICAL disease rather than current activity. The aim of therapy is to reduce pocket depths to <4mm

Attachment levels

Other anatomical factors e.g. enamel pearls, root


grooves
THE SITE-CHARACTERISTICS AT THE START OF MAINTENANCE = KEY REFERENCE POINT FROM WHICH TO MONITOR SITE STABILITY

Genetic Environmental Behavioural Life-style Metabolic Haematological

Poorly understood A family history of aggressive periodontitis: regular recall programmes with increased level of detail of examinations Early diagnosis of attachment loss and active pocket formation greatly simplifies therapy Single Nucleotide Polymorphism (SNP): can result in defects in PMNL function, leading to periodontal pathogens producing toxins to destroy or disable PMNLs

Down syndrome Chronic granulomatous disease Insulin-dependent juvenile diabetes Hypophosphatasia Papillon-Lefvre syndrome Ehlers Danlos syndrome Chediak-Higashi syndrome Jobs syndrome

DOWN SYNDROME defects of PMNL chemotaxis, killing and phagocytosis. Depressed T-cell antigen induced killing INSULIN DEPENDENT JUVENILE DIABETESHyperglycaemic state reduces PMNL function. Monocytes are hyper-reactive and excess IL1, PGE2, TNF and oxygen radicals are produced. Effects also on collagen solubility and vascularity reduce healing.

Drugs: -phenytoin -calcium channel blockers -ciclosporin

Can lead to drug induced gingival overgrowth, false pocketing and subsequently true pocketing. Discuss with medical practitioner - change drugs to non-calcium channel blocker? If gingival overgrowth, withdrawal of ciclosporin in transplant patients and substitute with alternative.

HIV Necrotising ulcerative gingivitis (NUG), Necrotising ulcerative periodontitis (NUP), Necrotising stomatitis (NS) are the most common in HIV patients -Chronic periodontits not linked -Attachment loss does not appear to progress at a higher rate in HIV patients, provided oral hygiene is comparable

Poor oral hygiene the most important factor in periodontal disease Improvement can lead to reduction in probing pocket depth, attachment gains and reduction in gingival inflammation Ability / Motivation of patient different issues Monitor by recording plaque and bleeding scores

Smoking Increased sites with deep pockets Greater levels of clinical attachment loss or bone loss Higher prevalence of furcation lesions Calculus accumulation Dose response between smoking habit and periodontal destruction (pack years = number of packs per day x number of years patient has smoked) Smokeless tobacco (e.g. chewing tobacco) are associated with attachment loss adjacent to the site of chewing

Nicotine causes vasoconstriction, reducing gingival bleeding and gingival redness Smoking leads to keratinisation of gingivae Therefore, smoking can mask clinical signs of periodontal inflammation

Non surgical therapy and surgical therapy are less effective in smokers -less probing pocket depth reduction -less clinical attachment gain -less bone height gain

Increased prevalence of Bf Harder to eradicate Aa, Pg and Bf Decreased levels of salivary IgA

Decreased serum IgG2 in smokers with aggressive periodontal disease


Decreased release of lysosomal enzymes and oxygen radicals by phagocytes Decreased ratio of T-helper and T-suppresser cells

Increased release of TNF, IL1-, IL-6 by monocytes when stimulated by lipopolysaccharides Decreased gingival blood flow initially (may compensate / self correct in chronic smokers) Increased destruction of extra-cellular matrix proteins Increased gingival keratosis and fibrosis

Stress potential risk factor - Financial strain and depression reduce dental attendance rates and oral health awareness therefore disease may be due to oral neglect rather than biological reasons - Link between NUG and stress because of reduced immune function - Reduces salivary flow

- Increases salivary viscosity, acidity and glycoprotein content increased plaque formation - Chronic stress leads to increased levels of noradrenaline and adrenaline which reduce gingival blood flow
-

Malnutrition Vitamin C has been shown to affect gingival bleeding Improved PMNL function with citrus fruit intake More research needeed

Diabetes mellitus type I and II increased risk for

periodontitis and other oral infections if poorly controlled. The greater the systemic complications of diabetes, the more severe the periodontitis. Independent of plaque control or calculus. Better the diabetic control = better the response to therapy.

Contributions to risk in diabetic patients: - PMNL function impaired chemotaxis, phagocytosis and
-

adherence. May be genetic / secondary to hyperglycaemia Collagen metabolism gingival fibroblasts synthesise less collagen. Increased levels of PMNL collagenase AGE products hyperglycaemia = proteins form advanced glycation end (AGE) products, which lead to decreased solubility of collagen. Monocytes/macrophages have AGE-receptors, AGE products bind to these, stimulating the release of IL-1, TNF, PGE2 and oxygen radicals Wound healing decreased due to decreased collagen solubility and increased collagenase removal of newly formed collagen

Pregnancy and oral contraceptive sex

hormones can cause gingival inflammation. Links to accelerated bone loss may be secondary to gingival inflammation, or due to oral hygiene behavioural changes Osteoporosis link with alveolar crest heights

Crohns disease Sarcoidosis

Acute/chronic myeloid leukaemia Myelodysplasia syndrome Agranulocytosis Cyclical or benign/familial neutropenia Hypo/agammaglobulinaemia Defects of lymphocyte formation (Di George syndrome, Wiscott-Aldrich syndrome)

rare and best referred for advice/therapy due to potential bleeding problems

Family history Smoking Medical problems e.g. diabetes mellitus

Severity of existing attachment loss in relation to age Whole mouth bleeding on probing at >25% sites Poorly controlled diabetes Smoking Plaque at >30% sites Local plaque-retentive factors Stress Poor nutrition (possibly)

A Consultation with patients physician B Pre-medication C Stress/fear management D Any necessary treatment considerations for systemic disease II: Acute phase A Emergency treatment for pain and infection B Addressing the urgent chief complaint III: Cause-related phase A Oral hygiene education, patient motivation and risk assessment B Mutual goal-setting for acceptable outcomes/endpoints of therapy

i: Implementation of strategies for risk reduction C Excavation of deep carious lesions i: Determine restorability D Extraction of hopeless teeth along with non-surgical periodontal debridement E Removal of plaque retentive factors F Necessary endodontic and occlusal therapy G Post-treatment re-evaluation i: Objective assessment of endpoints of therapy IV: Surgical corrective phase

A Resective/regenerative and implant surgical procedures B Post-surgical re-evaluation i: Objective assessment of endpoints of therapy C Definitive prosthodontic restoration V: Maintenance phase A Periodic professional supportive care B Reinforcement of oral hygiene instruction and motivation C Annual multi-pronged periodontal stability and risk re-assessment D Comprehensive professional supra- and subgingival plaque removal E Radiographic updates and therapeutic interventions (as needed)