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| Healthy Tissue Colour | Uniform pink, pigmentation may be present |
| Healthy Tissue Contour | Marginal gingiva: Meets the tooth in a tapered or slightly rounded edge Interdental papillae: Pointed papilla fills the space between the teeth (Knifed edged) |
| Healthy Tissue Consistency | Firm, resilient under compression |
| Healthy Surface Texture of Tissue | Smooth and/or stippled |
| Healthy Position of Gingival Margin | Slightly coronal to the CEJ |
| Healthy attachment | No attachment loss |
| Healthy radiological bone levels | No bone loss |
| Gingivitis Colour | Acute: bright red Chronic: Bluish red to purplish red |
| Gingivitis Tissue Contour | Marginal Gingiva: Meets tooth in a rolled, thickened edge Interdental papillae: Bulbous, blunted, cratered |
| Gingivitis Tissue Consistency | Spongy, ficid Indents easily when pressed lightly Compressed air deflects the tissue |
| Gingivitis Surface Texture of Tissue | Tissue appears “shiny” Stretched appearance |
| Gingivitis Position of Gingival Margin | Coronal to the CEJ (due to swelling) |
| Extent of Inflammation (Localised) | Inflammation confined to the tissue of a single tooth or a group of teeth |
| Extent of Inflammation (Generalised) | Inflammation of the gingival tissue of all or most of the mouth |
| Distribution of Inflammation | Papillary: Inflammation of the interdental papilla only Marginal: Inflammation of the gingival margin and papilla Diffuse: Inflammation of the gingival margin, papilla, and attached gingiva |
| Healthy Junctional Epithelium | JE coronal (above) to CEJ Tight intercellular junctions (to the enamel) |
| Healthy Connective Tissue Attachment | Intact supragingival fibre bundle |
| Healthy Alveolar Bone | Intact (crest of alveolar bone is located 2-3mm below the base of the JE) |
| What is Stage 1 of Periodontitis | Bacterial Accumulation (initial lesion) |
| What is Stage 2 of Periodontitis | Early Gingivitis (early lesion) |
| What is stage 3 of Periodontitis | Established Gingivitis (established lesion) |
| What is Stage 4 of Periodontitis | Periodontitis (advanced lesion): |
| Signs and Symptoms of Acute Gingivitis | Lasts for a short period of time, BOP, bright red, swelling/fluid in gingival connective tissue, tender or painful, heat- vasodilation, loss of function from swelling and pain |
| Signs and Symptoms of Chronic Gingivitis | Lasts for months or years, BOP, dark red or purple in colour, Enlarged and/or fibrotic gingival tissues due to excess collagen fibers, painless |
| Bacterial/Cellular Features Initial Lesion | Bacteria colonise along the gingival margin JE cells release cytokines, PGE, MMPs, TNF these calls stimulate an immune/inflammatory response which brings PMNs to the site of infection PMS pass into the gingival connective tissue and they release cytokines, cytokine destroy health gingival connective tissue to allow PMNs to quickly reach the infected tissue to destroy harmful bacteria PMN migration to the gingival sulcus to fight bacterial infection (phagocytize bacteria) If bacteria are destroyed tissues can be repaired and the infection can be stopped and progression to gingivitis will not occur |
| Tissue Level Initial Lesion | Increased vascular dilation Increase of gingival crevicular fluid |
| Clinical Features Initial Lesion | Gingiva looks clinically healthy Develops 2-4 days following plaque biofilm accumulation |
| Bacterial/Cellular Features Early Lesion | Bacterial accumulation continues and subgingival plaque biofilm maturation occurs. Intensified immune/inflammatory response (cytokines continue to cause destruction of connective tissue) Causes increased dilation and permeability of blood vessels which then brings PMNs to the site of infection and they destroy gingival connective tissue on the way Macrophages and T-cells migrate to the gingival connective tissue Macrophages release biochemical mediators – cytokines, PGE2, MMPs T-cells produce cytokines and antibodies Gingivitis is reversable when biofilm is controlled and inflammation is reduced, if not progression to established gingivitis occurs |
| Tissue Level Early Lesion | Collagen loss (by MMPs) in sulcular epithelium and epithelial ridges form |
| Clinical Features Early Lesion | Edema and redness of marginal gingiva (signs of gingivitis) Develops 4-7 days following plaque biofilm accumulation (can vary) |
| Bacterial/Cellular Features Established Lesion | Plaque biofilm extends subgingivally into the junctional epithelium Cytokines recruit more cellular defenders due to increased subgingival bacteria These cellular defenders (PNMs, macrophages, lymphocytes- B&T cells, plasma cells-produce antibodies) migrate to the site of infection and destroy connective tissue in the process Established gingivitis is reversable when professionally treated, if not advanced lesion/periodontitis occurs |
| Tissue Level Established Lesion | Junctional epithelium loosens its attachment and forms a pocket epithelium (thinner and more permeable) Continued collagen loss Deeper extension of epithelial ridges Increased cellular fluid |
| Clinical Features Established Lesion | All clinical features of gingivitis are evident and more pronounced than earlier stages Observed 21 days after plaque biofilm accumulation |
| Bacterial/Cellular Features Advanced Lesion | Plaque biofilm grows laterally and apically along the root surface Chronic inflammation from intense bacterial infection PMNs and macrophages produce cytokines that destroy gingival connective tissue and periodontal ligament fibres Macrophages produce lots of cytokines, PGE and MMPs that destroy connective tissue and alveolar bone MMPs destroy the extracellular matrix of the gingiva collagen fibres and periodontal ligament PGE destroy the bone by stimulating osteoclasts to resorb the crest of the alveolar bone Chronic inflammation causes irreversible damage to the periodontium and tissues causing the condition periodontitis |
| Tissue Level Advanced Lesion | Apical migration of junctional epithelium (development of perio pockets) Destruction of gingival connective tissue Destruction of periodontal ligament fibres Destruction of crest of alveolar bone by osteoclasts |
| Clinical Features Advanced Lesion | Periodontal pocket formation Bleeding on probing Destruction of ligaments Alveolar bone loss Furcation involvement Tooth mobility |
| What is the periodontium is made up of? | Gingiva = tissues which cover the crevicular portion of the teeth and the alveolar process of the jaw Periodontal ligament = fibres which surround the root of the tooth Cementum = thin layer of mineralised tissue which covers eh root of the tooth Alveolar bone = bone that supports the root of the tooth |
| Oral Epithelium | Outer layer that covers the free and attached gingiva |
| Sulcular Epithelium | Lines the sulcus but doesn’t come into contact with the tooth surface |
| Junctional Epithelium | At the base of the sulcus and join the gingiva to the tooth surface |
| Periodontal health on an intact periodontium | No clinical signs of gingival inflammation and no previous loss of periodontal tissue No alveolar bone loss |
| Periodontal health on a reduced periodontium in a non-periodontitis patient | Clinical signs of periodontal health on a periodontium with a pre-existing loss of connective tissue and/or loss of alveolar bone which is attributed to non-periodontitis reasons. (e.g., Gingival recession from toothbrushing) |
| Periodontal health on a reduced periodontium in a successfully treated stable periodontitis patient | Clinical signs of periodontal health on a periodontium with pre-existing loss of connective tissue an alveolar bone which is attributed to periodontitis but has been successfully treated and is currently stable. |
| Stage 1 Perio | Initial Periodontitis (No tooth loss) |
| Stage 2 Perio | Moderate Periodontitis (No tooth loss) |
| Stage 3 Perio | Severe Periodontitis (Tooth loss with potential for additional tooth loss) |
| Stage 4 Perio | Severe Periodontitis (Tooth loss with potential for additional tooth loss) |
| What does the Stages of Perio describe | (Severity/extent/distribution) |
| What does the Grade of Perio describe | (Progression/responsiveness to treatment/potential impact of systemic health.) |
| Grade A Perio | Slow rate of progression |
| Grade B Perio | Moderate rate of progression |
| Grade C Perio | Rapid rate of progression |
| Class I Neutrooclusion | Molar relation = MB cusp of maxillary first molar occludes with the B grove of the mandibular first molar Canine relation = The maxillary canine occludes between the mandibular canine and the first premolar |
| Class II (division between 1&2)- Distoclusion: | Molar relation: The buccal groove of the mandibular 1st molar is distal to the mesiobuccal cusp of the maxillary 1st molar by at least the width of a premolar Canine relation: The distal surface of the mandibular canine is distal to the mesial surface of the maxillary canine by at least the width of a premolar |
| Class II division 1 | All maxillary incisors are protruded |
| Class II division 2 | One or more maxillary incisors are retruded |
| Class III- Mesiooclusion (underbite) | Mandibular teeth are anterior to normal position in relation to maxillary teeth Molar relation: The buccal groove of the mandibular 1st molar is mesial to the mesiobuccal cusp of the maxillary 1st molar by at least the width of a premolar Canine relation: The distal surface of the mandibular canine is mesial to the mesial surface of the maxillary canine by at least the width of a premolar |
| Crossbite | Teeth positioned facially or lingually to their normal position |
| Open Bite | Lack of occlusion or incisal contact between certain maxillary and mandibular teeth |
| Overjet | Horizontal distance between incisal teeth measured in mm (usually Class II) |
| Underjet | Horizontal distance between incisal teeth measured in mm (usually Class III) |
| Overbite | Recorded as a % |
| Edge to Edge | Lncisal surfaces of maxillary teeth occlude with incisal mandibular teeth (don’t overlap) |
| Edge to Edge bite | Molars and premolars occlude cusp to cusp |
| What are the 3 Attrition Levels? | Level 1 – No need to be charted as only in enamel surface Level 2 - Wear has gone through to the dentine Level 3 - Outline of pulp is visible |
| Grade 1 Mobility | Tooth can be moved 1mm in BL direction |
| Grade 2 Mobility | Tooth can be moved 2mm in BL direction |
| Grade 3 Mobility | Tooth can be moved 3mm in BL direction & can depress tooth into socket in an apical occlusal direction |
| Class 1 Furcation | Where probe can extend 1mm into furcation |
| Class 2 Furcation | Where probe can extend 2mm or more into the furcation but not through |
| Class 3 Furcation | Where the probe can extend through one side (lingual/palatal) of the tooth to the other (buccal) |
| When os the probing depth physically charted | 4mm or more |
| Atrophy | A normally developed tissue that has decreased in size. |
| Hyperplasia | An increase in the size of a tissue that is caused by an increase in the number of constituent cells. |
| Hypertrophy | An increase in the size of a tissue that is caused by an increase in the size of constituent cells. |
| Bulla | A circumscribed, fluid containing, elevated lesion of the skin that is greater than 1cm in diameter. |
| Macule | A spot or stain on the skin or mucous membrane that is neither raised nor depressed. (E.g., café au lait spots, hyperaemia, erythema, petechiae, ecchymoses, purpura, and oral melanotic macules.) |
| Nodule | A circumscribed, usually solid lesion having the dimension of depth. Nodules are less than 1cm in diameter. |
| Papule | A small mass without the dimension of depth that is less than 1cm in diameter. When described as pedunculated, a papule is on a stalk. When described as sessile, a papule is attached at its base and does not have a stalk. |
| Plaque | An area with flat surface and raised edges. |
| Pustule | A well-circumscribed, pus containing lesion. Usually less than 1cm in diameter. |
| Ulcer | Loss of surface tissue caused by a sloughing of necrotic inflammatory tissue: the defect extends into the underlying lamina propria. (E.g., Aphthous Ulcer – Usually appears on the mucous membranes of the mouth. Is painful and typically heals spontaneously within 7-10 days.) |
| Systemic risk factors for dental disease | Is it something/risk factor that is increasing the risk of periodontal disease from their physical or general health (happening within the whole body, like other conditions, (E.g., heart disease, diabetes), is it that their immune response to the oral diseases is weakened because of their underlying general health issues. Diabetes Stress Hormonal fluctuations (puberty, pregnancy, menopause) Metabolic syndrome (high blood pressure, excess body fat, abnormal cholesterol) HIV/AIDS Neutropenia Down syndrome Leukemia |
| Local risk factors for dental disease | Is the something/risk factor that is increasing the risk of periodontal disease that is in the immediate environment of the oral cavity. Tooth and root morphology Calculus Occlusion Smoking Pellicle Clenching/bruxism Tongue thrust |
| Contributing Factor | A factor that lends assistance, adds or supplements to a condition or disease |
| Etiologic Factor | Factor that is actual cause of disease or condition |
| Predisposing Factor | Factor that renders a person susceptible to disease or condition |
| Risk Factor | An exposure that increases probability that disease will occur |
| What is acquired pellicle? | Is a thin acellular organic film composed of proteins, glycoproteins, amino acids and peptides, it also contains lipids, and other macro-molecules. Formation of Aqired pellicle is the adherence of salivary proteins to the tooth surface. This occurs as soon as the saliva touches the tooth surface, and the thickness reaches 10-20nm in just a few minutes. The pellicle acts as a ‘double sided sticky tape’ as well as adhering to the tooth’s surface on the inside, it also allows bacteria to adhere on the outside of it. |
| What is biofilm? | Is a slimy covering composed of extracellular polysaccharides, structural proteins, cell debris and nucleic acids. Biofilm formation begins with bacteria entering the oral cavity and slowly forming a layer over the teeth. Dental biofilm is a risk factor for gingivitis, dental caries, periapical periodontitis, periodontitis, and peri-implantitis. The oral cavity provides a moist, warm, and nutritious environment to promote the growth of biofilm. Biofilm produces acid which de-mineralises tooth surface and increases the risk of caries. The bacteria biofilm contributes to conditions such as gingivitis and periodontitis as it causes and inflammation, infection and destruction of periodontal structures. A build-up of Biofilm shows what surfaces you may be missing when brushing. |
| What is material alba | Translates to "White Material”, it is a white material which can be composed of cells of tissues and food debris etc. |
| What is dental calculus | Is hard calcified deposits on the teeth. This is formed when the soft deposits calcify with the minerals from our saliva. |
| What is the significance of pellicle? | Pellicle provides a barrier against different acids It is a lubricant- moistens surface to prevent drying, aid in speech and mastication. However, it also aids adherence of microorganisms and attachment of calculus to tooth surfaces. |