SAS 11: Gingival Diseases PDF

PERIODONTICS o Impaired venous return and; SAS 11: Gingival Diseases o Sluggish blood flow I (Inflammatory & other lesions)...

PERIODONTICS o Impaired venous return and; SAS 11: Gingival Diseases o Sluggish blood flow I (Inflammatory & other lesions) ▪ Anoxemia-leads to bluish hue on reddened gingiva o Color of gingiva deepen due to extravasation Page and Schroeder of erythrocytes and into CT and breakdown of ▪ Experimental study (group of people were made not to brush hemoglobin into its component pigments teeth for a certain period) ▪ Collagenase ▪ Found 4 stages of inflammation that occurs around the o Normally present in gingival tissue, produced periodontium in the presence of accumulation of dental by PMNs and by some bacteria plaque o Activity of collagenase increased in inflamed GINGIVAL INFLAMMATION gingival tissue which causes destruction of STAGE I: INITIAL STAGE gingival CT “Initial Phase or Subclinical Phase” ▪ Chronically inflamed gingiva ▪ Initial response to bacterial plaque; not apparent so referred o + levels of acid phosphatase, b-glucosidase, to as “subclinical gingivitis" b-galactosidase, esterases, aminopeptidase, and ▪ First manifestation of gingival inflammation cytochrome oxidase ▪ Vascular changes Histologically: o Dilated capillaries ▪ Presence of chronic inflammatory reaction o Increased blood flow ▪ + in # of plasma cells and B-lymphocytes ▪ If host response-good ▪ Intercellular spaces within JE widens o Initial lesion resolves rapidly leaving tissue to ▪ Intercellular spaces-filled with granular debris and some normal state lysosomes (derived from disrupted neutro, lympho, & mono ▪ If host response-do not respond well ▪ Tissue components o Lesion take up chronic form o Can be destroyed due to acid hydrolases o Infiltration of macrophages and lymphoid cells released by lysosomes HISTOLOGICALLY: ▪ Rete ridges-seen in JE, that protrude into the CT ▪ +leukocytes ▪ Collagen fibers also destroyed within CT, around, the ▪ +GCF flow infiltrate disrupted plasma cells, neutron, lympho, mono and o Due to +accumulation of leukocytes w/in gingival mast cells sulcus ▪ Leukocytes increase w/in JE and CT STAGE IV: THE PERIODONTAL BREAKDOWN (Periodontitis) ▪ Widening of blood vessels “Irreversible Tissue Destruction Phase (Periodontitis)” Clinically: ▪ Extension of lesion/inflammation into alveolar bone: ✓ Normal appearance of gingiva o Characterizes the advanced lesion STAGE II: EARLY LESION o Classified already as periodontitis “The Early Stage” ▪ Evolves from stage 3 gingivitis ▪ Early lesion evolves from initial lesion ▪ Phase of periodontal breakdown ▪ Process starts 1 week after the beginning of plaque Histologically: accumulation ▪ Extensive inflammation and immunopathologic tissue ▪ Erythema damage o Due to proliferation of capillaries and +formation ▪ Plasma cells continue to dominate CT of capillary loops between rete pegs or ridges ▪ PMNs dominate JE and crevice ▪ Bleeding on probing ▪ Gingiva becomes fibrotic ▪ Between 6 and 12 days after onset of clinical gingivitis, Clinically: gingival fluid flow and # of leukocytes reach max. level ▪ Attachment loss ▪ 70% collagen is destroyed around cellular infiltrate ▪ Destruction of alveolar bone ▪ PMNs-now evident in the gingival epithelium o Lengthening of tooth crown and gingival o Since they leave blood vessels and through destruction chemotactic stimuli from plaque, migrate to the CLINICAL FEATURES OF GINGIVITIS: epithelium 1. Color changes in the gingiva ▪ Phagocytosis 2. Changes in gingival contour o PMNs engulf bacteria 3. Changes in surface texture of gingiva ▪ Decreased capacity of collagen production, and fibroblasts 4. Changes in consistency of gingiva shows cytotoxic alterations 5. Changes in position of the gingiva HISTOLOGICALLY: 6. Gingival bleeding on probing ▪ 75% lymphocytes (mainly T-lymphocytes)-found in CT just 1. COLOR CHANGES IN THE GINGIVA beneath JE a. Acute Inflammation of the Gingiva ▪ Neutrophils, macrophages, and some amount of plasma and + blood flow to gingival tissue causes tissue to appear mast cells bright red o Also seen within CT b. Chronic Inflammation of the Gingiva ▪ Rete pegs-seen in JE Gingival tissue appear bluish-red/purplish-red due to ▪ Features of initial lesion aggravate in early lesions blood stagnation and burst of erythrocytes releasing Clinically: the hemoglobin content into the area ✓ Established gingivitis; mild to moderate Color change of gingiva may also be seen in the ff systemic ✓ Erythematous gingiva and bleeding on gentle probing conditions: a. Certain systemic factors which may influence the color STAGE III: THE ESTABLISHED GINGIVITIS (Subgingival Plaque of the gingiva Stage) b. Endogenous or exogenous source of pigments “The Established Gingivitis (Subgingival Plaque Phase” Endogenous oral pigments (cause oral pigmentation): ▪ Lesion-predominated by plasma cells and B-lymphocytes 1. Melanin ▪ B-lymphocytes-mainly immunoglobulin G1 (IgG1) and G3 2. Bilirubin (IgG3) subclasses 3. Iron ▪ Occurs around 2-3 weeks of plaque accumulation Melanin pigmentation – normal physiologic process found in ▪ Localized gingival anoxemia due to: highly-pigmented ethnic groups o Engorged & congested blood vessels Diseases where there is increased melanin pigmentation: EZRA. D. PERIODONTICS 1. Addison’s disease ✓ Isolated patches of discoloration 3. CHANGES IN SURFACE TEXTURE OF THE GINGIVA ✓ Bluish-black to brown Normal surface: stippled ✓ Due to adrenal dysfunction Stippling: 2. Peutz-syndrome ▪ Orange peel appearance caused by numerous small ✓ Causes intestinal polyposis depressions and elevations ✓ Melanin pigmentation in oral mucosa and lips ▪ Seen in interdental and attached 3. Albright syndrome (fibrous dysplasia) and von reckling Surface: hausen’s disease (neurofibromatosis) ▪ Can either be smooth and shiny or firm and nodular ✓ Produces areas of oral melanin pigmentation depending whether changes are exudative or fibrotic Bile pigments Nodular texture ▪ Stain the skin and mucous membrane ▪ Drug-induced gingival overgrowth Iron deposition ▪ Hemochromatosis 4. CHANGES IN CONSISTENCY ▪ Blue-grey pigmentation of the oral mucosa Both acute and chronic: Disorders related to blood can produce color changes of the ▪ Produce changes in consistency of gingiva oral mucosa: Chronic: ▪ Anemia ▪ Destructive (edematous and reparative which is fibrotic ▪ Polycythemia coexists and the form which is predominated will define the ▪ Leukemia consistency of gingiva Disorders related to endocrine system and metabolic CHRONIC GINGIVITIS disturbances Clinical changes Underlying microscopic feature ▪ Diabetes Soggy puffiness that Infiltration by fluid and cells of ▪ Pregnancy pits on pressure inflammatory exudate Exogenous factors Marked softness and Degeneration of CT and epithelium ▪ Irritants – Coal, metal dust, and coloring agents in food and friability, with ready associated w/ injurious substances lozenges) fragmentation on that provoke inflammation and ▪ Tobacco: exploration with inflammatory exudate; change in CT- o Increase in melanin pigmentation probe and pinpoint epithelium relationship, with o Hyperkeratosis of the gingiva surface areas of inflamed, engorged CT expanding to ▪ Amalgam implantation – localized bluish-black areas of redness and within a few epithelial cells of the pigmentation desquamation surface; thinning of epithelium and If a patient wants to get gingiva depigmented (esthetic degeneration associated w/ edema concerns): and leukocyte invasion, separated by a. Scalpels areas in which rete pegs are b. Chemicals elongated to CT c. Electrocautery d. Lasers Firm, leathery Fibrosis and epithelial proliferation consistency associated w/ long-standing chronic 2. CHANGES IN TISSUE CONTOUR (SIZE AND SHAPE) inflammation ▪ Diseased tissue o Free gingiva is no longer flat but rolled and ACUTE GINGIVITIS thickened as a result of edema (fluid) at the neck Clinical changes Underlying microscopic feature of the tooth Diffuse puffiness Diffuse edema of acute inflammatory Papillae-bulbous, blunted, or cratered and softening origin; fatty infiltration in 1. Bulbous – enlarged & appears to bulge out of the xanthomatosis interproximal space Sloughing w/ Necrosis w/ formation of 2. Blunted – flat & does not fill the interproximal space grayish, flakelike pseudomembrane (bacteria, PMNs, 3. Cratered – scooped out leaving a concave depression particles of debris and degenerated epithelial cells in in the midproximal area adhering to eroded fibrinous meshwork) Stillman’s cleft McCall’s festoon surface Vesicle formation Intercellular & intracellular edema w/ degeneration of nucleus and cytoplasm and rupture of cell wall 5. CHANGES IN THE POSITION OF MARGINAL GINGIVA ▪ Normal: CEJ ▪ Inflammation: above CEJ due to increased size ▪ Gingival enlargement: above CEJ covering clinical crowns ▪ Normal contour of marginal gingiva – scalloped and knife Other change in the position of the gingiva edged ▪ Change in the contour of gingiva – mainly seen in cases of Attachment loss: gingival enlargement ▪ Shift in the position of gingiva apical to CEJ, “Gingival ▪ In cases of disease – contour of gingiva becomes rolled or recession’’ rounded ▪ Recession-exposure of root surface by the apical shift in the ▪ Inflammatory changes in the marginal gingiva: position of gingiva o Lead to formation of clefts and narrow, triangular shaped gingival recession 2 positions of gingiva in recession: o As recession progress apically, cleft becomes broader, 1. Actual Position causing exposure of root cementum o Level of epithelial attachment on the tooth o Some suggest they occur due to traumatic occlusion o Determine severity of recession and the treatment would be occlusal adjustments 2. Apparent Position ▪ McCall festoons o Level of crest of gingival margin o Rolled thickened band of gingiva seen along canines when recession approaches mucogingival junction EZRA. D. PERIODONTICS o As the inflamed CT consists of engaged blood vessels w/c get enrobed by ulceration due to necrotic surface epithelium B. Systemic factors causing bleeding: ▪ Certain conditions have common feature of a hemostatic mechanism failure w/c result in abnormal bleeding in the skin, internal organ and other tissues including oral mucosa Hemorrhagic disorders (abnormal gingival bleeding): 1. Vascular abnormalities: vit C deficiency Causes of recession: 2. Allergy: Schonlein-Henoch purpura 1. Faulty tooth brushing techniques (gingival abrasion) 3. Platelet disorder: thrombocytopenic purpura 2. Tooth malposition 4. Hypoprothrombinemia: vit K deficiency 3. Friction from soft tissues (gingival ablation) 5. Other coagulation defects: 4. Gingival inflammation a. Hemophilia 5. Abnormal frenum attachment b. Leukemia 6. Iatrogenic dentistry c. Christmas disease 7. Trauma from occlusion d. Deficient platelet thromboplastic factor/PF3 8. Orthodontic treatment (resulting in uremia, multiple myeloma and post Clinical significance of gingival recession (lead to): rubella purpura) 1. Root caries 6. Effects of hormonal replacement therapy, oral 2. Cause abrasion or erosion of cementum contraceptives, pregnancy and menstrual cycle o Leading to hypersensitivity of dentin 7. Fluctuation in certain hormones: a. Androgenic hormones (modifying gingivitis esp. 6. PRESENCE OF BLEEDING IN GINGIVITIS puberty) Bleeding on probing: 8. Certain medications: ▪ One of the clearest signs of gingival inflammation seen a. Anticonvulsants before gingivitis is established b. Antihypertensive CCB (Other: Increase in GCF production rate) c. Immunosuppressants ▪ Appears before visual signs of inflammation; thus, a more o All 3 causes gingival enlargements causing objective sign that requires less subjective estimation by gingival bleeding secondarily the examiner In diseased tissue: ▪ Presence of bleeding: not a definite indicator of clinical ▪ Sulcus lining becomes ulcerated and blood vessels become attachment loss but its absence indicates excellent negative engorged predictor of future attachment loss ▪ When gingival tissues are disturbed by Factors causing gingival bleeding: probing/instrumentation they bleed easily A. Local ▪ Severity of bleeding depend on intensity of inflammation B. Systemic Describing gingival inflammation A. Local factors (other than plaque): 1. Duration 1. Anatomic and developmental tooth variations a. Acute gingivitis 2. Caries Sudden onset, painful, short duration 3. Frenum pull b. Chronic gingivitis 4. Iatrogenic factors Slow onset, painless, long duration 5. Malposition of teeth c. Recurrent gingivitis 6. Mouth breathing Reappears after being eliminated by treatment or 7. Overhangs disappearing spontaneously 8. Partial dentures 2. Extent of inflammation 9. Lack of attached G a. Localized gingivitis – confined to gingiva of a 10. Recession single tooth or group of teeth Chronic and recurrent bleeding: b. Generalized gingivitis – entire mouth Chronic inflammation 3. Distribution of inflammation ▪ Most common cause of abnormal gingival bleeding a. Marginal gingivitis Mechanical trauma Involves gingival margin and may include a ▪ Can provoke gingival bleeding (chronic or recurrent) portion of contiguous attached gingiva ▪ From tooth brushing, tooth picks, food impactions, or b. Papillary gingivitis biting into solid food (e.g., apple) Involves interdental papillae and often extends Severity of bleeding and ease of provocation: into adjacent portion of gingival margin ▪ Depends upon intensity of inflammation c. Diffuse gingivitis Once vessels are ruptured and damaged Affects gingival margin, attached gingiva and ▪ Mechanism of hemostasis starts: interdental papillae o Contraction of the vessel wall Use of descriptive terminology o Decrease in blood flow ▪ Localized marginal gingivitis o Platelets adhere to edges of the tissue o Confined to one or more areas of marginal forming a fibrous clot which contracts gingiva resulting in approximation of the edges of the ▪ Localized diffuse gingivitis injured area (when area is irritated, bleeding o Extends from margin to mucobuccal fold in a starts again) limited area Bleeding on probing ▪ Localized papillary gingivitis ▪ Sign of active tissue destruction o Confined to one or more interdental spaces in ▪ Injury can lead to active episodes of gingival inflammation a limited area Injury could be: ▪ Generalized marginal gingivitis ▪ Laceration of gingiva during tooth brushing o Involves gingival margins in relation to all ▪ Sharp pieces of hard food teeth ▪ Gingival burns from hot food or chemicals ▪ Generalized diffuse gingivitis Spontaneous bleeding o Involved entire gingiva, alveolar mucosa, and ▪ Also seen in ANUG attached gingiva, mucogingival junction is sometimes obliterated EZRA. D. PERIODONTICS o Semi-firm but have varying degrees of SAS 12: Gingival Enlargements softness & friability ▪ Painless, unless complicated by either accumulation of According to Carranza: debris under margin or interference w/ occlusion ▪ Size of gingiva – sum total of the bulk of all cellular and o Painful ulceration may occur intercellular elements and their vascular supply b. Puberty ▪ Alteration in size – common feature of gingival disease ▪ Both marginal and interdental papilla Current clinical descriptive terminology describing increase ▪ Characterized by: in size: o Prominent bulbous interproximal papilla Gingival enlargement ▪ Frequently only facial gingiva is affected mechanical Gingival overgrowth action of tongue prevent accumulation of food on lingual surfaces CLASSIFICATION ▪ Has all clinical features of chronic inflammatory I. ACCORDING TO ETIOLOGIC FACTORS AND PATHOLOGIC gingivitis CHANGES ▪ Distinguished from CIG by: A. Inflammatory enlargement o Degree of enlargement 1. Chronic o Tendency to develop massive recurrence ▪ Most common of all gingival enlargements ▪ 11-17 years old: high prevalence ▪ Brought about by prolonged local irritation of dental ▪ Capnocytophaga species-initiation of pubertal plaque/biofilm gingivitis o Localized or generalized o Progress slowly and painlessly unless c. Vitamin C deficiency complicated by acute infection or trauma ▪ Acute vit. C deficiency does not itself cause gingival o May come as discrete/tumor-like inflammation but causes: 2. Acute 1. hemorrhage ▪ Gingival abscess 2. collagen degeneration ▪ Localized, painful, rapidly expanding lesion 3. edema of gingival CT ▪ Sudden in onset o These changes modify response of gingiva to ▪ Usually as a result of bacteria carried into tissues when plaque foreign substance (toothbrush bristle or fragments of ▪ Gingival enlargement marginal and bluish-red, soft, food) is forcefully embedded into the gingiva friable, and has smooth, shiny surface ▪ ▪ Hemorrhage-spontaneous or on slight provocation B. Drug-induced enlargement (Phenytoin, cyclosporine A, CCB) d. Plasma cell gingivitis ▪ Starts within 3mos of taking medication ▪ AKA atypical and plasma cell gingivostomatitis ▪ Exaggerated inflammatory response in relation to plaque ▪ Mild-marginal gingival enlargement; extend to attached present gingiva ▪ Good daily plaque control limits severity of lesion ▪ Clinically gingiva appears red, friable and bleeds easily ▪ Higher prevalence among children ▪ Associated cheilitis and glossitis ▪ Exhibits change in gingival: ▪ Allergic in origin (possibly related to components of o Contour chewing gm and dentrifices) o Size e. Non-specific conditioned enlargement o Color ▪ Tumor-like ▪ Gingiva in anterior sextants: most commonly affected but ▪ Exaggerated conditioned response to minor trauma can also occur in posterior sextants ▪ Exact nature: Not yet identified ▪ Gingival enlargement first observed in interdental papilla ▪ Increased crevicular fluid flow and bleeding on probing f. Pyogenic granuloma ▪ NO attachment loss ▪ Lesion varies from discrete, spherical tumor-like mass ▪ Does not happen in edentulous spaces w/ pedunculated attachment to a flattened keloid-like enlargement w/ a broad base C. Enlargements associated w/ systemic diseases ▪ Bright red or purple; friable or firm depending on Systemic diseases/condition can affect periodontium in 2 duration mechanisms: ▪ Majority: surface ulceration & purulent exudation ▪ Lesion tends to involute spontaneously or persists I. Magnification of an existing inflammation initiated by dental relatively unchanged for years plaque ▪ TX: Surgical excision ▪ Local irritation is necessary ▪ Conditioned enlargement occurs when systemic II. Manifestation of systemic diseases, independently of the condition of px exaggerates usual gingival response to inflammatory status of the gingiva dental plaque ▪ The systemic disease, causing gingival enlargement a. Pregnancy and neoplastic enlargement [Tumor-like Gingival Enlargement (Pregnancy Tumor)] a. Leukemia ▪ Generalized, more prominent interproximally than on ▪ Diffuse or marginal, localized or generalized facial/lingual surface ▪ Oversized extension of marginal gingiva or a discrete ▪ Bright red or magenta, soft and friable, smooth shiny tumor-like interproximal mass surface ▪ Bluish-red w/ shiny surface ▪ Discrete mushroom-like flattened spherical mass that ▪ Consistency: protrude from interdental papilla or gingival margin o Moderately firm but tendency towards and is attached to a sessile or pedunculated base friability and hemorrhage (spontaneous/slight ▪ Tends to expand laterally and pressure from cheek & provocation) tongue increases its flattened appearance ▪ True leukemic enlargement: ▪ Dusky red/magenta w/ smooth glistening surface that o Common in acute leukemia frequently exhibit numerous deep red, pinpoint o May be seen in subacute leukemia markings o Seldom in chronic leukemia ▪ Consistency: b. Granulomatous diseases b.1 Wegener’s granulomatous EZRA. D. PERIODONTICS ▪ Rare disease characterized by granulomatous necrotizing lesion of respiratory tract including nasal & SAS 13: Acute Gingival oral defects Infections ▪ Initial manifestation: o Orofacial region Necrotizing Ulcerative Gingivitis o Oral mucosal ulceration ▪ Microbial disease of gingiva; impaired host response o Gingival enlargement ▪ Characterized by death and sloughing of gingival tissues o Abnormal tooth mobility Etiology: o Exfoliation of teeth a. bacteria (fusiform bacillus & spirochetes) o Delayed healing response b. impaired host response ▪ Etiology: Uknown 1. Local predisposing factors – smoking, existing gingivitis o Considered immunologically mediated tissue 2. Systemic predisposing factors – nutritional deficiency, injury debilitating diseases ▪ Usual outcome: Death from kidney failure 3. psychosomatic factors – stressful situations (induction in ▪ More recently made use of immunosuppressive drugs armed forces) produced prolonged remission Clinical signs and symptoms: b.2 Sarcoidosis ▪ Punched out, crater-like depressions at the crest of ▪ Also granulomatous disease of unknown etiology interdental papillae ▪ Starts in20s and 30s ▪ Surface – covered by gray, pseudomembranous slough ▪ Involve any organ including gingiva demarcated from remainder of gingival mucous by o Red, smooth enlargement pronounced linear erythema ▪ Spontaneous gingival hemorrhage after slightest stimulation D. Neoplastic Enlargement (Gingival Tumors) ▪ Extremely sensitive to touch, painful a. Benign tumors ▪ Fetid odor & increased salivation 1. Fibroma ▪ Metallic taste and pasty saliva 2. Papilloma Diagnosis: based on above clinical findings 3. Peripheral Giant Cell Granuloma Extraoral & Systemic Signs and Symptoms: 4. Central Giant Cell Granuloma ▪ Px usually ambulatory & minimum systemic symptoms 5. Leukoplakia ▪ Mild to moderate stages: 6. Gingival Cyst o Local lymphadenopathy o Slight elevation of temperature b. Malignant tumors ▪ Severe cases: 1. Carcinoma o High fever 2. Sarcoma o Increased pulse rate o Leukocytosis E. False Enlargement o Loss of appetite ▪ Not true enlargements o General lassitude (weakness) ▪ Appear as a result of increase in size of underlying osseous Clinical course: or dental tissues Stages of NUG Progression (Pindborg et al): a) Erosion of only tip of interdental papilla II. ACCORDING TO LOCATION AND DISTRIBUTION b) Lesion extends to marginal & cause further erosion EXTENT of papilla & potentially to complete loss of papilla 1. Localized – one or more group of teeth c) Attached gingiva affected 2. Generalized – entire mouth, gingiva is enlarged d) Exposure of bone DISTRIBUTION 1. Marginal – limited to marginal gingiva Stages of NUG Progression (Homing and Cohen) 2. Papillary – confined to interdental papilla Stage 1: Necrosis of the tip of interdental papilla 3. Diffuse – all parts of gingiva (marginal, attached, Stage 2: necrosis of the entire papilla interdental) Stage 3: Necrosis extending to gingival margin 4. Discrete – isolated sessile/pedunculated tumor-like Stage 4: Necrosis extending to attached gingiva enlargement Stage 5: Necrosis extending into buccal or labial mucosa Stage 6: Necrosis exposing alveolar bone (NUP) According to degree of Gingival Enlargement (Scoring) Stage 7: Necrosis perforating skin of cheek (Noma) Grade 0: No sign of GE Treatment: Grade I: Enlargement confined to interdental papilla 1. Alleviation of acute inflammation by reducing microbial Grade II: Enlargement involves papilla and marginal load and removal of necrotic tissue Grade III: Enlargement covers 3 quarters or more of crown 2. Treatment of underlying systemic condition 3. Alleviation of generalized symptoms (fever, malaise) 4. Correction of local systemic factors that contribute to initiation or progression of ANUG Patient instructions: 1. Avoid tobacco, alcohol, and condiments 2. Rinse w/ a glassful of an equal measure of 3% hydro pero and warm water every 2 hrs and/or 2x daily w/ chlorhexidine solution 3. Get adequate rest 4. Confine toothbrushing w/ bland dentrifice and ultrasoft brush to the removal of surface debris 5. Take the prescribed medications, antibiotic, pain relievers Primary Herpetic Gingivostomatitis ▪ HSV1, contagious ▪ Infants and children under 6 yrs. old ▪ Diffuse, erythematous, shiny involvement of the gingiva and adjacent oral mucosa EZRA. D. PERIODONTICS ▪ Initial stage – presence of discrete, spherical gray vesicles on gingiva, labial/buccal mucosa, soft palate, pharynx, tongue SAS 14: Desquamative Gingivitis ▪ After 24 hrs. vesicles rupture and form painful, small ulcers w/ a red, elevated halo-like margin and depressed yellowish or grayish central portion ▪ Prinz 1932; peculiar ▪ Course of disease is limited to 7-10 days ▪ Clinical description of gingiva w/c result from various Oral Symptoms: underlying conditions ▪ Generalized soreness of oral cavity; interferes w/ eating and ▪ Fiery, red, glazed, atrophic, or eroded looking gingiva drinking ▪ Loss of stippling; desquamate easily w/ minor trauma ▪ Ruptured vesicles – focal sites of pain & sensitive to touch, ▪ Painful, affects buccal & labial gingiva predominantly thermal changes, food (condiments & fruit juices), and action of coarse food Diagnosis (Systematic Approach): Extraoral & systemic signs and symptoms: ▪ Clinical history – data (symptomatology, when, how lesion ▪ Cervical adenitis start) ▪ Fever as high as 101 F ▪ Clinical exam – recognition of pattern of distribution of signs ▪ Generalized malaise ▪ Clinical maneuver – Nikolsky sign ▪ Treatment: ▪ Biopsy – foundation for diagnosis ▪ Early diagnosis and immediate initiation of antiviral therapy ▪ Immunofluorescence – direct or indirect ▪ Acyclovir suspension 15mg/kg 5x daily for 5 to 7 days (if o Lab technique; light microscopy; detect presence given within 3 days of onset) of proteins or antigens in cells/tissue sections by ▪ Reduce symptoms including fever, decreased oral symptoms binding specific antibody and reduce difficulty in eating from 7 to 14 days Diseases clinically presenting as desquamative gingivitis: ▪ After 3rd day of onset – palliative care is given 1. Lichen planus 2. Pemphigoid Acute Pericoronitis a. Bullous pemphigoid ▪ Inflammation of gingiva in relation to the crown of b. MMP (Cicatricial) INCOMPLETELY erupted tooth 3. Pemphigus vulgaris ▪ Mandibular 3rd 4. Lupus erythematosus ▪ Identified by varying degrees of inflammatory involvement of a. Systemic LE (SLE) pericoronal flap and adjacent structures by systemic b. Chronic cutaneous LE (CCLE) complications 5. Erythema multiforme ▪ Inflammatory fluid and cellular exudate – increase the bulk 1. Lichen planus of the pericoronal tissue w/c then interfere w/ complete ▪ Inflammatory mucocutaneous disorder; involve mucosal closure of jaws & can be traumatized surfaces (oral cavity, genital tract, other mucosae) and skin Treatment (depends on): (scalp, nails) 1. Severity of inflammation ▪ T-lymphocytes 2. Systemic complications Oral and gingival lesions 3. Advisability of retaining involved tooth (May occur as one or more types of 4 distinctive patterns) 4. Treatment can take more than 1 visit 1. Keratotic lesions – raised, white lesions; groups of Treatment (consists of): individual plaques, linear or reticular 1. Gently flushing area w/ warm water to remove debris 2. Erosive or ulcerative lesions – extensive erythematous and exudate areas w/ patchy distribution; present as focal or diffuse 2. Swabbing w/ antiseptic after elevating flap gently from hemorrhagic areas tooth w/ a scaler 3. Vesicular or bullous lesions – raised, fluid filled, o Underlying debris is removed and area is flushed uncommon and short-lived on gingiva, quickly erupting w/ warm water and leaving an ulceration 3. Instructions to px 4. Atrophic lesions – atrophy of gingiva w/ ensuing o Hourly rinses w/ solution of teaspoonful of salt in epithelial thinning results in erythema confined to the warm water, rest, copious fluid intake, & admin. of gingiva systemic antibiotics if toxic symptoms present Microscopically (3 main features) Occlusion – evaluated to determine if an opposing tooth is 1. Hyperkeratosis or parakeratosis occluding w/ pericoronal tissue 2. Hydropic degeneration of basal layer Removal of tissue (operculectomy) or occlusal 3. Dense, bandlike infiltrate of primarily T-lymphocytes in adjustment may be necessary lamina propria Antibiotics can be prescribed in severe cases Immunopathology After acuter symptoms subside – decide whether to 1. Direct immunofluorescence (of lesional and retain or extract perilesional areas) o Decision is governed by the likelihood of further o Reveal fibrillar deposits of fibrin in the eruption into a good functional position basement membrane zone w/ IgM deposits in o Operculectomy is done the lamina propria 2. Indirect immunofluorescence – negative Gingival Abscess Treatment ▪ Localized, painful, rapidly expanding lesion of sudden onset Keratotic lesions – do not require treatment, however, follow up ▪ Marginal gingiva or interdental papilla px every 6 to 12 mos. to monitor suspicious clinical changes ▪ Result of bacteria carried deep into tissues when foreign ▪ Erosive, bullous, or ulcerative lesions – high potency topical bodies are forcefully embedded into gingiva steroids: ▪ May become fluctuant and pointed w/ surface orifice from o 0.05% fluocinonide ointment (Lidex 3x daily) w/c purulent exudates are expressed ▪ Severe cases: Treatment: o Intralesional injections of triamcinolone 1. If cause is still there – it should be removed (remove cause) acetonide (10-20 mg) 2. Drainage by warm salt water mouthwashes every 2 hrs o 40 mg of prednisone daily for 5 days; 10 to 3. Lesion persists – curette under local anesthesia or incise if 20 mg daily for 2 weeks pointing (Because of potential side-effects, administration of systemic 4. Persistent and severe systemic – prescribe antibiotic steroids should be prescribed and monitored by dermatologist) 5. Residual pocketing – removed by subgingival curettage or localized gingivectomy EZRA. D. PERIODONTICS 2. Pemphigoid Treatment – topical & systemic steroids (prednisone and ▪ Number of cutaneous, immune-mediated, subepithelial immunosuppressive drugs) bullous diseases characterized by separation of basement a. SLE membrane Severe disease w/ proliferation for women over men 2 conditions: Affects vital organs (kidney, heart, skin, and mucosa) a. Bullous Pemphigoid – disease is non scarring; skin Oral lesions similar to lichen planus b. Cicatricial Pemphigoid (mucous membrane) – confined Direct immunofluorescence to mucous membrane of oral cavity, conjunctiva, nose, o IgG or IgM and C3 deposits at dermal- vagina epidermal interface Cicatricial pemphigoid o Antinuclear antibodies (ANA) 95%, DNA, and ▪ Desquamative gingivitis, typically areas of erythema, extractable nuclear antigen (ENA) in >50% of desquamation ulceration and vesiculation of ATTACHED patients gingiva ▪ Vesiculobullous lesions – appear elsewhere in the mouth 5. Erythema Multiforme o Bullae – thick roof w/c rupture 2 to 3 days, leaving Acute bullous and macular inflammatory mucocutaneous irregularly-shaped ulceration disease o Healing – 3 weeks or longer Caused by 3 common etiologic factors: ▪ Ocular lesions (histologic exam) – entire epithelium is 1. Herpes simplex infection separated from underlying connective tissue 2. Mycoplasma infection ▪ Ocular lesions of cicatricial pemphigoid – characterized by 3. Drug reactions (sulfonamides, penicillins, unilateral conjunctivitis; becomes bilateral within 2 years phenylbutazone, phenytoin) ▪ Adhesion of eyelid to eyeball; eventually produce scarring, 2 types: corneal damage, and blindness 1. Erythema multiforme minor – last for 4 weeks Histopathology 2. Erythema multiforme major (Steven-Johnson syndrome) ▪ Striking subepithelial vesiculation, w/ epithelium separated o lasts for months or longer from underlying lamina propria; leaves intact basal layer o affects skin, conjunctiva, oral mucosa, ▪ Separation of epithelium and connective tissue occurs at genitalia basement membrane zone IRIS or target lesion – hallmark of EM Immunofluorescence Oral lesions ▪ Both direct & indirect – positive along basement membrane ▪ Multiple, large, shallow, painful ulcers w/ erythematous IgG and C3 main immunoreactants border Treatment ▪ Affect entire oral mucosa ▪ Topical steroids – fluocinonide and clobetasole propionate ▪ Buccal & tongue mucosa (most frequent site), then labial m. 0.05% 3x daily for up to 6mos ▪ Floor of mouth, hard & soft palate (less frequent) ▪ Systemic steroids – ocular involvement ▪ May be confined to gingiva alone as desquamative type ▪ Hemorrhagic crusting of vermilion border of lips 3. Pemphigus vulgaris Immunofluorescence – negative ▪ Autoimmune bullous disorder; produce cutaneous and Treatment mucous membrane blisters ▪ No specific tx – some lesion resolves spontaneously ▪ MOST COMMON of pemphigus diseases ▪ Mild symptoms – local antihistamines w/ topical anesthetics ▪ Lethal and chronic w/ 10% mortality rate ▪ Severe cases – corticosteroids ▪ Predilection: women 40 yrs. ▪ Idiopathic / unknown cause ▪ Penicillamine and captopril – produce drug-induced pemphigus Oral lesions ▪ Heralds the 1st sign of the disease ▪ Range from small vesicles to large bullae ▪ When ruptured, leaves extensive areas of ulceration, virtually, any region of oral cavity may be involved: o Soft palate (more common), buccal mucosa, ventral/dorsum tongue, and lower labial mucous o Less often in gingival tissues as desquamative lesion Clinically looks the same w/ pemphigoid lesions but histologically: ▪ Vesicle formation and sloughing of superficial layer of gingiva occurs intraepithelially ▪ Basal cell layer – remains attached to connective tissue, TOMBSTONE appearance Histopathological exam ▪ Intraepithelial separation – occurs above basal cell layer ▪ Tombstone appearance to epithelial cells ▪ Acantholysis – separation of epithelial cells of lower spinosum characterized by presence of round rather than polyhedral epithelial cells 4. Lupus Erythematosus a. Systemic Lupus Erythematosus (SLE) b. Chronic cutaneous lupus erythematosus (CCLE) o no systemic signs or symptoms o symptoms limited to skin and mucosa only o produces scarring on skin c. subacute Cutaneous Lupus Erythematosus (SCLE) o similar to CCLE but no scarring and atrophy EZRA. D. PERIODONTICS Gingiva – fibrotic and pink in outer surface while SAS 15: Periodontal Pathology: inner surface of soft tissue wall is inflamed and Periodontal Pocket ulcerated Pocket – pathologically deepened gingival sulcus (According to disease activity) Clinically healthy or normal gingival sulcus – 2 to 3mm depth 1. Active pockets (margin to base of sulcus); increase in measurement result to Periods of exacerbation (activity) pocket Characterized by bone and connective tissue Occur in 3 ways: attachment loss w/c results to deepening of pockets 1. Coronal movement of gingival margin (gingival pocket) Clinically: bleeding spontaneously or w/ probing and 2. Apical displacement of gingival (epithelial) attachment greater amounts of attachment loss, presence of (periodontal pocket) exudation/pus 3. Combination of the above 2. Inactive pockets Periods of remission or quiescence (inactivity) CLASSIFICATIONS OF POCKETS characterized by reduced inflammatory response (According to morphology) Little or no loss of bone or connective attachment Clinical Features 1. Gingival pocket (Pseudo or false pocket) Signs: ▪ It is seen as gingivitis a. Enlarged, bluish-red marginal gingiva w/ rolled edge ▪ It is formed by the gingival enlargement w/out any separated from tooth surface destruction of underlying periodontal structures b. Bluish-red vertical zone extending from gingival ▪ The gingival sulcus is deepened because of the increased margin to alveolar mucosa bulk of the gingiva c. Break in faciolingual continuity of interdental gingiva d. Shiny, discolored and puffy gingiva associated w/ 2. Periodontal pocket (Absolute or true pocket) exposed root surfaces ▪ Occurs as periodontitis e. Gingival bleeding, purulent exudates from gingival ▪ Due to apical migration of JE and destruction of supporting margin periodontal tissues that lead to tooth loss f. Development of diastema where none existed 2 kinds: previously 1. Suprabony pocket (supracrestal or supraalveolar Symptoms: pocket) a. Localized pain or sensation of pressure in the gingiva Bottom of pocket – coronal to underlying alveolar after eating w/c gradually diminishes bone b. Foul taste in localized areas Lateral wall – consists of soft tissue alone c. Tendency to suck material (blood) from interproximal Pattern of bone destruction – Horizontal spaces Interproximally – transseptal fibers arranged d. Radiating pain “deep in the bone” horizontally (between base of pocket and alveolar e. “Gnawing” feeling or feeling of itching in the gingiva bone) f. Urge to dig a pointed instrument into the gingiva and Facial & lingual surfaces – PDL fibers follow relief is obtained from resultant bleeding horizontal oblique course g. Patient complains food “sticks between teeth” or teeth feel loose” or a preference to “eat on the other side” 2. Infrabony pocket (Subcrestal or intraalveoalar h. Sensitivity to heat and cold; toothache in the absence pocket) of caries Bottom of pocket – apical to crest of alveolar bone Pocket contents Lateral wall – soft tissue & bone Debris principally containing microorganisms and their Pattern of bone destruction – Vertical products (enzymes, endotoxins, and other metabolic Interproximally – transseptal fibers are oblique products) dental plaque, gingival fluid, food remnants, (extend from cementum beneath base of pocket salivary mucin, desquamated epithelial cells, and along bone and over crest of cementum of leukocytes adjacent tooth) Purulent exudates – living degenerated and necrotic Facial & lingual surfaces – PDL fibers follow PMNs, living and dead bacteria, serum, and scanty angular pattern amount of fibrin Pus formation – common in periodontal disease but 3. Combined pocket only a secondary sign According to number of tooth surfaces involved: o Merely reflects nature of inflammatory 1. Simple pocket – involves only one surface changes in the pocket 2. Compound pocket – more than one surface Presence of pus in the pocket – accumulate and form 3. Complex/Spiral pocket – originate on one tooth periodontal abscess (also called, “lateral or parietal surface, twisting around the tooth to involve one or abscess” more additional surfaces (but open into oral cavity on Pocket depth vs Clinical Attachment Level/Loss the surface of origin) ▪ Probing depth – tip of gingival margin to probable depth or base of pocket According to the Nature of the Soft Tissue Wall of the Pocket ▪ Clinical attachment level – CEJ to base of pocket ▪ Periodontal pockets – inflammatory lesions and constantly Pseudo vs true pocket undergoing repair ▪ Clinical attachment level measurement should be considered ▪ Complete healing does not occur due to persistence of ▪ Clinical detection of attachment level – done by first bacterial attack w/c continue to stimulate an inflammatory identifying CEJ w/ probe tip (since JE is attached to CEJ), if response causing degeneration of new tissues: probe passes beyond point of CEJ then it is considered TRUE a. Edematous pockets POCKET Inflammatory component predominates Lateral wall – appears soft, edematous, friable, w/ smooth shiny surface and bluish red discoloration b. Fibrotic pockets Reparative changes predominate EZRA. D. PERIODONTICS Accdg to Carranza et al SAS 16: Bone Loss and Patterns of Locally produced bone resorption factors may need to be Bone Destruction in Periodontal present in the proximity of the bone surface to exert their action Disease Range of effectiveness of about 1.5-2.5mm within w/c bacterial plaque can induce loss of bone Periodontitis vs Gingivitis Beyond 2.5mm – no effect; interproximal angular defects can ▪ Perio – loss off attachment accompanied by bone loss appear in spaces wider than 2.5mm bec narrower spaces would ▪ Alveolar bone – never stable be destroyed entirely o Continuous balanced process of bone resorption and bone formation Loe et al ▪ However, in the presence of inflammation, disease and Rate of bone loss (when periodontal disease was allowed to susceptibility, bone resorption exceeds formation and bone progress untreated) density and height are reduced Periodontitis 0.2mm/ year for facial surfaces ▪ Bone level – indication of the past pathologic changes 0.3mm/year – proximal areas ▪ Soft tissue changes (periodontal pockets) – indicative of present inflammatory changes 2. Trauma from Occlusion ▪ Although infectious, changes that occur in bone are crucial because its destruction is responsible for tooth loss 3. Systemic Disorders ▪ Bone loss patterns associated w/ periodontal disease – ▪ Osteoporosis, osteopenia, Paget’s disease, varied and the type of management depend upon type of hyperparathyroidism and diseases that affect skeletal loss disturbances may also have a relative effect to periodontal destruction Normal anatomy of alveolar bone Factors Determining Bone Morphology in Periodontal Alveolar bone – part of jaw that surrounds and supports teeth Disease o Has facial and lingual cortical plate or compact 1. Normal Variation in Alveolar Bone bone between w/c cancellous is sandwiched o Thickness, width and crestal angulation of the o Shape and size – vary in different regions of the interdental septa mouth o Thickness of facial and lingual alveolar plates o Margins of alveolar crest run parallel to CEJ at a o The presence of fenestrations and dehiscences remarkably constant distance of 1 to 2 mm o The alignment of the teeth Causes of bone destruction in Periodontal Disease o Root and root trunk anatomy and position in the 1. Extension of Gingival inflammation alveolar process ▪ Most common cause of bone loss o Proximity with another tooth surface ▪ Sequela of chronic gingivitis in some individuals 2. Exostoses ▪ Inflammation spreads form gingiva into deeper tissues along 3. Trauma from occlusion 2 pathways w/c marks transition from gingivitis to 4. Buttressing bone formation (lipping) periodontitis 5. Food Impaction ▪ Transition – associated w/ changes I the composition of 6. Aggressive periodontitis bacterial plaque and resistance of the host ▪ Lesion – presents w/ most pathogenic bacteria, Bone Destruction Patterns in Periodontal Disease: inflammatory cell infiltrate 1. Horizontal Bone Loss o Lesion becoming more progressive and ▪ Most common pattern of bone loss in periodontal disease destructive w/ the conversion of T-lymphocyte to ▪ Bone is reduced in height but the bone margins remain B-lymphocytic lesion and; roughly perpendicular to the tooth surface o Release of high concentrations of cytokines, PGE2, and MMPs by immune cells lead to more tissue 2. Vertical or Angular Defects destruction that overwhelms any tissue repair ▪ Oblique direction, leaving a hollowed-out trough in the bone alongside the root ▪ Base of the defect – apical to the surrounding bone ▪ Most situations angular defects are accompanied by infrabony pockets Angular defects are classified on the basis of number of walls present as: 1. One-walled or hemiseptal defect 2. Two-walled defect 3. Three-walled or intrabony defect (common on mesial 1 – into gingival connective 1 – into gingival connective surfaces of upper and lower molars) tissue tissue 4. Combined osseous defect (best seen upon surgical 2 – into alveolar bone 2 – into PDL exposure) 3 – into PDL (final) 3 – into alveolar bone (final) After inflammation reaches bone – it spreads into marrow spaces and replaces the marrow w/ leukocytic and fluid exudates, new blood vessels and proliferating fibroblasts Multinuclear osteoclasts and mononuclear phagocytes – increase in number, and have to be present in the proximity of the bone surfaces appear lined w/ Howship lacunae in marrow spaces Resorption proceeds from within, causing thinning and 3. Osseous Craters reduction in bone height ▪ They are concavities in the crest of the interdental bone confined within the facial and lingual walls Bone destruction – episodic, intermittent manner, w/ periods of ▪ Make up two-thirds of all mandibular defects inactivity or quiescence ▪ Reasons for high frequency of occurrence: EZRA. D. PERIODONTICS o interdental areas are more prone to the accumulation of plaque and more difficult to SAS 17: Trauma from Occlusion clean o the normal flat or even concave faciolingual Adaptive capacity shape of the interdental septum in lower ▪ Periodontium especially the alveolar bone is a highly molars may favor crater formation dynamic tissue in the accommodation of the forces exerted o vascular patterns from the gingiva to center on the crown of the tooth. of the crest may provide a pathway for ▪ This varies in different persons and in the same person at inflammation different times. ▪ It can be diagnosed by transgingival probing ▪ In periodontitis, the primary etiologic factors are the microorganisms (bacterial plaque and their byproducts ▪ The role that occlusion plays in the initiation and progression of disease process is secondary and it is mainly affected by the influence of the following factors of the forces that would be exerted on to the tooth: a. Magnitude or Amount of Force Exerted: ▪ When occlusal forces are increased, periodontium responds w/: o Widening of PDL space o Increase in number and width of PDL 4. Bulbous Bony Contours fibers ▪ Bony enlargement caused by exostoses, adaptation to o Increase in the density of alveolar function or buttressing bone formation (lipping) bone ▪ Frequently found in maxilla than in mandible b. Direction: ▪ Changing the direction of occlusal forces causes a 5. Reversed Architecture reorientation of the stresses and strains within the ▪ Produced by loss of interdental bone, including the facial periodontium and lingual plates without concomitant loss of radicular ▪ Principal fibers of the PDL fibers are arranged so bone, thereby, reversing the normal architecture that they best accommodate occlusal forces along the long axis of the tooth ▪ Lateral (horizontal forces) and torque (rotational)forces are more likely to injure the periodontium c. Duration: ▪ Constant pressure on bone is more injurious than intermittent forces d. Frequency: ▪ The more frequent the application of intermittent 6. Ledges force, the more injurious is the force to the ▪ They are plateau-like bone margins caused by resorption of periodontium thickened bony plates Trauma from occlusion (according to Orban and Glickman et al) ▪ Tissue injury in the periodontium when occlusal forces exceed the adaptive capacity of the periodontal tissues ▪ An occlusion that produces such injury is referred to as traumatic occlusion ▪ The criterion that determines if an occlusion is traumatic is whether it produces periodontal injury, not how the teeth occlude. 5. Furcation Involvements ▪ ▪ Invasion of the bifurcation and trifurcation of multirooted There are different types of traumas from occlusion depending teeth by periodontal diseases on the following factors: ▪ Mandibular molars – most common sites 1. Depending on onset and duration ▪ Maxillary premolars – least common sites a. Acute trauma from occlusion ▪ Diagnosis is made by careful probing with Naber’s probe Results from an abrupt occlusal impact, such as that produced by biting on a hard object. Restorations or prosthetic appliances that interfere with or alter the direction of occlusal forces on the teeth may also induce acute trauma. Results in pain, sensitivity to percussion and increased tooth mobility. If force is dissipated by shift in position of the tooth or by wearing away or correction of restoration, injury heals and the symptoms subside o Otherwise, periodontal injury may worsen and develop into necrosis, abscess formation, or may persist as a symptom-free, chronic condition b. Chronic Trauma from Occlusion More common than the acute form and is of greater clinical significance EZRA. D. PERIODONTICS Often develops from gradual changes in ▪ Pain and spasm in muscles of mastication. occlusion produced by tooth wear, ▪ Food impaction caused by forceful wedging by opposing drifting movement and extrusion of teeth. teeth, combined with parafunctional ▪ TMJ or myofacial pain/dysfunction syndrome. habits such as bruxism and clenching ▪ Looseness of teeth, vague “itching’ and tendency to grind or 2. Depending on the cause initiate parafunction on certasin teeth. a. Due to alterations in the occlusal forces ▪ Thermal hypersensitivity of teeth Primary Occlusal Trauma Radiographic Signs Injury from excessive occlusal force ▪ Alteration in the lamina dura acting on a periodontium that has not Uneven thickening may be associated w/ been altered by disease (healthy tensional forces periodontium) Severe occlusal force may cause a complete Result of excessive occlusal forces loss of lamina dura associated with such factors as ▪ Alteration in the periodontal ligament space. parafunctional habits, high restorations ▪ Widening ma mean increased function or periodontal and removable partial dentures traumatism No attachment loss Widening may be compensatory, especially if Lesion – reversible and can usually be lamina dura is thickened and intact corrected by eliminating the local factors ▪ Root resorption and adjusting the occlusion. ▪ Hypercementosis b. Reduced capacity of the periodontium (In the ▪ Osteosclerosis presence of inflammation ▪ Angular bone loss and bone loss in furcation areas-a vertical Secondary Occlusal Trauma rather than horizontal destruction of the interdental septum. Injury from a normal occlusal force ▪ Root fracture placed on a weakened periodontium Often observed after treatment of advanced cases of chronic destructive periodontitis The greater the loss of periodontal support, the more important the occlusal factors become in the prognosis and treatment of the disease. Combined Periodontal Trauma Injury from an excessive occlusal force on a diseased periodontium In effect, inflammation is present, pocket formation, and excessive occlusal forces exaggerate and or exacerbate the disease process Trauma from occlusion may be a co- destructive factor in combination with the existing active periodontal lesion Resultant lesion is not reversible by occlusal adjustment Current Concepts ▪ Trauma from occlusion in the absence of gingival inflammation does not cause periodontal pocket. ▪ Trauma from occlusion does not affect the loss of the connective tissue attachment. ▪ Teeth move in the direction of occlusal force. ▪ Unilateral trauma may cause bone resorption on the pressure side and bone apposition on the tension ▪ side. ▪ Bone loss may occur on all sides of a tooth or may be extensive enough to cause tooth mobility ▪ Trauma from occlusion, in the presence of inflammation, may contribute to angular bone loss. ▪ Trauma from occlusion may alter the healing response of the periodontium, following treatment. ▪ The less the tooth mobility, the more favorable the postoperative level of periodontal attachment. Clinical Signs ▪ Passive mobility of teeth ▪ Fremitus ▪ Migration of teeth, especially “fanning of anterior teeth” ▪ Unusual wear patterns of teeth (facets) ▪ Hypertonicity of masticatory muscles ▪ Periodontal abscess formation, especially in deep infrabony defects and furcas Symptoms ▪ Soreness on percussion and in function Often associated with new restorations and has a short-term history ▪ In chronic periodontal traumatism, pain may be more vague and generalized EZRA. D. PERIODONTICS 3. Larger and mini larger curettes SAS 18: Periodontal Set of three Instrumentation and their Combines shank design of the standard Gracey 5-6, Principles of Usage 11-12 and 13-14 with a universal blade of 90°. Can be adapted to both the mesial and distal sides of the tooth without changing the instruments. Periodontal instruments – designed for specific purposes like: 4. American Gracey Curettes ▪ Removal of calculus Set of 4 Mini bladed curettes ▪ Smoothening the root surfaces, Length of blade is 50% of that of the conventional ▪ Debriding the soft tissue walls of the periodontal pocket curettes and the blade is slightly curved upward. Parts: a. blade; b. shank; c, handle Sub-0 and number 1-2 are for anterior and premolar 11-12 for posterior mesial surfaces 13-14 for posterior or distal surfaces Sonic and Ultrasonic Instruments Power driven instruments for removing plaque, scaling and curetting and removing stains. Classification of Periodontal Instruments: C. The Periodontal Endoscope A. Diagnostic Instruments: –used to visualize deep pockets and furcations during scaling 1.Periodontal Probe-used to locate, measure and mark pockets and root planing. Types: color-coded; noncolor coded 2.Explorer –used to locate calcular deposits and caries D. Cleansing and Polishing Instruments Examples: Rubber cups, brushes, dental tapes B. Scaling and root planing and Curettage Instruments Air-driven abrasive system (EVA system) ▪ For supragingival scaling; Scalers (sickle, Jacquette scaler, Morse scaler, E. Surgical Instruments cingulum scaler 1. Excisional and incisional instruments: ▪ For subgingival scaling: o Periodontal knives (gingivectomy knives: ex: Kirkland Hoe scaler, chisel and file scalers o Interdental knives ex: Orban knife Curettes o Surgical blades Curettes – instrument of choice for removing deep subgingival o Electrosurgical unit calculus, and altered cementum are used to plane the root 2. Surgical curettes and sickles- for the removal of granulation surfaces by removing altered cementum and also used for tissue scraping the soft tissue wall of the pocket 3. Periosteal elevators –to reflect and move the flap after incision 2 kinds of curette: 4. Surgical chisels and hoes – for bone removal and reshaping a. Universal curette – it can be used in any surface of the 5. Surgical files –smoothen rough bone, ledges tooth 6. Scissors and nippers b. Area-specific curette –site specific, designed and 7. Needle holders angled to adapt to specific anatomic areas of the dentition To use effectively the instruments, it is governed by a number of Gracey 1-2 & 3-4 anterior teeth general principles that are common to all periodontal Gracey 5-6 anterior and premolar instruments. These are the following: Gracey 7-8 posterior teeth-facial & lingual surface Gracey 9-10 posterior teeth facial & lingual surfaces A. Accessibility: Gracey 11-12 posterior teeth mesial surfaces Proper positioning of patient in the dental chair Gracey 13-14 posterior teeth distal surfaces o Accessibility helps in thoroughness of instrumentation. o Position of the patient and operator should provide Recent Additions maximal accessibility to the area of operation. Gracey no. 15-16 (modification of Gracey no. 11-12) – mesial o Decreased accessibility impedes thorough surface of the posterior teeth instrumentation, prematurely tires the operator and Gracey no. 17-18 (modifications of lowers their effectiveness. Gracey no. 13-14) Position of Operator Gracey curettes can be obtained as a single ended, as a set of o Back – straight; Head – erect; Shoulders – relaxed 14 instruments. o Distance from the patients mouth to eyes of clinician: Offset blade i.e., the face of blade is at 60– 70° to the lower 14–16 inches shank o Forearm and thighs – parallel to the floor; This angulation allows the blade to be inserted in the Hip angle should be 90° precise areas for subgingival scaling and root planing. o Weight should be evenly balanced. Recent additions of Gracey curette are 15-16 and 17-18 o Height of the seat – positioned low enough so heels of feet touch the floor Modifications of Gracey Curette o When working from 9 to 12 position of the clock, feet 1. Extended shank curettes should be spread apart so that the legs and the chair Terminal shank – 3mm longer base form tripod which creates a stable position o Allows extension into the deeper periodontal pockets of 5 mm or above) Patient Position 2. Miniblade curettes o Supine position and mouth is close to resting elbow of Hu-Friedy mini five curettes are modifications of after the clinician five curettes o Back of the chair –nearby to floor for maxillary; slightly Size of blades – half the length of the after five or raised for mandible. standard Gracey curette o Patient’s head – even w/ upper edge of the head rest Mini fives are available in all standard Gracey numbers o Mandible – chin down; Maxilla – chin up except for the number 9-10. EZRA. D. PERIODONTICS o Head rest – raised or lowered; patient’s neck and head Angulation are aligned with torso It means the angle between the face of a bladed instrument and the tooth surface. B. Visibility, illumination and retraction. To insert beneath the gingival margin, the face to tooth o Direct vision w/ direct illumination from the dental surface angulation should be at an angle between 0° light should be present. and 40°. o If this is not possible then indirect vision may be For removal of calculus, angulation should be between obtained by using a mouth mirror to reflect light where 45° and 90°. it is needed. o Indirect vision and indirect illumination are often used The exact blade angulation depends on the amount and nature simultaneously. of calculus, the procedure being performed and condition of tissue during scaling or root planing. C. Maintaining of clean field. o Angulation should be greater than 90° for curettage. A clean field can be maintained by: o Adequate suction Lateral pressure o By removing all obstacles in the operating area. It is the pressure created when force is applied against the surface of a tooth with the cutting edge of a bladed D. Sharpening of instrument. (Refer to the Internet) instrument. Exact amount of pressure depends upon the procedure E. Instrument stabilization: Grasp and finger rest. performed. Stability of the instruments and the hand – primary requisites It can be firm, moderate or light. for controlled instrumentation If insufficient lateral pressure is applied, rough ledges or lumps may be shaved to thin, smooth sheets of Stability and control – essential for effective instrumentation and burnished calculus. to avoid injury to the patient or clinician. Careful application of controlled and varied amounts of lateral pressure during instrumentation is an important ▪ The two factors that provide instrument stability are: part of effective scaling and root planing techniques 1. Instrumental grasp 2. Finger rest G. Controlled strokes for scaling and removal of calculus ▪ Instrument Grasp w/out injury to tissues o A proper grasp is important for precise control of Stroke – activated by a pull or a push motion in a vertical, movements made during periodontal instrumentation: oblique or horizontal direction. ▪ There are three types of grasps: 1. Standard pen grasp There are mainly three types of strokes: 2. Modified pen grasp 1. Exploratory stroke – light, feeling stroke 3. Palm and thumb grasp o Probe and explorers ▪ Finger Rest 2. Scaling stroke – short powerful pull stroke o Helps in stabilizing hand and instrument by providing o Bladed instrument for removal of subgingival firm fulcrum, as movements are made to activate and subgingival calculus instruments. 3. Root planing stroke – moderate to light pull stroke o Good finger rest – prevents injury and laceration of o Final smoothening and planing of the roo