Tissues of the periodontium (Chapter 2) Periodontium * The tissues that surround, support, and attach to the teeth Components of the periodontium 1. Gingiva 2. Periodontal ligament 3.
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Cementum 4. Alveolar bone Function of the periodontium * To support the teeth and oral structures The gingiva * The visible component of the periodontium inside the mouth * Described as: pink, pink-red, blue, purple, or pigmented * It can appear much darker when melanin pigmentation is present * Factors that mask the color change of gingiva: * Food * Medications The three types of gingiva 1. Free gingiva 2. Attached gingiva 3.
Alveolar mucosa Mucogingiv al junction * Appears as a line that marks the connection between the attached gingiva and the alveolar mucosa Alveolar mucosa * The moveable tissue loosely attached to the underlying boe * It is attached but moveable * The surface is smooth and shiny Attached gingiva * Extends coronally from the mucogingival junction * It is continuous with the oral epithelium and is covered with keratinized stratified squamous epithelium * It is firmly attached to the alveolar bone unlike the free or marginal gingiva * It DOES have attachment fibers, which is why on the lingual aspect of maxillary teeth the ttached gingiva will blend with the attached palatal mucosa Rete pegs * Ridges of epithelium that form the connection between the free or attached gingiva and the underlying connective tissue * If gingiva is healthy, it appears stippled, which is due to the rete pegs * If gingiva is not healthy, it will appear flat and shiny, due to a lack of rete pegs Function of rete pegs 1. Add strength to the gingiva 2. Nourish the gingiva Free gingiva or free marginal gingiva * Surrounds the tooth and crests a cuff or collar of gingiva extending coronally about 1. mm * Usually a groove called the free gingival groove demonstrates the free marginal gingiva from the attached gingiva * Appears to be attached to the tooth but maybe separated by an instrument like a periodontal probe Gingival sulcus or crevice * A crevice or groove around each individual tooth * Sulcular epithelium is the continuation of the oral epithelium covering the free gingiva * Healthy sulcus is 1 to 3 mm probing depth Sulcular or gingival crevicular fluid * Liquid in the gingival sulcus Components diffuse through the basement membrane and the junctional epithelium Components of crevicular fluid 1. Connective tissue 2. Epithelium 3. Inflammatory cells 4. Serum 5. Microbial flora Functions of the crevicular fluid 1. Cleanses the sulcus 2. Antimicrobial action 3. Plasma proteins improve adhesion of the epithelium to the teeth 4. Antibody activity to defend the gingiva Junctional epithelium * Separates the periodontal ligament form the oral environment * Protects the attachment to the tooth to the surrounding tissues * Approximately 15-20 cells If the base of pocket is damaged, it takes 4-6 weeks to heal Interdental papilla (interdental gingiva/gingival papilla) * The gingiva that fill embrasure spaces, which is the interproximal space beneath a contact point of 2 teeth * Shape depends on the teeth it is between but we generally consider the papillae pyramidal or triangular * In health, it should fill embrasure and the tip pointed, not blunt or swollen * Other descriptions: pointed, bulbous, blunted, absent, or cratered Col Depression between the lingual and facial papillae in posterior teeth that conforms to the proximal contact area * Usually absent in anterior teeth because of the lack of lingual facial width at most coronal portion * Often susceptible to infection because of its non-keratinization Keratinization * The process whereby keratinocytes migrate from the basal layer of the epithelium to the surface and flatten out in the process * These flattened cells produce a superficial layer that is similar to skin where no cell nuclei are present * Least common form of epithelium in oral cavity
Oral epithelium * The oral cavity is primarily made of stratifies squamous epithelium cells * The majority of cells are keratinocytes and melanocytes which produce melanin which gives the gingiva a pigmented appearance (dark brown) Parakeratinized * The epithelium appears keratinized but the cells of the superficial layers retain their nuclei * Lightly keratinized (dorsal surface of tongue) Non-keratinized * No signs of keratinization (no keratin) are present (epithelial surface) Keratinized| Non-keratinized|
Palate (most)| Sulcular epithelium| Tongue| Alveolar mucosa| Attached gingiva| Junctional epithelium| Oral epithelium| Cols of papillae| Cheeks (least)| Buccal mucosa| Components Gingival epithelium 1. Oral epithelium 2. Sulcular epithelium 3. Junctional epithelium Normal “healthy” gingiva Color| Uniformly coral or light pink varying with thickness and degree of keratinization may also vary due to amount of melanin (pigment)| Size| Fits snuggle around the tooth, not enlarged when healthy| Contour| 1.
Marginal gingiva: flat/knife edged 2. Papilla: 1. Pointed and pyramidal in normal contact 2. Blunted/absent if diastema is present| Texture| 1. Free gingiva: smooth 2. Attached gingiva: stippled of rete pegs| Consistency| Firm and resilient (bounces back quickly)| Bleeding| No spontaneous bleeding upon probing| Exudate (pus)| None| Probing depth| Average is 1. 8mm (0-3mm is the normal range)| Periodontal ligament * Fills the space between the cementum and bone * Remember that teeth have a “shock absorbing cushion” space of 0. -1. 5 mm next to the bone and they are not rigidly fixed in their sockets * The attachment apparatus consists of: 1. Alveolar bone 2. Periodontal ligament 3. Cementum * The fibrous connective tissue that surround and attaches the roots of the teeth to the alveolar bone * This connective tissue is made of fiver bundles (mainly collagen) and cells * The fiber bundles in the PDL are made of collagen arranged in bundles and spread throughout the PDL Function of the periodontal ligament 1.
Maintains the relation of a tooth to hard/soft tissues 2. Supplies nutrients and removes waste via blood and lymph vessels 3. Protect the vessels and nerves from injury 4. Resists occlusal forces (shock absorbers) 5. Transmits occlusal forces to the bone Sharpey’s fibers * The terminal brush-like fibers of the principle fiber bundles in the periodontal ligament that are partially inserted into the outer portion of the cementum at 90 degrees and then attached to the alveolar bone at the other end Five principal fiber groups of the periodontium
Apical fibers| * Run from the root apex to adjacent surrounding bone * Function: to resist vertical forces| Oblique fibers| * Run from the root above the apical fibers obliquely toward the occlusal * Function: to resist vertical and unexpected strong forces| Horizontal fibers| * From the cementum in the middle of each root to adjacent alveolar bone * Function: To resist intrusive forces| Alveolar crest fibers| * From the alveolar crest to the cementum just below the CEJ * Function: to resist intrusive forces| Interradicular fibers| * Run from the cementum between the roots of multi-rooted teeth to the adjacent bone * Function: to resist vertical and lateral sources| Cementum * Outer most layer of the root of a tooth * Helps anchor the teeth * Made of a mineralized fibrous matrix (collagen and fibers) and cells (cementoblasts and cementocytes) * Attaches teeth to the alveolar bone b anchoring the periodontal ligament * No vascular or nerve connections * Cannot transmit pain, therefore not sensitive to scaling procedures * Renewable Cementoenamel junction * The junction point between enamel and cementum * Not always smooth, can be due to alterations in cemented surface and the tissues involved Three scenarios occur at the CEJ 1.
Cementum will overlap enamel (60%) 2. Cementum and enamel meet (30%) 3. Cementum and enamel fail to meet leaving a narrow zone of exposed dentin (10%) Alveolar process * Support system for teeth * Extensions of the bone from the body of the mandible and maxilla * Lines the sockets of the teeth and provides support for the sockets * The walls of the sockets are called the lamina dura * The process also provides attachments for the periodontal ligament Components of the alveolar process * Alveolar bone * Compact bone * Trabecular and cancellous bone The alveolar process functions as a unit, as indicated by it’s gradual resorption when teeth are lost
Current concepts of microbiology and periodontal disease (chapter 4) Microorganism * Microscopic living organisms which include bacteria, viruses, and fungi * Bacteria: single-cell * Viruses: very small and not capable of growth or reproduction without living hosts * Fungi: plant-like organisms that occur as yeasts or molds Bacterial classifications 1. Morphologic forms (shape) 2. Cell wall structure 3. Oxygen environment 4. Metabolism 5. Motility Morphologic forms (shape) * Involved in plaque biofilm formation 1. Cocci: spherical, most common form in plaque is streptococci 2. Rods or bacilli: generally rectangular or rod like 3. Spirochetes: spirals Cell wall structure Bacteriologic technique (gram staining) of using a double dye staining system to differentiate the structure of the cell walls * Two wall types: 1. Gram positive: stains purple (crystal violet dye applied first) 2. Gram negative: stains red (safranin dye applied second) Oxygen environment Aerobe/Aerobic organism| Requires oxygen to live and grow| Anaerobe/Anaerobic organism| Grows in complete or almost complete absence of oxygen| Facultative anaerobic organism| Can use oxygen when present but can use anaerobic fermentation when oxygen is absent| Obligate anaerobe| Cannot survive in an aerobic environment| Aerotolerant anaerobes| Grow in both types of environment| Capnophile| Requires or prefers carbon dioxide for growth| Metabolism The sum of total of chemical changes occurring in the body; chemical process of transforming foods into complex tissue elements and or transforming complex body substances into simple ones, along with the production of heat and energy * Anabolism: The building up of tissue; maintenance and repair of the body * Catabolism: The breaking down of tissue into smaller parts from energy production and excretion Motility * Bacteria either are or aren’t motile * Flagella are long fine wavy filamentous structures used for motility * May have one or more flagella * Flagella may be located at either end, both ends, or encircling cell Microbial succession * Flora: organisms together in a locale * Oral flora: various bacterial and other microscopic organisms that inhabit the oral cavity Normal oral flora * Predominant microorganisms present in healthy state: * Streptococcus mitis * Actinomyces species Streptococcus oralis (sanguis II) Dental plaque: “The cause” * Dental plaque is THE major etiologic factor in the initiation and progression of periodontal disease * Epidemiologic studies have shown that poor oral hygiene increases the prevalence and severity of periodontal disease * Microorganisms other than bacteria can be found in plaque (ex. yeasts, protozoa, and viruses) * The difference between dental plaque and material alba is the strength/adherence of the deposit * Material alba is loosely adherent, soft accumulations of bacterial/cellular debris and can be removed by mechanical action (ex. strong water) The definition of dental plaque (Not on test) An accumulation of bacteria on the surface of teeth or other solid oral structures and is not readily removed Plaque formation: 3 stages 1. Pellicle formation * The acquired pellicle forms on the tooth surface * It is acellular * It is an organic and tenacious film composed of glycogen proteins from saliva * It will start to form within minutes after a tooth surface is entirely polished 2. Bacterial colonization * Bacteria from indigenous oral micro flora attach to the pellicle and form microbial colonies in layers as the bacteria grow and multiply * An intermicrobial substance is formed mainly from saliva and from polysaccharides produced by certain bacteria from sucrose or sugar in the diet 3. Plaque Maturation As plaque ages, a change in the types of microorganisms occurs within plaque * Plaque that is up to 2 days old consists primarily of cocci * By 2-4 the filaments replace the cocci * By days 4-7, filamentous forms increase and rods and fusiform bacteria appear * By 7-14 vibrios and spirochetes and more gram negative and anaerobic microorganisms appear * Bacterial plaque, if not mechanically disturbed, produces a great proportion of those microorganisms associated with periodontal disease Dental plaque growth * After the first day of plaque growth, gram (+) streptococci decrease in number * During the next 3 weeks of undisturbed plaque formation, cocci continue to decrease because of an increase in filamentous bacteria.
These filaments actually invade and replace many of the streptococci that inhabit the deeper levers * As plaque increase in thickness, further changes occur in the environment * When plaque is allowed to grow undisturbed, it becomes more anaerobic * The level of oxygen diminishes as a result of O2 consumption by facultative organisms * This lowers 02 level and allows the growth of obligate anaerobes * A more mature plaque harbors increasing number of obligate anaerobic organisms such as spirochetes and gram (-) rods * At this point, no additional bacterial species join the plaque, although the volume of bacteria may continue to increase * Mature plaque has the potential to invade the subgingival space and to cause localized gingival disease Page 74 (figure 4-9) The difference between supra/subgingival plaque Characteristic| Supragingival| Subgingival|
Location| * At or above (coronal to) the margin of the free gingiva| * Apical to the margin of the free gingiva, between tooth and gingival pocket epithelium| Origin| * Salivary glycoproteins form pellicle * MO’s from saliva are selectively attached to the pellicle| * Apical growth of bacteria from supragingival plaque| Distribution| * Starts on proximal surfaces * Heaviest on areas not cleaned daily by patients * Cervical 3rd * Lingual mandibular molar * Pits and fissures| * Shallow pocket * Attached plaque covers calculus * Unattached plaque extends to the periodontal attachment| Adhesion| * Firmly attached to acquired pellicle, other bacteria and tooth surfaces| * Adheres to tooth surface: calculus| Sources of nutrientsFor bacterial proliferation| * Saliva * Ingested food| * Tissue fluid (sulcus) * Exudates * Leukocytes| Bacteria | * Early plaque: mostly gram + cocci * Older plaque: increases in filaments (3-4 days) * More complex flora increase rods (4-9 days)| * Depends on pocket depth. Apical part dominated by spirochetes, cocci, and rods; coronal part has more filaments. * Environment is conducive to growth of anaerobic population| Significance| * Etiology of: * Gingivitis * Supragingival calculus * Dental caries| * Etiology of: * Gingivitis * Periodontal infections * Subgingival calculus| Pathogens in plaque The virulence for pathogenicity of a microorganism is its ability to cause disease * For a microorganism to be virulent it must: * Be established in close proximity to the periodontal tissue * Must be able to withstand the forces of saliva and gingival crevicular fluid that are capable of sweeping it away * Normally cellular defense systems are able to rid the microbe from the host * However, periodontal pathogens have developed a variety of strategies to evade or overcome these mechanisms * Example: Actinobacillus Actinomycetemcomitans (AA) defends themselves against phagocytosis by: 1. releasing inhibitors of directed migration (inhibits chemotaxis) 2.
Produces anti-phagocytic surfaces that prevent the polymorphonuclear lymphocytes (PMN’S) or neutrophils killing mechanisms * Has very slippery surface: slippery surface makes it extremely difficult to latch onto bacteria, therefore PMN’s cannot properly engulf it and PMN’s may be destroyed releasing toxins that produce osteoclasts * AA is a major pathogen Plaque tissue destruction 1. Bacteria themselves do not need to be present within the tissue to be a major participant in the destructive process 2. Some bacterial products may directly injure the hose cells and tissues 3. Others may interact with a variety of cells and activate the humeral and cellular immune reactions that secondarily affect the integrity of the periodontium Direct effect of plaque * P. gingivalis * Produces collagenase, the enzyme that degrades collagen * LPS or endotoxins ( which is a component of a gram (-) bacterial outer membrane) nduces inflammatory reactions and stimulates osteoclasts Indirect effects of plaque * Toxins from p. gingivalis and other gram (-) organisms stimulate the immune response, releasing prostaglandin E2, and interleukin 1B from macrophages and fibroblasts, which can induce bone resorption Gingivitis associated plaque * Increase thickness and mass of plaque * Increase in gram negative motile rods and spirochetes which are usually aerobic (require o2) * Fuso-bacterium nucleatum * Various species of prevotella and treponema * Campylobater rectus Periodontitis associated plaque * Prophyromonas gingivalis * Prevotella intermedia * Bacteroides forsythus * Treponema denticola * Peptostreptococcus micros Plaque biofilm summary Plaque is a biofilm meaning that it is an accumulation of microbes on the surface of teeth or other solid surfaces, not readily removed by rinsing * Plaque biofilm provides some protection for its resident microorganisms, increasing their survival * Therefore essential to physically remove plaque biofilms DAILY to maintain gingival and periodontal health- keeps plaque immature * Bacteria that colonize in the first few hours do not possess pathogenicity as the bacteria that dominate plaque after 34 hours. (plaque virulence increase with age) The role of calculus and other extrinsic factors in periodontal disease (chapter 5) Calculus * Calculus (tartar) is mineralized bacterial plaque, a hard tenacious mass that’s forms on natural teeth, dentures, and other dental appliances generally by the deposit of calcium and phosphate salts * 90% of treatment time on calculus removal and 5 % on plaque control * Not all plaque calcifies.
Generally it takes 24 hours to 2 weeks to begin mineralization * Plaque can be mineralized in 2 days and up to 90% in 2 weeks * Formation rates influenced by diet and composition of microbial flora * Calculus can reduce drainage from a pocket by helping to trap bacteria and debris * Healing is prevented and advancement of the disease is encouraged Role of calculus in periodontal disease- pathogenicity * Originally the focus was on calculus as a mechanical irritant * Now the focus is on calculus as a rough surface for plaque growth and retention, and a reservoir for toxic microbial and tissue breakdown products because of its permeable surface * Spicules: small pieces and usually subgingival * Granular: similar to spicules but are a lot smaller * Veneer: common in lower anteriors and the buccal of the upper molars. It is important to air dry before checking if all is removed
Comparison of clinical characteristics of calculus: supragingival vs. subgingival Characteristic| Supragingival| Subgingival| Also known as:| * Supramarginal calculus or salivary calculus | * Submarginal calculus or serumal calculus| Source of minerals| * Saliva| * Crevicular fluid| Formation starts| * Along inner surface of supragingival plaque| * In attached subgingival plaque| Attached to/by| * Acquired pellicle directly to tooth surface| * Penetration into cementum Intercrystalline bonding, mechanically locking into surface irregularities (caused by loss of Sharpey’s fibers)| Composition| * Inorganic Material(70-90%) :1. Calcium phosphate(75. 9%)2. Calcium carbonate(3. %) * Traces of magnesium, sodium, potassium, fluoride, zinc, strontium| * Similar to supra but increase in calcium, magnesium and fluoride (higher % in crevicular fluid) * Sodium content increases with pocket depth| Factors that influence formation| * Elevated salivary pH * Concentration of calcium in saliva * Concentration of salivary bacterial protein and lipid * Low individual inhibitory factors| * Higher total salivary lipid levels * Some medications(beta blockers, diuretics, thyroid supplements reduce the formation of supra | Commonly found (individual teeth)| * Coronal to margin of gingiva * Can be fine line near gingival margin * Cover large portion of clinical crown | * Apical to gingival margin * Can extend to bottom of the pocket and follows contour of soft tissue attachment. * As tissue recedes, subgingival calculus can become supra| Common Distribution Patterns| * Lingual surface of mandibular anteriors (Wharton’s Duct) * Facial surface of max. molars (Stenson’s Duct) * Does not necessarily mean there are SUB deposits.
Generally symmetrical except when: * Teeth are malpositioned * Functional irregularities * Oral hygiene inconsistent| * Heaviest in interpoximal areas * Lightest on facial surfaces * Occurs with or without SUPRA deposits| Shape| * Determined by tooth anatomy, contour of gingival tissue, pressure from lips, tongue and cheeks * Generally bulky gross deposits may form ‘calculus bridge’ between teeth or cover gingival margin or extend to incisal/occlusal edges| * Generally flattened to conform with pressure from pocket wall: * Ledge or ring like * Thin, smooth (veneers) * Spiny, spur-like * Granular (grainy) * Spicules (irregular amounts)| Consistency/Texture| * Moderately hard * Porous (may come off in pieces that easily break off from adjoining calculus) * Newer deposits are softer| * Harder and more dense than supra * Brittle/flint like * May feel a ‘snap’ as calculus is dislodged * Newest deposits (bottom of pocket) are less hard| Size and Quantity| * Depends on: * Efficacy of personal oral care * Diet * Function/use * Tobacco use| * Related to same as supra plus: * Pocket depth * duration| Supragingival calculus * Porous and rough * Provides lattice on which plaque can grow * Brings the bacteria close to the tissue * Interferes with oral self-cleaning mechanism * Makes plaque removal more difficult * Found on the clinical crowns of any tooth above the margin of the gingiva * Readily visible * Tightly adherent to the teeth * Yellowish-white in color, darkens with age * It is an organic matrix of plaque, microorganisms, glucans, lycol-proteins and lipids * Calcium is deposited in layers * 70-90% is inorganic mineral content Subgingival calculus * Associated with the progression of periodontal disease * Periodontal pockets almost always contain subgingival calculus * Provides a reservoir for bacteria and endotoxins that are related to the disease process * Can cause greater disease progression than plaque alone * Located below the gingival margin * Attached to cementum or dentin * Tenacious and black in color * Also dark green due to organic matrix products of the subgingival plaque * Color also comes from blood products * Commonly deposited in rings or ledges on root surfaces The mineral content is derived from crevicular fluid rather than from saliva as supra * Similar inorganic mineral content as supra * Can be found anywhere subgingivally * Attaches by means of attached pellicle or mechanical locking into undercuts and irregularities in tooth surfaces * Therefore more difficult to remove * Improper removal of calculus will leave a smooth outer collar called burnished calculus Calculus removal * Calculus is more readily removed from some tooth surfaces than others * Ease of removal related to mode of attachment of the calculus to tooth surface * Can be attached to acquired pellicle, mechanical locking into undercuts or minute irregularities in tooth surface or direct contact between intercellular matric and tooth surface
Conditions that affect periodontal health 1. Malocclusion * Is not a cause of periodontal disease * Poorly aligned teeth will make it harder for daily plaque control, but malocclusion is not an imitator of pathology 2. Missing teeth * Teeth harder to clean as they can tip in if one is missing 3. Bulky restorations * Poorly contoured restorations may cause plaque traps, increase gingival inflammation, may complicate plaque control and this does contribute to periodontal disease 4. Partial dentures * They should be cleaned daily * Calculus can stick on plastic teeth and stain on dentures * Poor fitting dentures can also irritate the gingiva Stress to remove dentures at night. Soak in water 5. Mouth breathing * This can lead to localized gingival inflammation * Usually on maxillary anterior facials * It is associated with an increase in plaque and gingivitis 6. Food impaction * A common local factor that contributes to the initiation and progression of periodontal disease * Food is an excellent breeding ground for bacteria * Forceful wedging of food may also tear epithelial attachment 7. Orthodontic appliances * Fixed appliances have increased plaque retention and are difficult for self-care * Minimal increase in periodontics but increase in gingivitis Tobacco use on periodontal disease It is a risk factor for periodontal disease (can help cause it) * Smoking will constrict white blood cell supply and retard PMN’s (type of leukocyte). PMN’s have reduced ability to phagocytosis * It has been determined that smokers are 2. 5 times more likely to have periodontal disease * The vascular reaction to inflammation is reduced in smokers THEREFORE?? Gums look normal and pink and there less bleeding and less response to fighting disease * Smokeless tobacco is associated with a specific type of gingivitis called gingivitis toxica it is associated with the destruction of gingiva and bone underling the area where the smokeless tobacco rests in the mouth Systemic factors in periodontal disease (chapter 16) Systemic factors * Systemic: pertaining to or affecting the whole body Systemic factors may complicate or intensify the periodontal disease * Systemic problems in some patients may: * Increase their susceptibility to infection * Interfere with wound healing * Require modification of standard approaches to treatment * Complicate factors associated with patient cooperation * More significant responses to bacterial plaque and other local predisposing factors Blood disorders (Dyscrasias) * A blood dyscrasia is any disorder that affects cellular elements of the blood (red or white blood cells) * Most common are anemia (need to know tablet or capsule form of iron taken), leukemia, abnormal bleeding * Most have an oral manifestation * In addition to changes to tissue there is: * Increased bleeding Lowered resistance to infection due to the impaired function of defensive white blood cells-polymorphonuclear neutrophilic leukocytes (PMNs or neutrophils) Aplastic Anemia * Bone marrow has very reduced ability to produce most of the components of blood * May be due to exposure to toxic chemicals or certain drugs * May have no known etiology, ie. Idiopathic aplastic anemia * Patients have: * Rapidly progressing periodontitis * Reduction in neutrophils Agranulocytosis * A rare disease involving destruction of bone marrow * Caused by antipsychotic drugs or an autoimmune diseases such as Lupus (corticosteriods) * Sharp drop in WBC’s; bacterial invasion is rapid * Patients have: * Ulcerations in mouth or pharynx Gingival bleeding * Increase in salivation * An odor in the mouth Cyclic Neutropenia * Unknown etiology * Periodic reduction in neutrophils * Patients have: * Flare-ups of periodontal disease during depletion of neutrophils Leukemia * Cell malignancies of bone marrow with a decrease in WBC and platelets * Etiology is unknown, although linked to certain viruses and ionizing radiation exposure * Abnormal WBC proliferate and suppress the normal WBC function (fighting infection) * Reduction in blood platelets means clotting ability is reduced * Clients with chronic leukemia have: * Increase susceptibility to infections * Decrease healing ability Spontaneous gingival bleeding * Acute forms have sudden onset and lead to death if not treated in a few months * Oral manifestations include painful ulcerations, spontaneous gingival bleeding, dry mouth, and secondary infections Endocrine dysfunctions * Periodontal disease is associated with endocrine changes or endogenous sex hormone changes * Puberty associated gingivitis: dramatic increase in hormone levels causes gingival inflammation * Menstrual cycle associated gingivitis: significant observable changes especially at ovulation * Menopause: tissue can be fragile. May have osteoporosis with loss of alveolar bone Diabetes Mellitus Usually hyperglycemic due to defect in insulin (hormone) secretions or insulin action * Either a relative or absolute lack of insulin or inadequate function of insulin * Type I (juvenile diabetes): absolute insulin deficiency * Type II (adult diabetes): most common * Insulin secretion may be lower or higher than normal * Cannot use insulin effectively * Oral findings: * Increased gingival inflammation * Periodontitis is more frequent and often more sever * Increase in tooth mobility * Decrease in saliva flow * Fruity (acetone) breath due to glucose in sulcular fluid * Delayed healing and an increased chance for oral candidiasis (thrush) Pregnancy Increase in gingival inflammation * Tissues are red, swollen * Can lead to periodontitis with loss of alveolar bone * Inflammation due to plaque * Due to increase in estrogen and progesterone * These can cause dilation of gingival capillaries and thus increase permeability and increase in gingival crevicular fluid. This allows for more bacteria to enter and form plaque Nutritional deficiencies * Healthy tissues depend on adequate supply of nutritive material * Hard or fibrous foods provide stimulation necessary for the maintenance of the PDL and alveolar bone and also stimulate the gingival tissues Vitamins| Function| Oral manifestations (deficiencies)|
Vitamin A| Growth and bone development| XerostomiaHyperkeratosis of gingiva| Vitamin K| Synthesis of blood clotting factors| Prolonged bleeding| Vitamin D| Promotes absorption of calcium and phosphorus| Hypo-calcification of enamel, bone, dentin, and cementum| Vitamin B| Helps with growth and tissue regeneration and maintains integrity of the oral mucosa| Poor wound healing, gingival inflammation, angular chelosis| Vitamin C| Collagen formation, promotes healing| Blue to red gingiva, bleeding, loss of PDL support, poor wound healing| Infectious diseases * Acquired immune deficiency (AIDS) * Caused by HHHIV (human immunodeficiency virus) * Transmitted by: needle sharing, sexual activities, infected mothers to their newborns, transfer of blood, possibly saliva * HIV infects and eventually kills a wide range of cells but particularly ‘CD4-positive helper T cells’ * Helper T cells are thymus derived lymphocytes that promote certain immunologic reactions * The depletion of these helper T cells can result in severe immune-suppression that makes the person susceptible to any life threatening fungal, bacterial, and viral infections * Oral manifestations: * Hairy leukoplakia: usually on lateral border of tongue * Those with AIDS usually have rapidly progressive periodontitis Cardiovascular disease 1. Hypertension * Blood pressure exceeds 160/95 mmHg (systolic/diastolic) * Normal is 120/80 mmHg * Avoid elective treatment if uncontrolled * Typical medications are diuretics and vasodilators * Drugs often cause xerostomia 2. Cardiac arrhythmias * Irregular heartbeat * Often due to stress 3. Anticoagulant therapy * Blood thinners to reduce the risk of blood clots that can block circulation to vital organs * Consult with doctor prior to seeing Instrumentation can cause prolonged bleeding * Usual medications are: a) Warfarin (Coumadin) (INR levels) b) Heparin c) Aspirin Psychological stress * Emotional stress is associated with an increased risk of developing periodontitis * Stress may induce secretion of Norepinephrine which may make the periodontal tissues more susceptible to damage from plaque Neurological disorders * Patients with nervous and neuromuscular diseases present with 3 basic problems: 1. Physical inability to perform adequate oral hygiene procedures due to a decrease in motor skills 2. May have a mental or physical inability to cooperate with the clinician 3.
May have changes in oral tissues that increase the risk from dental disease * Ex. phenytoin-influenced gingival enlargement: gingival enlargement with administration of anticonvulsive drugs that are used to control seizures. Mechanism is not completely understood Oral Cancer * Most frequent type is squamous cell carcinoma, develops from epithelial cells * Strongly linked to tobacco and pipe smoking * Chronic use of snuff (smokeless tobacco) * Be suspicious of long standing un-healing sores (anything longer than 2-3 weeks) * Red or white lesions on the lips or in the mouth What you can do * A thorough head and neck examination should be a routine part of each patient’s dental visit.
Clinicians should be particularly vigilant in checking those who use tobacco or excessive amounts of alcohol * EXAMINE your patients using the head and neck examination described here * TAKE A HISTORY of their alcohol and tobacco use * INFORM your patients of the association between tobacco use, alcohol use, and oral cancer * FOLLOW-UP to make sure a definitive diagnosis is obtained on any possible signs/symptoms of oral cancer The exam * This exam is abstracted from the standardized oral examination method recommended by the World Health Organization. The method is consistent with those followed by the Centers for Disease Control and Prevention and the National Institutes of Health.
It requires adequate lighting, a dental mouth mirror, two 2×2 gauze, and gloves; it should take no longer than 5 minutes Oral cancer screening Incidence and survival * Oral or pharyngeal cancer will be diagnosed in an estimated 30,000 Americans this year, and will cause approximately 8,000 deaths. On average, only half of those with the diseases will survive more than five years The importance of early detection * Early detection saves lives; deaths from oral cancer could be dramatically reduced. The five-year survival rate for those with localized disease at diagnosis is 76% compared with only 19% for those whose cancer has spread to other parts of the body.
Early detection of oral cancer is often possible. Tissue changes in the mouth that might signal the beginnings of cancer often can be seen and felt easily Warning signs 1. Lesions that might signal oral cancer * Two lesions that could be precursors to cancer: a) Leukoplakia (white lesions) b) Erythroplakia (red lesions) * Although less common than leukoplakia, erythroplakia and lesions with erythroplakic components have a much greater potential for becoming cancerous * Any white or red lesion that does not resolve itself in two weeks should be reevaluated and considered for biopsy to obtain a definitive diagnosis 2. Other possible signs/symptoms of oral cancer A lump or thickening in the oral soft tissues * Soreness or a feeling that something is caught in the throat * Difficulty chewing or swallowing * Ear pain * Difficulty moving the jaw or tongue * Hoarseness * Numbness of the tongue or other areas of the mouth * Swelling of the jaw that causes dentures to fit poorly or become uncomfortable * If the above problems persist for more than two weeks, a thorough clinical examination and laboratory tests, as necessary, should be performed to obtain a definitive diagnosis * If a diagnosis cannot be obtained, referral to the appropriate specialist is indicated Risk factors 1. Tobacco /alcohol use * Increases the risk of oral cancer Using both tobacco and alcohol poses a much greater risk than either substance alone 2. Sunlight * Exposure to sunlight is a risk factor for lip cancer 3. Age * Oral cancer is typically a disease of older people usually because of their longer exposure to risk factors * Incidence of oral cancer rises steadily with age, reaching a peak in persons aged 65-74 * For African americans incidence peaks about 10 years earlier 4. Gender * Oral cancer strikes twice as often as it does women Oral changes due to drugs 1. Xerostomia: dry, smooth, shiny mucosa * Diuretics (Dyazide) * Histamines (Benadryl) * Antidepressants (Tofranil) * Antihypertensive (Seroasil) 2.
Glossitis/Stomatitis: lesions o the tongue; small multiple ulcers * Anticoagulants (Warfarin) 3. Lichenoid eruptions: white striations; red patched of ulcers * CNS drugs (Aldomet) * Diuretics (Lasix) 4. Oral candidiasis/thrush: multiple with patches * Antibiotics (Vibramycin) 5. Hairy tongue: elongations of filiform papillae * Antibiotics (Tetracycline) Dental hygienist’s role * Consult with other health care providers for clients with systemic factors * Hygienists may be in a position to recognize changes at an early stage * Cautions: 1. Heart attack: need to wait at least 6 months before treating 2. Pregnancy: must finish 1st trimester 3.
Cancer: deep scaling could be open channel for infection to reach bone so treatment contraindicated during chemo and radiation 4. Medical histories * Antibiotics: a) What? b) How long? c) How much? * Cancer: a) How long ago? b) Advised against cleaning or pre-meds? * Kidney disease: a) On dialysis? b) How long has treatment been going on? c) Pre-med? * Blood thinners: a) Advised against cleanings? b) What are they on? c) Dose? d) How long on meds? e) Date of last work up? The diseases of the gingiva (chapter 6) Gingivitis * Inflammation of the gingival tissue with no apical migration of the junctional epithelium beyond the cementoenamel junction (CEJ) * Manifests as: Color change (red/pink-red) * Edema (swelling of tissues) * Exudates (pus) * Tendency to bleed readily * Major indicators of gingivitis are: * Bleeding in response to gentle probing * Clear gingival fluid flow, or exudates, which appears to increase with the severity of the gingivitis * Gingivitis appears directly related to the amount of plaque on the tooth surface and the amount of time that the plaque is allowed to remain undisturbed- the plaque is considered nonspecific because it is not associated with any specific type of microorganisms Three stages of gingivitis 1. Stage I gingivitis: (initial or sub-clinical) * No clinical signs yet Occurs in the first few days of contact between microbial plaque and gingival tissues * Is an acute inflammatory response characterized by dilation of the blood vessels * PMN (neutrophils) are the principal defense in acute inflammation- they phagocytoze (engulf) bacteria and their products * Small amounts of plasma leak into surrounding tissues causing edema * Exudate from early gingival inflammation is composed mostly of serum and it is referred to as ‘gingival fluid flow’- the fluid is clear, not yellow like pus, because few cells are present at this point * Lymphocytes will also appear at this stage (almost all are T-lymphocytes) * Collagen degradation will start to occur (collagen will start to break down) 2. Stage II gingivitis (early stage) * These lesions begin to form 4-7 days after plaque has accumulated in the gingival sulcus * Increase in T-lymphocytes- they are localized in the connective tissue under the epithelium of the gingival sulcus * Exudates increases and may appear white or yellow Clinically tissues will appear slightly red and swollen * Collagen fibers in connective tissue is destroyed by the inflammation and is replaced by blood plasma and inflammatory cells * Collagen fibers that attach the underlying connective tissue to the junctional epithelium are also destroyed * Gingival stippling if present, will begin to disappear causing the gingiva to appear shiny * The junctional epithelium will slightly start to lengthen against the root surface * Bleeding will occur upon probing * This stage may continue for 21 days or longer * It is the earliest clinical evidence of gingivitis 3. Stage III (established stage) * Occurs between 15-21 days * T and B lymphocytes are found in equal amounts indicating that tissue destruction by the inflammatory reaction is taking place * More collagen destruction during this stage * Junctional epithelium also continues lengthening Clinical probing depths will increase for 2 reasons: a) Probe can penetrate deeper due to collagen destruction b) Edema causes swelling of tissue and therefore may present as a deepening of the pocket * The increase of blood vessels and inflammatory cells in that area will cause visible plus formation * Capillary proliferation also causes the gingiva to appear red * Tissues may appear cyanotic (blue) in extreme cases of congested blood cells within the gingiva * The presence of many O2 depleted RBC’s give the bluish color * This stage can persist for many months or years Summary of stages Stage| Clinical signs| Pathogenic events|
Stage I (Initial) | * None| * Blood vessels * Polymorphonuclear (PMN’s) leukocytes migrate into CT * Plasma leaks into CT * Gingival fluid exits pockets * T-lymphocytes predominate| Stage II (Early)| * Gingiva may redden * Stippling disappears * Exudates may appear * Bleeding usually occurs on probing| * T-lymphocytes increase * Cells congregate under sulcular epithelium * Gingival fluid increases * Collagen is destroyed * Lengthened JE is disrupted * Fibroblasts destroyed| Stage III (Established)| * Gingiva is redden * Gingiva may appear blue-red * Probing depths increase * Pus forms * Tissue swells| * Capillaries proliferate * T and B lymphocytes occur in equal numbers * Extensive collagen destruction * JE thickens and rete pegs extend into the CT * Plasma cells infiltrate * Edema increases| Microbiology review * The mature plaque found in long-standing gingivitis has a large % of gram-bacteria (this change from gram (+) plaque associated with health, to predominantly gram (-) plaque, or pathogenic plaque is a characteristic of gingivitis) Types of gingivitis 1. Plaque associated gingivitis * Most common form of gingivitis in general population Directly related to presence of bacterial plaque on tooth surface * Clinically, gingivitis causes a redden gingival margin, with pocket formation as a result of gingival swelling and edema, hypertrophy, and deepened penetration of periodontal probes on clinical evaluation * Surface of the gingiva may appear glazed or smooth, and stippling when present in health, usually disappears; microscopically there is an increase in capillaries along the gingival margin, and the epithelium lining in the sulcus is ulcerated when periodontal probe is placed in the crevice 2. Necrotizing ulcerative gingivitis * A disease that occurs occasionally in young adults Is a periodontal disease that can occur with NO BONE LOSS and a bacterial component * Related to excess stress-common outbreaks at universities and colleges * Very painful * AKA ‘trench mouth’ widespread among soldiers in WWI (stress or poor oral hygiene) * Sudden onset of burning mouth and inability to eat * Disease most commonly begins in the interdental papillae after a few days, the tips of the papillae appear punched out and covered by a white necrotic pseudomembrane * Attached gingival tissues usually appear inflamed * Often a distinctive odor termed ‘fetor oris’ that is unique to the disease * There is a presence of two microorganisms a) Fusiform bacillus b) Spirochetes * May have a fever Antibiotics (penicillin and metronidazole) are useful in treatment, but only if the patient has systemic symptoms of fever and severe malaise * Treatment is to completely debride the tissues of plaque and to begin a home regiment of plaque control * Careful debridement with curettes or ultrasonic scaler can be performed over a few appointments; after appointment can rinse with a dilute solution of hydrogen peroxide and warm water * Untreated, this disease may lead to bone loss and become Necrotizing Ulcerative Periodontitis (NUP) or periodontitis 3. Endocrine-influenced gingival disease * Gingivitis is often influenced by steroid-type hormones produced by the endocrine glands. These include: a) Puberty b) Pregnancy: several changes in the gingiva have been associated 1. As hormone levels increase during 2nd trimester, gingival inflammation may * Increase, even with good plaque control The gingiva may be come dark red or hyperplastic and may bleed excessively * Changes may occur as the pregnancy progresses but most improves with good home care and removal of irritants- some not till after the baby is born 2. Some may also get a pregnancy tumor-tissue is highly inflamed, bleeds easily, and may cause teeth to become mobile * When female hormone levels are increased, there is an increase in some subgingival bacteria, such as bacteroids species, and gingival inflammation may be greater * Estrogen may also regulate cellular proliferation, keratinization, and vascular proliferation, and vascular fragility in the gingival tissues * The extent of hormone related changes is related to the level of plaque control- poor plaque control aggravates the condition 4. Drug-induced gingival enlargement Various medications can cause changes in gingival tissue * Anti-seizure meds most commonly associated with gingival overgrowth * Gingival tissue may become fibrotic and enlarged (enlargement may be caused by changes in the epithelial cells and the fibroblasts that create a more dense CT) * Overgrowth begins with interdental papillae which enlarge until they coalesce involving all of the attached gingiva * An increase in bacterial plaque causes an increase in gingival overgrowth in patients taking these medications-excellent plaque control is needed here * Patients may have heavy calculus and increased levels of inflammation because of plaque retention * Treatment requires good oral home care, regular debridement, root planning, and often surgical reduction of the enlargements * Some cardiac meds also cause overgrowth-include nifidine and verapamil used to control BP * Cylcosporine (immunosuppressant in transplant patients) also causes gingival overgrowth; also used to treat MS; can cause excessive accumulation of CT in many other tissues of the body Plaque induced gingivitis can be modified by: crowded teeth, restorations, orthodontic appliances, etc Gingival disease can be modified by malnutrition: vitamins A, B1, B2, B6, and C The Diseases of the supporting tissues of the periodontium (chapter 7) Periodontal disease * Broad term referring to any disease of the tissues surrounding teeth * 2 basic classifications: 1. Gingivitis 2. Periodontitis Periodontitis: an inflammatory disease of the periodontium characterized by the loss of connective tissue attachment, destruction of bone, and possible tooth mobility * Periodontal pockets: a clinical manifestation of tissue destruction associated with bone loss (apical migration of sulcus) Periodontitis: pathogenesis of periodontal pockets 1. Bacterial challenge from plaque biofilm * In the early stages of periodontitis, the bacterial flora of the gingival pocket is similar to that of gingivitis * As the disease becomes more sever, the flora become more complex 2. Connective tissue loss * Associated with enzymes secreted by healthy and inflammatory cells (collagenase degradation) * Phagocytosis of collagen by fibroblasts 3. Epithelial cells proliferate and migrate apically 4. Junctional epithelium detaches from root surfaces * As it becomes engorges with inflammatory cells 5.
Gingiva swells and moves coronally from increased amount of cellular and serum elements 6. Epithelial lining of pocket loses integrity * Leukocytes and products of inflammatory response escape into pocket space and in opposite direction the tissue is permeable to bacterial products * This process results in a periodontal pocket the patient cannot clean adequately. This the disease cycles as follows: * Biofilm > gingival inflammation > pocket formation >biofilm formation * Exposed cementum absorbs bacterial products and becomes soft and necrotic * Repair is minimal unless necrotic tissue is removed by root planning Periodontitis: microbiology The continued presence of pathogenic plaque bacteria causing the inflammatory process to extend into the PDL, cementum, and alveolar bone leading to the loss of attachment of the gingiva to the tooth and the loss of supporting bone * The predominant organisms are gram – anaerobic rods * P. gingivalis seems to be the most important periodontal pathogen based on its numeric presence (highest in numbers) Periodontitis: spread * Two mechanisms have been proposed for the initiation of the spread of infection 1. The bacteria and their products may break down the wall between the junctional and sulcular epithelium and cause detachment of the JE 2.
The bacteria products may interfere with the normal growth and maintenance of the junctional and sulcular epithelium permitting it to break down * In either case, as inflammation progresses the sulcular epithelium increases in thickness and begins to infiltrate into the underlying connective tissue * Pockets deepen because of the breakdown of collagen fibers by enzymes such as collagenase, which is released by some of the plaque bacteria and the hosts inflammatory response * Because bone is an active tissue with continuous resorption and formation it is not possible to determine histologically exactly when bone loss has occurred as a result of periodontitis * When bone resorption exceeds apposition, a net decrease in the amount of bone occurs Periodontal bone loss The loss of crestal alveolar bone through the inflammatory process * Osteoclast bone resorption is driven by plaque and most derived mediators such as bacterial enzymes, prostaglandins, interleukins, and tumor necrosis factor * When disease established, plasma cells and lymphocytes present * Plasma cells important in antigen-antibody reactions which activates events attracting additional inflammatory cells * These cells cause additional destruction of collagen fibers * Bacteria stimulate lymphocytes which release lymphokines * Lymphokines have many effects on inflammatory system including production of chemical factors that activate osteoclasts * Osteoclasts increase osseous resorption Types of bone loss 1. Horizontal: Occurs when entire width of interdental bone is resorbed evenly 2.
Vertical: Defect produced when interdental bone adjacent to root surface is more rapidly resorbed, leaving angular uneven morphology Two types of periodontal pockets * Describes relationship of pocket to crestal bone 1. Suprabony: base of pocket occurs above the crest of the alveolar bone 2. Infrabony: pocket base is apical to crest of alveolar bone Clinical attachment loss * Total attachment loss from CEJ * Combines recession and probing depth (pocket depth) (only exists when recession is present) * Provides more complete assessment of loss of support than probing alone * Why? Crest of alveolar bone is not at CEJ but 1-2 mm apical to it * Page 131 figure 7-2 Furcation * When attachment lose occurs vertically and horizontally between toots of multi-rooted teeth Etiology As in gingivitis, plaque biofilm is the principle cause of all forms of periodontitis * Therefore, treatment directed at its elimination or reduction * The composition of the flora differ significantly from patient to patient and from pocket to pocket, as does patients susceptibility to it * This variability makes causes of periodontitis less obvious than plaque biofilm + gingivitis relationship * All conditions that retain biofilms or prevent its removal play significant roles as they do in gingivitis * In addition, deeper periodontal pockets house greater amounts of subgingival plaque that is impossible for the patient to remove * Most patients with periodontitis have high proportions of anaerobic gram –ve bacteria Classification of periodontal disease * American academy of periodontology * Periodontitis can be: * Localized (? 30% of involved sites) * Generalized (> 30% of involved sites) The defining element for classifying periodontal disease is probing depth, the level of attachment loss from the CEJ indicates bone loss * Page 130 box 7-2 Chronic periodontitis * Most common form of periodontal disease * Bacterially induced inflammation of the periodontium * True periodontal pockets result from apical migration of JE * A degree of false pocketing resulting from gingival edema or fibrosis is commonly present * Characterized by bone resorption that progresses slowly and predominantly in a horizontal direction * May have pre-clinical onset in adolescence and if not halted by therapy it appears to progress continually for life * Usually not clinically significant until 35 years of age may occur at any age * More common in males than females Severity of this disease is directly related to the accumulation of plaque and calculus on the surface of the teeth * Preventable! (not associated with abnormalities in host defense) * Rate of periodontal destruction varies depending on disease activity and patient’s resistance * Can be localized or generalized * Progresses slowly until teeth are lost by exfoliation or extraction * Appears to occur in episodic bursts (can be quiet and then rapidly comes on) * Progresses in the presence of dental plaque * Disease activity halts or stops when the host resistance controls the disease process through therapy or natural defenses * Classified as slight, moderate, or severe Aggressive periodontitis Applied to those periodontal diseases that progress rapidly with massive bone loss * Attachment loss > 1mm/year is considered to be an aggressive type * Can be localized or generalized * Often associated with young people * Microbiology similar to chronic periodontitis Types of aggressive periodontitis * Early onset periodontitis (page 137-140) 1. Prepubertal periodontitis * Rare; may affect 1o or 2o with bone severe gingival inflammation, rapid bone loss, early tooth loss 2. Juvenile periodontitis * Localized juvenile periodontitis (usually 2o molars and incisors, minimal plaque and calculus, AA) * Generalized juvenile periodontitis (rarer, heavy calculus and plaque, p. gingivalis +E corrodens with AA) * Rapidly progressive periodontitis (page 140-142) * Refractory periodontitis (page 142) Unresponsive to thorough and varied periodontal treatments) Class VI: periodontitis as a manifestation of systemic disease 1. Associated with hematologic disorders 2. Associated with genetic disorders 3. Not otherwise specified Class IV: periodontitis as manifestation of systemic disease * Lesions associated with HIV: * Oral candidiasis * Karposi sarcoma: type of oral cancer usually seen on the palate * A malignant neoplasm associated with HIV infection and manifesting as brown or purplish tumors on the gingiva near the teeth or on the skin * Xerostomia * Unilateral/bilateral swelling of the salivary glands * Gingivitis * Spontaneous bleeding
Class V: necrotizing periodontal disease 1. NUG: necrotizing ulcerative gingivitis 2. NUP: necrotizing ulcerative periodontitis * Necrotic gingival tissue-pseudo membrane * Pain * Fetid breath odor * Punched out papillae * Gingival bleeding * Progression of NUG * Bone loss AND connective tissue attachment loss Class IV: abscess of periodontium * Acute localized purulent infection * Usually untreated choric periodontitis * Pockets’ pathogenic bacteria becomes occluded (cannot escape) * Associated with rapid bone loss * Requires immediate attention * Untreated- seeks drainage route and becomes chronic * Episodes of localized swelling * Periocoronitis is associated with the 8’s Treatment involves debridement and systemic antibiotics Class VII: periodontitis associated with endodontics * Periodontal pocket can progress to join an endodontic lesion * Treatment: endodontic therapy must be completed before scaling Class VIII: developmental or acquired deformities and conditions The role of abnormal occlusion and jaw dysfunction in periodontal treatment (chapter 10) Normal * Occlusal function- the dynamic state during talking, chewing, swallowing * Orthofunction: the state if morphofunctional harmony in which the forces developed during function are within adaptive range; means health and comfort with no pathological change Abnormal Dysfunction is a state of morphofunctional disharmony in which forces developed during mastication cause pathogenic/pathologic changes in tissue Role of abnormal occlusion and jaw dysfunction * These changes can cause bone loss * Poor occlusion alone does not cause or create periodontitis, it only exacerbates it * Antiaxial forces directed along tooth and periodontium can cause resorption or a hypertrophic response * Some areas will break down, others show no injury Factors * Certain factors affect the response of teeth and periodontal structures to normal and abnormal functions: * Size/shape of roots * Quality/quantity of alveolar bone * Presence of plaque * Missing teeth * Oral habits (parafunctional activity ie. grinding and clenching) Parafunctional activity 1. Bruxism Grinding or gnashing of teeth when not chewing or swallowing , usually during sleep * May lead to acute pulpitis, wear faucets, occlusal trauma, and muscle fatigue (summed up in periodontal injury, pain and jaw discomfort) 2. Clenching * Clamping and forcing the teeth together without grinding 3. Crepitation (crepitis) * A grinding noise in the TMJ from damage to the disc and articulating joint surfaces Traumatic occlusion * An occlusion that has caused injury to the teeth, muscles or TMJ * Primary traumatic occlusion is made when heavy occlusal forces exceed the adaptive range causing injury to tissues and bone * Secondary traumatic occlusion is made when normal forces exceed capability of a periodontium already affected by periodontal disease (ie. denture wear or lack) Assessing TMJ/occlusal dysfunction 1. Muscle palpation Normal muscles are equal in length and they should contract and relax without discomfort or pain * Myalgia is a pain in the muscle 2. Mandibular movement * Normal opening/closing of the jaw should be smooth and symmetrical * On average a person should be able to open about 40 mm * Page 222 and 223 3. Assessing occlusion * There should be a firm well disturbed pattern of occlusal contacts * Observe the patient opening and closing * You should note on closing any deviation to the left or right * The posterior teeth should have even contact and maximum inter-cuspation * Anterior teeth should have light to no contact 4. Radiographic evaluation These changes from excessive forces can be observed in periapical films * Widening of PDL (caused by resorption of bony support) * Increased density of surrounding bone (hypertrophic response) * Increased cementum at apices (hypertrophic response) 5. Subjective questionnaire * Screens for patient reported signs and symptoms * Several questions assessing pain, noises, comfort level, headaches, injury, arthritis, previous treatment * Ex. questions page 221 Prevention is key * Attention to form and function of aspects of head and neck: * Form: morphology of teeth, bones, and TMJ * Function: morphology including neuromuscular system * Masticatory system is complex but adaptive to function When adaptive capacity exceeded, dysfunction ranges from discomfort to debilitation Temporal Mandibular Disorder (TMD) * Group of musculoskeletal conditions that produce pain or dysfuction in the masticatory system * When it involves muscles and not joint, it is referred to as extracapsular * When it involves the TMJ, it is referred to as intracapsular Etiology * Multifactorial therefore difficult to diagnose and treat * Stress * History of other diseases: arthritis and psychological problems * Car accident * Sports injury Microtrauma * Number of minor habits or events that cause damage to masticatory structures: * Bruxism * Postural habits * Oral habits (pen, pin, nail holding, nail biting, etc. Symptoms of temporal mandibular disorder (TMD) * Pain and tenderness in the muscles of mastication * Pain and tenderness in the TMJ * Painful clicking of the joint during function * Limitation of mandibular motion * You may also see muscle swelling and patient may complain of ringing in the ears * Arthralgia: pain in a joint structure Consideration for treatment * Short appointments * Aids during treatment- bite blocks to help keep mouth open * Home care suggestions- small tooth brush heads * Post treatment care- no gum chewing, possible medication, soft diet, warm towel * Frequent recalls Clinical Assessment (chapter 8) Clinical assessment of periodontal disease Assessment: represents the 1st phase of the dental hygiene process, provides the foundation for the subsequent diagnosis, planning, implementation, and evaluation of dental and dental hygiene care * Data collection: a systemic process of collecting information from multiple sources to help evaluate the health status of the patient. An example of data collection is the medical history * Documentation: this is the information gathered during the assessment and is a reference tool, an historical record; also has a medical and legal function * Examination: includes extraoral and intraoral, oral hygiene, periodontal and dentition assessments * Evaluation: At this point, the patient’s current progress (or lack thereof), is compared with baseline data and the stated goal.
The evaluation is used to determine if the patient should be re-treated, referred, or placed on a maintenance program * Interpretation: being able to decipher and understand your findings clinically or radiographically Examination of gingival tissues: clinical markers * Periodontal screening and recording system (PSR) * Was introduced in 1993 * Is a periodontal disease detection system * To be used in the screening process * A specifically designed probe is used * Bleeding, overhangs, defective margins, supra/subgingival calculus are assessed while pocket depth is measured * A PSR code is given to each sextant * The code that best describes the most periodontally involved tooth in a sextant is assigned to that sextant PSR scale Code| Description| | * Colored area of the probe remains completely visible * No calculus or defective margins are detected * Gingival tissues are healthy, with no bleeding on probing| 1| * Colored area of the probe remains completely visible in the deepest probing depth in the sextant * No calculus or defective margins are detected * There is bleeding on probing| 2| * Colored area of the probe remains completely visible in the deepest probing depth in the sextant * Supra or sub gingival calculus is detected or defective margins are detected| 3| * Colored area of the probe remains partly visible in the deeper probing depth in the sextant| 4| * Color