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C L I N I C A L D I A G N O S I S O F P E R I O D O N T A L D I S E A S E PRESENTED BY: AKANKSHA GROVER IInd YEAR PG
CONTENTS  Introduction  What is diagnosis?  Categories of periodontal diseases.  The gingival diseases  Various types of periodontitis  Periodontal manifestation of systemic diseases.  First visit  Second visit  Clinical examination  Extra oral  Intra oral  Oral hygiene  Caries  Wasting disease of teeth  Dental Stains  Halitosis  Quality and quantity of saliva  Soft tissue examination
 Examination of periodontium  Introduction  Gingiva  Mucogingival Junction  Width of attached gingiva  Plaque and calculus  Periodontal probing  Furcation  Tooth mobility  TFO  Pathologic tooth migration  Determination of disease activity Variations in soft tissue & Bone  Alveolar bone loss  Palpation  Suppuration  Lab tests  Efficacy of diagnostic tests  Summary
INTRODUCTION • Diagnosis” is the ability and skill of the clinician to detect, recognize, and know the nature of the disease process • DIAGNOSIS: The correct determination, discriminative estimation, and logical appraisal of the conditions found during examination as evidenced by signs and symptoms of health and disease. • WHO Definition: It is the art of chronological organization and critical evaluation of the information obtained of patients’ history, lab investigations, clinical examination so as to identify the disease type and etiology. PRINCIPLES OF DIAGNOSIS: • SPECIFICITY: The ability of a test or observation to clearly differentiate one disease from another. • SENSITIVITY: The ability of a test or observation to detect the disease whenever it is present. • PREDICTIVE VALUE: The probability that the test result (ie. the proportion of true positive results and true negative results combined) agrees with the disease status.
• In general diseases that can afflict the periodontium fall into 3 broad categories. The gingival diseases The various types of periodontitis The periodontal manifestation of systemic diseases
Classified by AAP World Workshop in Clinical Periodontics (1989). • Adult Periodontitis. • Early Onset Periodontitis – -Prepubertal -Juvenile -Rapidly progressive. • Necrotizing Ulcerative Periodontitis. • Refractory Periodontitis.
CLASSIFIED BY AAP INTERNATIONAL WORKSHOP FOR PERIODONTAL DISEASES (1999).
CLASSIFICATION OF GINGIVAL DISEASES PLAQUE INDUCED GINGIVAL LESIONS 1. Gingivitis associated with dental plaque only 2. Gingival diseases modified by systemic factors Associated with endocrine system Associated with blood dyscrasias 3. Gingival diseases modified by medications 4. Gingival diseases modified by malnutrition
CLASSIFICATION OF GINGIVAL DISEASES NON-PLAQUE INDUCED GINGIVAL LESIONS 1. Gingival diseases of specific bacterial origin 2. Gingival diseases of viral origin 3. Gingival diseases of fungal origin 4. Gingival diseases of genetic origin 5. Gingival manifestations of systemic conditions 6. Traumatic lesions 7. Foreign body reactions
CLASSIFICATION OF PERIODONTITIS • 1. Chronic Periodontitis* – Localized – Generalized • 2. Aggressive Periodontitis – Localized – Generalized • 3. Periodontitis Associated with Systemic Diseases • 4. Necrotizing Periodontal Diseases • 5. Abscesses of the Periodontium • 6. Periodontal Diseases associated with Endodontic Lesions • 7. Developmental or Acquired Deformities and Conditions • *Can be further classified on basis of extent and severity
PROPER DIAGNOSIS -BASIS • Proper evaluation of history of the disease process • Signs & symptoms present • Laboratory data • Special tests & radiographs • The value of establishing a diagnosis is to provide a logical basis for treatment & prognosis
• Periodontal diagnosis should first determine whether disease is present, then identify its type, extent, distribution & severity and finally provide an understanding of the underlying pathologic process and its cause.
RECOMMENDED SEQUENCE FOR DIAGNOSIS 1ST VISIT - OVERALL APPRAISAL OF PATIENT - MEDICAL HISTORY - DENTAL HISTORY - INTRAORAL R/G SURVEY - CASTS - CLINICAL PHOTOGRAPHS - REVIEW OF INITIAL EXAMINATION
FIRST VISIT: OVERALL APPRAISAL OF THE PATIENT: • Consideration of the patients mental and emotional status • Temperament • Attitude • Physiologic age
Observation of patient’s general health and appearance Commences when the patient enters the dental office • Body weight: recent weight loss may indicate serious underlying pathology e.g. cancer Excessive weight may suggest risk of heart attack or stroke, type 2 diabetes mellitus • Awkward gait: degenerative joint disease, a nervous system disorder such as multiple sclerosis • Complexion: pallor with anemia, yellow with jaundice • Breathlessness with minor exertion may indicate cardiac or lung disease
PERSONAL INFORMATION NAME-  Full name includes pt’s name, father’s or husband’s name and surname  For - Record Communication Certification. AGE-  Recorded in years  In case of periodontal disease helps in diagnosis of puberty gingivitis, ANUG, Prepubertal periodontitis, Juvenile periodontitis and Adult periodontitis. SEX  Hormonal disturbances during puberty, menstrual period & pregnancy modifies tissue response to local irritation in females.  Certain systemic conditions also seen with significant sex difference( e.g. hemophilia in male)also affects overall condition.
RESIDENCE-  This should be noted in details mentioning the house number,street, society, city or village, pincode and district. Previous visit or residency also noted.  Due to high fluoride content in water fluorosis is more common in certain regions.  Also gives information about convenience of patient for recall visits. OCCUPATION-  Both the present and past occupations should be noted.  Erosion is commonly seen in persons associated with acid fume works  Some occupational habits (e.g. holding nails by anterior teeth in carpenters, shoe makers and tailors.) causes notching of incisal edges of maxillary incisors.
HISTORY OF PERIODONTAL PATIENTS • The history of the patient is a revealing document as a basis for comprehensive treatment planning and understanding of the patient’s needs, social and economic situation, as well as general medical conditions. • The assessment of the patient’s history required an evaluation of the following six aspects: – Chief complaint – Social and family history – Dental history – Oral hygiene habits – Smoking history – Medical history and medications
CHIEF COMPLAINT The presenting problem of the patient Has to be recorded in the patients own words Obtained by asking the patient to describe the problem for which help is being sought or reason for visit It is essential to realise the patient’s needs and desires for treatment. If a patient has been referred for specific treatment, the extent of the desired treatment has to be defined and the referring dentist should be informed of the intentions for treatment.
• Patients reporting independently, however, usually have specific desires and expectations regarding treatment outcomes. • These may not be congruent with the true assessment of a professional with respect to the clinical situation. • Optimal treatment results may only be achieved if the patient’s demands are in balance with the objective evaluation of the disease and the projected treatment outcomes. Therefore, the patient’s expectations have to be taken seriously and must be incorporated in the evaluation in harmony with the clinical situation.
History of the present illness: Elaboration of the chief complaint In case of pain:  Mode of onset  Duration  Type of pain  Radiation or localization of the pain  Severity  Aggravating and relieving factors  Whether the patient has taken any medication or has consulted a doctor
In case of lesion: When was the lesion first observed Mode of development Symptoms Previous treatment Bleeding gums: Time of onset Spontaneous/ on brushing/ while eating Duration of bleeding Manner of stopping
• In case of mobility – History of trauma – Time duration – Pain – Pre treatment • In case of Recession – Time duration – Tooth brushing – hypesensitivity
• In case of Hypersensitivity – On cold or hot stimulus – Timing – Generalized or localized • In case of Food Impaction – Area – Use tooth pick or pin-area of use – On eating what food items
• In case of Supperation – Time duration – Swelling – Pain • In case of Bad Breath – Time duration – Timing – Association with burps
MEDICAL HISTORY(Armitage ,2004) • Most of the medical history is obtained at the first visit. Health history can be obtained verbally by the questioning of the patient. • Importance of medical history should be explained to the patient. • Medical history will aid the clinician in diagnosis of oral manifestations of systemic disease, detection of systemic conditions that may be affecting the periodontal tissue response to local factors that require special precautions and or modifications in treatment procedures.
Medical history should include reference to the following  Whether the patient is under the care of a physician. Name,address, telephone no. of the physician should be recorded.  Hospitalization and operations: Kind of operation, untoward effects such as anesthesia, hemorrhagic, infectious complications.  All medications being taken : Special inequity should be made regarding the dosage and duration of therapy with anticoagulant and cortico steroids.  History of all medical problems :Cardiovascular,hematologic, endocrine etc. Infectious diseases, sexually transmitted diseases, AIDS.  Possibility of occupational disease
Medical history should include reference to the following • Abnormal bleeding tendencies : Nose bleeds, prolonged bleeding from minor cuts, spontaneous echymosis, tendency towards excessive bruxism, excessive menstrual bleeding. • History of allergy including : Hay fever, asthma, sensitivity of foods, sensitivity to drugs - Aspirin, Codeine, Barbiturates, Sulfonamides, Antibiotics, Procaine, Laxatives. Sensitivity to dental materials – Eugenol /Acrylic resin. • Information regarding the onset of puberty : Menopause, menstrual disorders, hysterectomy, pregnancies, miscarriages. • Family medical history, including bleeding disorders and diabetes.
• Relevant dental history A list of dental visits, recent visit, nature of treatment and oral prophylaxis or cleaning by a dentist or hygienist including frequency & date of most recent cleaning. • Patient’s oral hygiene regimen – Toothbrushing frequency. – Method of brushing. – Time of day. – Type of toothbrush or datun – – Type of dentifrice – Interval at which brushes are replaced. – Other aids.
• Previous tooth loss due to caries or periodontal lesion may change the treatment plan. • Any orthodontic treatment including duration and approximate date of termination. • Pain -Whether in teeth or gum -Manner by which provoked -Manner in which relieved -Nature and duration.
Bleeding gums- • Since what time • Spontaneously, on brushing or eating. • At night or with regular periodicity whether associated with menstrual period or other specific factors • Duration of bleeding • Manner in which it is stopped. Bad taste and areas of food impaction. Tooth mobility-If teeth feel loose or insecure -Difficulty in chewing
• Habits -grinding or clenching during day or night -Unilateral chewing -Mouth breathing -Tobacco smoking or chewing -Nail biting or foreign objects. • Previous periodontal problems -Nature & condition -If treated, type of treatment and approximate period of termination of treatment. -In the patient’s opinion present problem is recurrence of previous disease.
FAMILY HISTORY History of any hereditary linked problems Diabetes Hemophilia Hypertension Is taken to determine if there is a familial predisposition to disease or if there are diseases in which inheritance is an important factor. e.g. diabetes mellitus. A patient with a strong history of diabetes mellitus and no apparent signs or symptoms should be evaluated periodically since clinical features may appear later in life.
PERSONAL HISTORY • May assist in determining the patient’s response to the demands and conflicts of modern society. It explains the untoward incidence of patients to health problems and to therapeutic recommendations. DIET SMOKING/ TOBACCO USE: • Cigarette smoking has been documented to be the second most important risk factor after inadequate plaque control (Kinane et al, 2006) in the etiology and pathogenesis of periodontal disease. DRUG USE BRUSHING HABITS PARAFUNCTIONAL HABITS
EXAMINATION OF THE PATIENT 1. Observation of patient’s general health and appearance 2. Extraoral examination 3. Intraoral examination
EXTRAORAL EXAMINATION Is carried out using the principles of inspection, palpation. Thus it includes: 1. Head, face and neck • Swelling • Space infection 2. Eyes, nose • Icterus ,pallor 3. Skin • Skin allergy or infection 4. Lips • Angular chielitis • Infection-Herpes labialis STRESS STRESS
1. Lymph nodes • Palpable-infection,malignancy 2. TMJ • Dislocation,clicking 3. Salivary glands • Tumour,genetic disease,sialolithiasis 4. Nails • Clubbing,infection 5. Masticatory apparatus • Hypertrophy of muscles
RADIOGRAPHIC EVALUATION •Radiographs are an indispensable aid in identifying the presence of pathogenesis and the conditions that affect the prognosis and treatment of periodontal diseases. •Proper angulation of the film and of the head of the x-ray machine minimizes distortion. •For periodontal purposes, it is useful to position bite-wing radiographs vertically so that both maxillary and mandibular bone crests are visible. •Individual periapical radiographs are superior in detail to panoramic radiographs and preferred for a more accurate analysis.
THE RADIOGRAPH IS A VALUABLE AID IN THE: 1. Diagnosis of periodontal disease. 2. Determination of prognosis. 3. Evaluation of the outcome of treatment Radiograph is only an adjunct to the clinical examination, not a substitute for it.
INTRAORAL RADIOGRAPHIC SURVEY -Minimum of 14 intraoral films and 4 posterior bitewing films. -Panaromic radiographs more convenient. -Provides information of distribution and severity of bone destruction in periodontal disease.
EXTRAORAL RADIOGRAPHY •Panoramic radiography •Digital radiography •Digital subtraction radiography (DSR) •Tuned aperture tomography (TACT) •Computed tomography (CT)
CASTS Casts from dental impressions are extremely useful adjuncts in the oral examination. Casts indicate : • the position of the gingival margins and • the position and the inclination of the teeth, • proximal contact relationships and • food impaction areas. • Developmental deformities in teeth • lingual-cuspal relationships
• visual aids in discussions with the patient • pre-treatment and post-treatment comparisons. • Reference at checkup visits • Wear facets • Plunger cusp • Vestibular depth • Implants-Bucco-lingual width
CLINICAL PHOTOGRAPH • Not essential but useful for recording before and after treatment tissue appearance • Can not always be relied on for comparing color changes in gingiva but they depict gingival morphologic changes • Record keeping for mucogingival problems like – Areas of gingival recession – Frenum involvment – Papilla loss
REVIEW OF INITIAL EXAMINATION • If no emergency care is required the patient is dismissed and instructed when to report for 2nd visit. • Before second visit, a correlated examination is made of the radiographs and casts to relate the radiographic changes to unfavorable condition represented on the casts. • Casts should be checked for-Abnormal wear -Plunger cusps or ridges -Malposed teeth -Cross bite. • Such areas are marked for future reference. • The radiographs and casts are valuable diagnostic aids. However, clinical findings constitute the basis for diagnosis.
SECOND VISIT Clinical examination Intra oral Oral hygiene • The cleanliness of the oral cavity is appraised in term of the extent of  Accumulated food debris  Materia alba  Tooth surface stains  Plaque - detected well by disclosing solutions. - Quality rather than quantity decides - severity of periodontal destruction
EXAMINATION OF TEETH –should note for  caries  developmental defects  wasting diseases of teeth  proximal contact relationship
WASTING DISEASE OF THE TEETH • Loss of tooth structure may occur through noncarious processes. Regressive alterations may vary in etiology, extent and clinical presentation among individuals and may be associated with physiologic or pathologic processes. • Traditionally, those entities have been classified as attrition, erosion, and abrasion . Attrition is defined as the physiologic loss of tooth structure as a result of the masticatory processes. • Erosion is the chemical dissolution of structure that does not involve the carious process; and Abrasion is the mechanical wearing away of structure.
FORMS OF WASTING ARE Erosion : •Tooth surface loss caused by chemical or electrochemical action is termed 'corrosion.' (John O,2004) •Cupping of occlusal surfaces(incisal grooving)with dentin exposure •Broad concavities with smooth surface enamel , Increased incisal translucency •Sources of Erosion 1) Endogenous sources of Erosion 2) Exogenous sources of Erosion
Endogenous sources of Erosion Bulimia produces a unique pattern of enamel loss. The corrosion, called perimolysis, is most marked on the palatal surfaces of maxillary anterior teeth and, in more severe cases, on the buccal surfaces of posterior teeth. This pattern is consistent with the head's position while vomiting. The forcefully directed movement of the vomitus, which has a mean pH of 3.8, determines the site and extent of dental Erosion
Exogenous sources of Erosion. It has been reported that any food substance with a critical pH value of less than 5.5 can become a eroded and demineralize teeth. This may occur as a result of consuming and/or mulling highly acidic foods and beverages such as mangoes and other citrus fruits, drinking carbonated soft drinks and sucking sour candies.
ABRASION : • The pathological wearing away of tooth structure resulting from direct frictional forces between the tooth and the external objects or from frictional forces between contacting teeth components in the presence of an abrasive medium. • Forms of dental abrasion may be related to habit or occupation. • Tooth brushing is the most common cause.(Kitchen PC,1941) • Notching of incisal edges may be caused by pipe smoking, nut and seed cracking, nail biting, and hairpin biting. • The appearance is commonly described as saucer shaped or wedge shaped indentations with a smooth and shiny surface • If teeth are worn on their occlusal surfaces, incisal surfaces or both by friction from the food bolus,this wear is termed “masticatory abrasion”(John O,2004) • The teeth most commonly affected are premolars and canines.
ATTRITION : • The physiological wearing away of the tooth structure as a result of tooth to tooth contact as in mastication of abrasive foods or Para functional activity such as bruxism. • This is an age-related process that can occur at the incisal or occlusal surfaces and sometimes on the proximal surfaces. • Clinically, the first manifestation is the appearance of a small polished facet on a cusp tip or ridge or an incisal edge. • Shiny ,smooth and curviplanar facets.In severe attrition- cuneiform occlusal surface. • Occlusal and incisal attrition can occur during deglutition and clenching; (Kydd WL,1957) • Proximal attrition (which occurs at contact areas) can cause a reduction of the dental arch(Murphy TR,1964) • Severe attrition may lead to dentinal exposure, which may increase the rate of wear.
ABFRACTION : • Abfraction is the microstructural loss of tooth substance in areas of stress concentration.(Grippo JO,2004) • This occurs most commonly in the cervical region of teeth, where flexure may lead to a breaking away of the extremely thin layer of enamel rods, as well as microfracture of cementum and dentin. • These lesions, which appear to result from occlusal loading forces, frequently have a crescent form along the cervical line, where this brittle and fragile enamel layer exists. (Lee WC,1984) • This is believed to cause V-shaped depressions on the side under tension and C-shaped depressions on the side under compression. • Mechanical microcracks on cementum and dentin may act as the initial contributor to the formation of cervical defects. • Abfraction has a possibility of being the initial factor and the dominant progressive modifying factor in producing cervical lesions. CERVICAL ABFRACTION ON THE MANDIBULAR LEFT INCISOR
ABRASION EROSION ABFRACTION The pathological wearing away of tooth structure resulting from direct frictional forces between the tooth and the external objects or from frictional forces between contacting teeth components in the presence of an abrasive medium. The loss of tooth structure by a chemical dissolution without the involvement known of bacteria (corrosion or physico-chemical wear). Abfraction is the microstructural loss of tooth substance in areas of stress concentration. CAUSE-faulty tooth brushing with highly abrasive tooth pastes CAUSE-Acidic beverages,GERD CAUSE-cervical tensile stress under cuspal loading. Loss of enamel can lead to exposed dentin •Wedge shaped ditch Usually located at the cervical areas of the teeth. The exposed dentin appears highly polished. •Lesions are more wide than deep •Cupping of occlusal surfaces(incisal grooving )with dentin exposure •Broad concavities with smooth surface enamel •Increased incisal translucency •Wear on non occluding surfaces •Loss of surface characteristics of enamel in young children •Deep, narrow V shaped notch Premolars and cuspids Palatal surface of upper anteriors single teeth with eccentric occlusal loads
CAUSE OF DENTAL STAINS • Oral cavity is subjected to many exogenous and endogenous substances that stains the teeth. • Also the oral flora contains many type of chromogenic deposits which also causes stain deposit. • Intrinsic stains are seen in porphyria, erythroblastosis fetalis and tetracycline therapy. DENTAL STAINS : •Pigmented deposits on the teeth. Carefully examined to determine their origin.
Types of dental stains & Physical characteristics • Extrinsic stains:(Harris, 1991). Discoloration include brown, black, gray, green, orange, and yellow. The scratch test is usually used to distinguish between extrinsic and intrinsic discoloration. • Intrinsic stains: (Shafer et al, 1983) Discoloration colours include brown, black, gray, green, orange, and yellow. Unlike extrinsic discoloration, teeth with intrinsic discoloration may be red or pink. Under ultraviolet light, teeth with tetracycline staining and congenital porphyria may fluoresce yellow or red, respectively. Intrinsic discoloration cannot be removed by using the scratch test.
EXTRINSIC STAINS Predisposing factors • Certain factors predispose children and adults to extrinsic stains, include – enamel defects - accumulation of stain-producing food, beverages, tobacco, and other topical agents. – salivary dysfunction- decreased removal of food debris and dental plaque from the outer and interproximal tooth surfaces, – poor oral hygiene. • Deposition of tannins found in tea, coffee cause brown stains . • Tobacco stains -dark brown and black stains • Pan chewing - red-black stain on the teeth, gingiva, and oral mucosal surfaces. • Metallic compounds -Industrial exposure to iron, manganese, and silver –black stain. Mercury and lead dust - blue-green stain.(Gaffar et al., 1977).
Contd… • Chromogenic bacteria cause stains, typically at the gingival margin of the tooth. – black stain caused by Actinomyces species. – Green stains are attributed to fluorescent bacteria and fungi such as Penicillium and Aspergillus species. – Orange stain is caused by chromogenic bacteria such as Flavobacterium lutescens. • Topical medications cause staining. – Chlorhexidine rinse causes brown staining after several weeks of use (Solheim et al, 1980), – Iron-containing oral solutions used for treatment of iron deficiency anaemia cause black stains. – Potassium permanganate mouthwash (violet-black stain), – silver nitrate (black stain), – stannous fluoride (brown stain) – systemic medications (e.g. minocycline, doxycycline) can also cause extrinsic staining.
Red extrinsic stain at gingival margin and interproximal and incisal region-habit of chewing pan. Sever tobacco stain
Causes of intrinsic dental stains • Numerous causes for intrinsic tooth discoloration exist. • Stain distribution varies from localized (e.g. 1 or 2 teeth) to a regional or generalized involvement of primary and secondary teeth. • Following are some of the causes of intrinsic stains. • Dental restoration (Feinman et al., 1987) • Amalgam restorations can generate corrosion products leaving a gray-black colour in the tooth • Composites, and glass ionomer and acrylic restorations gradually can leave a gray hue in the tooth adjacent to the material. • Other dental materials that cause intrinsic discoloration include eugenol, root canal sealers, and polyantimicrobial pastes. – The erosion of enamel can lead to a yellow tooth discoloration. – Caries
– Trauma can cause intrapulpal hemorrhagic and iron sulfide deposition along the dentinal tubules, producing a bluish black cast. – Periapical odontogenic infections, maternal rubella or cytomegalovirus infection and toxaemia of pregnancy and Systemic postnatal infections (e.g. measles, chicken pox, streptococcal infections, scarlet fever) can also cause enamel hypoplasia – MEDICATION- (McEvoy, 1989a) • Tetracyclin-When the affected teeth first erupt, they have a bright-yellow band like appearance that fluoresces under ultraviolet light, although upon exposure to sunlight, the color gradually changes to gray or brown • Minocyclin- a green-gray or blue-gray colour • Doxycycline – Flourosis – Genetic defects in enamel or dentin formation include amelogenesis imperfecta , dentinogenesis imperfecta , and dentinal dysplasia . (Shafer et al., 1983)
Intrinsic dental discoloration caused by trauma to the mandibular incisors that led to pulpal necrosis. Tetracycline staining of mandibular teeth caused by the ingestion of tetracycline when the patient was aged 3 years. Severe fluorosis of the teeth.
HYPERSENSITIVITY : DIAGNOSIS- Root surfaces exposed by gingival recession may be hypersensitive to thermal changes/tactile stimulation located by gentle exploration with a probe/cold air. EVALUATION •MECHANICAL STIMULATION •CHEMICAL(ELECTRICAL) STIMULATION •DEHYDRATING(EVAPORATIVE) STIMULI •THERMAL STIMULATION
OBJECTIVE EVALUATION  MECHANICAL STIMULATION-(Tactile stimuli) Pader M 1998 • Sharp Dental explorer or Yeaple probe is used to identify regions of sensitive dentin. • Subjects will then evaluate their level of tactile sensitivity using a Verbal Rating Scale (VRS). 0 - no discomfort 1 - mild discomfort 2 - marked discomfort 3 - marked discomfort that lasted more than 10 sec DEHYDRATING(EVAPORATIVE) STIMULI(Kleinberg et al,1990) • Evaporation of fluids from dentin is seen when relatively dry air is directed at a tooth. The time is within a second. The direction of air blast should be 90 degrees to dentin.
CHEMICAL(OSMOTIC) STIMULATION • This requires the use of very HYPERTONIC solution to induce enough fluid movement to cause pain. • A cotton pellet saturated with the solution(Sucrose or Calcium chloride) is placed on the suspected area. ELECTRICAL STIMULATION • Directly stimulates pulpal nerves. • Evaluates only the presence or absence of pulp vitality. THERMAL STIMULATION • In using cold water, each tooth is isolated with a rubber dam and then water at known temperature is slowly flowed on exposed dentin surfaces for a maximum of 3 sec.
FOOD IMPACTION • FOOD IMPACTION-Forceful wedging of food into the periodontium by occlusal forces • CAUSE(Hirschfeld,1930) – Uneven occlusal wear – Light or open proximal contact – Extrusion – Congenital morphologic abnormalities – Faulty restorations – Excessive anterior open bite – Plunger cusp • PLUNGER CUSP-Cusps that tend to wedge food forcibly into interproximal embrasures – As teeth wear down ,their originally convex proximal surfaces become flattened and wedging effect of the opposing cusp is exagerrated – Missing teeth are not replaced and the relationship between proximal contacts of adjacent teeth is altered
PROXIMAL CONTACT RELATIONS: •Slightly open contacts - permit food impaction. •Tightness of contacts - Checked by means of clinical observation & with Dentalfloss •Abnormal contact relationships may also initiate occlusal changes.Such as: Shift in the median line between incisors. Labial version of the maxillary canine Buccal/lingual displacement of the posterior teeth Uneven relationship of the marginal ridges
OPEN BITE RELATIONSHIPS(Hirschfeld,1930)  Abnormal vertical spaces exist between the maxillary and mandibular teeth.  Accumulation debris, calculus formation,  Mechanical cleansing by the passage of the food.  Most often occurs in anterior region. Posterior open bite is occasionally seen.  Mouth breathing habit-marginal & papillary gingivitis- maxillary anterior region  No effect on prevalence or extent of gingivitis except when large amounts of calculus is present  Crowding of teeth aggravates (Alexander A,1970)
• Most frequently in the anterior region may cause . Impingement of the teeth on the gingiva, food Impacation. • Attachment loss ,gingival inflammation, gingival enlargement and pocket formation. • Food impaction on the lingual surface of maxillary anterior teeth and facial surface of opposing mandibular teeth Excessive Overbite :(Hirschfeld,1930)
CROSSBITE : Normal relationship of the mandibular teeth to the maxillary teeth is reversed. Maxillary teeth being lingual to the mandibular teeth. Crossbite may be unilateral/bilateral. Leads to: TFO, Food impaction, Flaring of the mandibular teeth, associated gingival and periodontal disturbances. Check for Functional Occlusal Relationships : Important part of the diagnostic procedure. Dentitions that appear normal when the jaws are closed may present marked functional abnormalities.
MOUTH ODORS INTRODUCTION • Also termed as fetor exore, fetor oris and oral malodor, bad breath. • Common complain of adult population .Prevalence may be as high as 50%, in most cases originate from oral cavity. • In many studies but not all, periodontal disease related parameters have been found to be associated with bad breath levels. • DEFINITION – “It is foul or offensive odor emanating from the oral cavity.” – First described by howe in 1874.
ETIOLOGY MULTIFACTORIAL ETIOLOGY 1. Local factors of pathologic origin  -Poor oral hygiene  -Extensive caries  -Gingivitis and Periodontitis  -Open contact which allows food impaction -Vincent’s disease -Hairy or coated fissured tongue -Dry socket  -Necrotic tissue from ulceration  -Cyst with fistula draining in oral cavity • 2. Local factors of non pathologic origin  In the morning due to lack of cheek and tongue movement,(Collins,1987)  Smoking.  Denture traps food debris and causes denture breath.
EXTRAORAL SOURCES OF MOUTH ODOUR  ENT(Rosenberg,1996)  Bronchial and lung(Lorber,1975)  Gastro intestinal tract (Norfleet,1993)  Liver-liver insufficiency(cirrhosis)-sweetish amine odour(Chen S,1970)  Alcoholics- Alcoholic breath  Systemic metabolic disease-Diabetes- Acetone odor  Kidney dysfunction- Ureamic breath  Halitosis due to xerostomia (Kleinberg,1995)  Hormonal –increase in progestrone level during menstrual cycle  Medications-metronidazole, antineoplastic agents ,diuretics,etc  Eucalyptus containing medication  Arsenic smells of rotten eggs
PATHOGENESIS • The most common cause of mouth odor is being local causes. • Sulphur compounds such as indole & volatile sulfur compounds hydrogen sulphide, methylmercapten and dimethyl sulphide (Tonzetich,1977)
Diagnosis of halitosis through  Medical history  Clinical / laboratory examination  Self examination  Organoleptic Rating  Specific character of breath odor  Portable volatile sulfide monitor  Gas chromatography  field or phase contrast microscopy  Saliva incubation test  Electronic nose
SALIVARY GLANDS • These are exocrine glands that are responsible for the secretion of saliva • The salivary glands are categorized as major and minor • The major salivary glands are the parotid, submandibular and sublingual glands • Minor glands that produce saliva are located in the lower lip, tongue, palate, cheeks and pharynx
• The major salivary glands contribute to maximum saliva production. The average daily flow of saliva is between 1 to 1.5 liters in healthy individuals. Percentage contribution from different salivary glands are as follows: • Parotid gland: 20% • Submandibular:65% • Sublingual: 7 to 8% • Minor salivary glands: 10% These percentages are described for unstimulated whole saliva. Stimulated high flow rates change the percentage contribution from different salivary glands with the maximum from parotid gland:50%(serous)
SALIVA FLOW • There is a great variability in salivary flow rates in different persons • The accepted flow rate of unstimulated saliva is anything above.1 ml per minute. For stimulated saliva, the accepted norm is .2 ml per minute. Salivary flow is highly individualized and should be recorded. • On an average, the flow rate for unstimulated saliva is .3 ml per minute. With the average total of 16 hours of unstimulated flow being 300 ml. (Fox et al,1987) • Stimulated flow of saliva is 7 ml per minute on an average. Stimulated saliva is supposed to contribute as much as 80 to 90 % of the daily secretion.(Daniel et al,1984)
Quality and quantity of saliva Protective and maintain oral soft tissue in a physiologic state •Plaque is mechanically cleansed by saliva from oral surfaces. •By buffering acids produced by bacteria. •Controlling bacterial activity. Antibacterial factors Salivary antibodies • Preponderant Ig A. (secretary) • Lesser amount Ig G and Ig M. Salivary secretion decreases in certain conditions causing xerostomia Salivary secretion increases whenever local irritation in oral cavity & in certain gingival disease states
QUANTITY OF SALIVA Physiological Causes • In the same individual, salivary flow has a circadian rhythm • Salivary flow is minimum to zero in the night and peaks during the day • In the year low salivary flow rates occur in summer and peak in winter • In the mouth, there are areas with high and low flow. The mandibular lingual areas have high flow while maxillary anteriors have a low flow rate Pathological Changes Xerostomia(Fox et al,1987) • Medications - – Antihypertensives, antidepressants, analgesics, tranquilizers, diuretics and antihistamines – Cancer Therapy - Chemotherapeutic drugs can change the flow and composition of the saliva. – Radiation treatment that is focused on or near the salivary gland • Sjogren's syndrome - An autoimmune disease, • Other conditions -such as bone marrow transplants, endocrine disorders, stress, anxiety, depression, and nutritional deficiencies may cause xerostomia. • Nerve Damage - Trauma to the head and neck area from surgery or wounds can damage the nerves that supply sensation to the mouth.
Ptyalism • Medications – central nervous system depressants such as barbiturates, anticholinergics such as belladonna alkaloid. (Van Dinter MC,1991) • During pregnancy • Oral infections-abscesses,Respiratory diseases,gastrointestinal,cardiovascular causes • Neoplasia • Pain
Quality of Saliva • Systemic Diseases(hereditary, autoimmune, malignancy, and infectious) – congenital adrenal hyperplasia – Cystic fibrosis – Sjögren's syndrome • Viral diseases – Herpes virus,HIV,CMV,EB virus • Medications – Antipyrine – Caffeine – Carbamazepine
• patient’s response to a health questionnaire and the outcome of clinical evaluation as the basis for identification and assessment of dry mouth. For example, “yes” responses to the following four questions have been significantly associated with salivary gland hypofunction: – Does the amount of saliva in your mouth seem too little? – Does your mouth feel dry when eating a meal? – Do you have difficulty swallowing any food? – Do you sip liquids to aid in swallowing dry food?(Fox PC,1987) • Visual Analogue scale, an ordinal scale based on rank-ordered categories (for example, I have no/slight/severe/ annoying feeling of dry mouth) or both to assess salivary gland function. • Objective measurements of qualitative or quantitative changesin saliva are best captured by collecting saliva from individual glands or from all that contribute to whole saliva. (avazesh M, 1982) • Commonlyused stimulants include – gum base, paraffin wax, rubber bandsand citric acid. Secretagogues such as pilocarpine and cevimeline hydrochloride ( Chambers MS, 2007) – mechanical stimuli such as a transcutaneous electrical nerve stimulator and powered toothbrushes have been used to stimulate salivary flow. (Hargitai IA,2005) DIAGNOSIS
SOFT TISSUE EXAMINATION • Floor of mouth • Oropharyngeal region • Tongue • Lips
• Soft tissue should be examined for o -Keratotic or nonkeratotic white lesions o -Ulcerative lesions o -Vesiculobullous lesions o -Precancerous lesions Particularly in case of desquamative gingivitis, oral soft tissue examination is very important.
PLAQUE AND CALCULUS : • Many methods for assessing plaque and calculus accumulation. • Supragingival plaque and calculus  Directly observed  amount measured with a calibrated probe. • Sub gingival calculus :  Each tooth surface is carefully checked to the level of the gingival attachment with a sharp explorer no. #17or #3A explorer.  For Visualization of the Calculus : • Warm air may be used to deflect the gingiva
EXAMINATION OF PERIODONTIUM GINGIVA • Color • Generally described as coral pink, produced by • Vascular supply • Thickness and degree of keratinization • Presence of pigment containing cells(Dummett,1946)
Systemic diseases Addison’s Disease
CONTOUR AND FORM • Is related to teeth, underlying bone and presence or absence of disease. • Normal gingiva: tissue fills interdental space and gingival margin ends in a knife like edge coronal to CEJ and interdental papilla are tucked beneath contact points. • Depends on -Shape of teeth. -Alignment in the arch. -Location & size of the area of proximal contact. -Dimensions of facial & lingual embrasures. -Caries • The marginal gingiva follows scalloped outline on the facial and lingual surfaces. • Gingival contour changes with gingival enlargement such changes may also occur in other conditions. e.g. Stillman’s cleft ,Mc call’s festoons.
• Marginal gingiva in diastema-Flat or saddle shaped • In disease- • Marginal gingiva-Rounded or rolled out • IDP- – Bulbous – Flattened – Blunted – Cratered
• STILMAN’S CLEFT(Stilman PR,1921) – Apostrophe shaped indentations exteding from and into gingival margin for varying distance – Triangular shaped gingival recession-Common on the facial surface – Cause-occlusal trauma • Clefts are divided into – Simple Clefts – Compound clefts • MCCALL’S FESTOONS – Liver shaped enlargements of the marginal gingiva – Canines and premolar
CONSISTENCY • It is firm and resilient with the exception of the movable free margin,tightly bound to underlying bone. • In chronic gingivitis it may be destructive with edematous soft consistency and reparative with fibrotic changes. • In case of acute gingivitis diffuse puffiness, softening, eroded surface and vesicle formation can be seen. • .
DIAGNOSIS • DIAGNOSIS-Gently pressure ongingiva with the side of the periodontal probe. – Soft & edematous- Pits on pressure – Fibrotic,Firm & leathery- No imprint left on gingiva
SIZE • Sum total of bulk of cellular & intercellular elements and their vascular supply. • Alteration in size is a common feature of gingival disease.
ACUTE GINGIVAL DISEASES CHRONIC GINGIVAL DISEASES DIGO Gingival abscess-marginal gingiva or IDP Slight ballooning of IDP & marginal gingiva then to attached gingiva Bead like enlargement of IDP extending to facial and lingual margins Periodontal abscess- involves supportive periodontal tissues with gingiva Gingival abscess DIAGNOSIS
SURFACE TEXTURE • Stipples are small regularly spaced depressions in the surface of the attached gingiva that give it an ‘orange peel’ appearance.(owings ,1969, orbans, 1948). • The absence of stippling is not a sign of disease, and conversely its presence is not necessarily a sign of gingival health.(greene,1962.) • Best viewed by drying the gingiva • Attached gingiva and center of interdental papilla is stippled. • Microscopically produced by alternate rounded protuberances and depressions in the gingival surface. The papillary layer of connective tissue projects into the elevations and the elevated & depressed areas covered by epithelium.
DIAGNOSIS - Best viewed by drying the gingiva Healthy gingiva- small regularly spaced depressions in the surface of the attached gingiva that give it an ‘orange peel’ appearance PHYSIOLOGIC • Stippling varies with age. Absent in infancy, appears in some children at about 5 years of age, • Increases until adulthood and • Begins to disappear in old age. PATHOLOGIC • Loss of surface stippling is an early sign of gingivitis. • In chronic inflammation -the surface is either smooth & shiny or firm & nodular, depending on whether the dominant changes are exudative or fibrotic. • In atrophic gingivitis- gingival atrophy is seen • In desquamative gingivitis- peeling of surface • Drug induced gingival overgrowth- nodular surface and leathery
Magnified model of the outer surface of the oral epithelium of the attached gingiva. The surface exhibits minute depressions. Subsurface of epithelium characterised by the presence of ridges.
POSITION • Refers to the level at which the gingival margin attached to the tooth. when the tooth errupts in the oral cavity the margin and the sulcus are at the tip of the crown, as the erruption progresses, they are seen closer to the tooth. • The position of the gingiva on the surface of the tooth changes with time. • When the tooth first reaches the plane of occlusion one third to the one fourth of the enamel still remains covered by the gingiva. • Actual position is the level of epithelial attachment on the tooth. • Apparent position is the level of the crest of the gingival margin. • Visible gingival recession- clinically observed • Hidden recession- detected by periodontal probes
Tooth in occlusion
Gingival recession Gingival recession is the exposure of the root surface by an apical shift in the position of the gingiva. •Recession is often of major concern to patients since it is a readily visible manifestation of periodontal damage and can cause esthetic problems when it occurs around anterior teeth. •Indeed, many patients have a chief complaint of ‘receeding gums’. Therefore, at the initial examination it is important to record the amount and location of gingival recession.
Etiology: • Anatomy of the buccal plate of alveolar bone. • Periodontal disease • Frenum pulls • Overzealous tooth brushing • Dentifrice Abrasivity • Non surgical procedures (Root planing) and surgical periodontal Procedures • Orthodontic movement of teeth or roots outside the alveolar housing • Root prominence in the presence of thin mucosa • Chronic use of fingernails , toothpick or placement of tongue or lip jewellery and studs.
• Classification of Recession-By Sullivan & Atkins Four morphologic categories –shallow narrow –shallow wide –deep narrow –deep wide
BY P.D.MILLER(1985) Class-I This includes marginal tissue recession that does not extend to the mucogingival junction. There is no loss of bone or soft tissue in the interdental area. This type of recession can be narrow or wide. Class-II Consists of marginal tissue recession that extends to or beyond mucogingival junction. There is no loss of bone or soft tissue in the interdental area. Sub classified into wide and narrow. Class-III There is marginal tissue recession that extend to or beyond the mucogingival junction in addition there is bone &/or soft tissue loss interdentally or there is malpositioning of teeth. Class-IV There is marginal tissue recession that extend to or beyond the mucogingival junction with severe bone and soft tissue loss interdentally &/or severe tooth malposition.
FRENUM • A frenum is a fold of mucous membrane, usually with enclosed muscle fibers, that attaches lips and cheeks to the alveolar mucosa &/or gingiva and underlying periosteum. Tension test • A frenum becomes problem if the attachment is too close to the marginal gingiva. Tension on the frenum may pull the gingival margin away from the tooth. This condition may be conductive to plaque accumulation an inhibit proper brushing of teeth.
Classification of Frenum(Placek et al,1974) • Mucosal • Gingival • Papillary • Papilla penetrating DIAGNOSIS- • PULL TEST-Lip is stretched-gingival margin or papilla is moved awaynfrom the tooth • BLANCHING TEST-On stretching frenum blanching is produced at the base of the frenum.
ANKYLOGLOSSIA • CLASSIFICATION 1. Clinically acceptable,normal range of free tongue:greater than 16mm 2. CLASS I:Mild ankyloglossia:12 -16mm 3. CLASS II:Moderate ankyloglossia:8-11mm 4. CLASS III: Severe ankyloglossia:5-7mm 5. CLASS IV:Complete ankyloglossia:less than 3mm
DIAGNOSIS • Tip of the tongue should:(Ayer F,1977) – protrudes outside mouth without clefting – Sweep the upper and lower lip,without straining – Normal swallowing pattern – Speech difficulties
Mucogingival junction • The apical boundary of the attached gingiva is located at the mucogingival junction where the cornified epithelium merges abruptly with the non cornified epithelium of the alveolar mucosa (Schroeder et al) • Stable landmark probably genetically predetermined.(Ainamo et al.)
Methods to identify mucogingival junction • Jiggling Method (Roll Method) Place the blunt end of an instrument over the alveolar mucosa and roll or jiggle coronally, the alveolar mucosa will bulge at the mucogingival junction
Anatomical method By distinguishing between color of attached gingiva and alveolar mucosa
Schiller’s Iodine solution Stains the alveolar mucosa and thus demarcates the mucogingival junction Local Anesthesia Inject LA into alveolar mucosa ; it swells up (elastic fibers)
ALVEOLAR MUCOSA – Darker red. – Apical to Mucogingival junction – Loosely bound to the underlying bone. – Epithelium-Thin non keratinised stratified squamous epithelium – Mucosa –short papilla,Elastic fibres and capillary loops. – Lamina propria and submucosa of alveolar mucosa contain numerous elastic fibres.
WIDTH OF ATTACHED GINGIVA • “Distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or periodontal pocket.” • Adequate amount of attached gingiva is detected by a positive or a negative tension test. . Adequacy of attached gingiva is important in maintenance of proper cleanliness around that particular tooth. . Inadequacy = increased alveolar mucosa which usually gets hurt during brushing so patients avoid cleaning that area. • Greatest in incisors – Maxilla -3.5 to 4.5mm, – Mandible -3.3 to 3.9mm. • Least in first premolar – Maxilla -1.9mm, – Mandible -1.8mm. • Width of attached gingiva increases with age and in supraerupted teeth. .(Ainamo et al.)
The horizontal probe has located the mucogingival junction (the most apical area where nonmovable tissue is found), while other probes measure the probing depth (2 mm) and the width of the keratinized gingiva (7 mm). In this example, the amount of attached gingiva is 5 mm. The amount of attached gingiva can be recorded on the chart, or the relative amount, no attached gingiva (NAG), or minimal attached gingiva (MAG) can be indicated.
VESTIBULAR DEPTH • Measured from gingival margin to the depth of vestibule. • ETIOLOGY for reduced vestibular depth – Physiological – Gingival recession • Reduced vestibular depth –oral hygiene measures jeopardized – Placement of removable prosthesis
EXUDATE ON DIGITAL PRESSURE • At times found in gingivitis but most often in chronic periodontitis • PUS-Neutrophil rich exudate • Presence-Site is inflamed and infected • Not a good stand alone predictor of the progression of chronic periodontitis(Armitage GC,1996) • Seen in large amount in periodontal abscess  Clinically presence of pus is determined by placing the ball of the index finger along the lateral aspect of the marginal gingiva and applying pressure in a rolling motion toward the crown.
BLEEDING ON PROBING • The insertion of a probe to the bottom of the pocket elicits bleeding if the gingiva is inflamed and the pocket epithelium is atrophic or ulcerated. • Objective sign of gingival inflammation.It is an earlier sign than color changes. • Depending on the severity of the inflammation bleeding can vary from a tenuous red line along the gingival sulcus to profuse bleeding.
BLEEDING ON PROBING • Bleeding on probing is not a good diagnostic predictor for CAL.Absence of gingival bleeding –low risk of future attachment loss(long et al,1990) • When to probe For diagnosis Monitoring course of treatment Monitoring maintenance • Probing around implants To prevent scratching of the implant surface, plastic probes should be used instead of steel probes. • At the initial examination the percentage of sites that exhibit bleeding on probing prior to treatment is a clinically useful piece of information since it provides a full mouth pre treatment assessment of the extent of gingival inflammation
THE PERIODONTAL EXAMINATION
FACTORS TO CONSIDER EVALUATING AT THE INITIAL PERIODONTAL EXAMINATION Medical Periodontal Radiographic Systemic diseases Gingival status Appropriate and diagnostic radiographs Medications Gingival recession Pattern of bone loss Medical consultations Periodontal probing Accretion Prophylactic antibiotics Loss of attachment Root caries Risk factors Mobility Crown-to-root ratio Family history Furcation involvement Periapical pathology Age Mucogingival defect Widened periodontal ligament Halitosis Food impactions Overhanging restorations Mental status Poor margins on restorations Root proximity Physical and dexterity statuses Occlusal examination Root trunk length TMD*/Parafunctional habits Restorative rehabilitation *TMD: Temporomandibular joint disorder. Some clinical information on TMD may be gathered at the initial periodontal examination, but a comprehensive evaluation of the Temporomandibular joint requires radiographs
PROBING Periodontitis is characterized clinically by loss of attachment (LOA) and the formation of pockets and osseous defects. The documentation of LOA is essential in establishing baseline data, monitoring treatment results, and determining periodontal stability. Probes vary in design by length, thickness, and millimeter markings.
The probe is inserted gently into the gingival sulcus and stepped around the tooth at about 1 mm increments. The probe should be kept as close as possible to the axial direction of the tooth while the tip remains in contact with the root surface. Measurements are made from the gingival margin for pocket depth and from the cementoenamel junction (CEJ), or a similar fixed point, to the gingival margin for recession. PROBE WALKING
• Characteristics of a good periodontal probe include a thin shaft with a rounded tip, durable markings that are easily read, and ease of sterilization. Commonly, six measurements are recorded per tooth. • Special attention should be directed to detecting the presence of interdental craters and furcation involvement. • Naber’s probe is used specially for easier and more accurate exploration of the horizontal component of furcation lesions. • The probing depth and recession measurements added together determine the LOA. • Factors such as the health of the surrounding gingiva, probing force applied by the operator, and discomfort tolerance of the patient can make a difference of 1 to 2 mm in probe readings.
PERIODONTAL POCKET • It is a pathologically deepened gingival sulcus. • Classification – Gingival pocket- Pseudo pocket . – Periodontal pocket • Two types – Suprabony (Supracrestal /Supraalveolar) – Intrabony (Infrabony /Subcrestal or Intra alveolar) • According to involved tooth surfaces it may be classified as – Simple pocket – Compound pocket – Complex pocket
• Signs -Color changes to bluish red -Rolled edge of gingival margin -Edematous gingiva -Presence of bleeding -Suppuration -Loose extruded tooth. • Symptoms -generally painless or localized or dull radiating pain. -sensation of pressure after eating. -foul taste in localized area. -sensitivity to hot and cold. -toothache in absence of caries.
DETECTION OF POCKETS(Armitage,2004) •The only accurate method of detecting and measuring periodontal pockets is careful exploration with a periodontal probe. •Gutta purcha points or calibrated silver points can be used with the radiograph to assist in determining the level of periodontal pockets.
POCKET DEPTH • The biologic depth is the distance between the gingival margin and the base of the pocket, measured only in carefully prepared & adequately oriented histologic sections. • The probing depth is the distance to which an ad hoc instrument (probe) penetrates into the pocket. • Depth of penetration depends on - Size of the probe - Force with which it is introduced - condition of gingival tissue - angulation of the probe • The probing forces have been explored by several investigators, forces of 0.75N have been found to be well tolerated.
TRANSGINGIVAL PROBING Introduced by Laser & Listgarten (1976) Transgingival probing or sounding, under local anesthesia confirms the extent and configuration of the intra bony component of the pocket or furcation defect.
Prior to surgical therapy it is highly desirable to have an accurate assessment of bony defect morphology. This allows development of a surgical treatment plan that best addresses the degree of existing periodontal destruction. Revert et al (1981) found a mean difference of 0.3mm between transgingival probing and surgically determined bone level. Ursell (1989) reported a mean difference of 0.12mm intra bony defects it was found to be less accurate than horizontal defects.
To obtain the most accurate manual readings, use a thin probe positioned as parallel to the long axis of the tooth as possible PROBING OF POCKETS
LEVEL OF ATTACHMENT VERSUS POCKET DEPTH POCKET DEPTH • It is the distance between the base of pocket and the gingival margin. LEVEL OF ATTACHMENT • The distance between the base of the pocket and the cementoenamel junction. • It is a better indication because changes in the level of attachment can only be due to gain or loss of attachment and periodontal destruction.
DETERMINING THE LEVEL OF ATTACHMENT • Gingival margin on anatomic crown-Level of attachment = pocket depth - distance from gingival margin to C-Ejunction. • Gingival margin coincides with C-E junction - Loss of attachment = pocket depth • Gingival margin apical to C-E junction-Loss of attachment = pocket depth + distance between the C-E junction and gingival margin.
Advances in measurement of periodontal attachment loss 1)Tolerance method to determine thresholds for probing measurements This method uses two replicate measurements of each site which are made for each subject. Their standard deviation is then calculated.. Thus using this method any change below 3mm is considered to be unreliable and this makes it possible to measure small changes of attachment using manual probing. 2) Computer linked electronic constant pressure probes currently available includes: The Florida probe incorporates constant force, precise electronic measurement and constant storage of data. The Interprobe which has an optical encoder transduction element. The Birek probe which works by constant air pressure and uses the occlusal surface as its reference point . The Jeffcoat probe automatically detects CEJ.
FURCATION INVOLVMENT •In treating molar teeth, it is essential to differentiate furcation involvement on the basis of severity and to keep a record of the observed data and the treatment decisions involved. •In general, a furcation is a common site for active bone loss accompanying periodontitis. •Some studies report that the most common sites of recurrent periodontitis are the distal furcations on the maxillary first molars. (Larato,1970) •Problems with plaque control in involved furcations may be explained by these differences.
Facial furcations for a maxillary (A) and a mandibular (B) first molar. The portion of the furcation facing apicaily or toward the bone is the vault (vt), or roof. The vertical concavity on the common root trunk is the flute (fl). FURCATION FLUTES
NABER’S probes are useful for mesial and distal furcae of maxillary molars and interproximal furcae of maxillary premolars. The furcae can be classified in one of the following manners: Approach 1 Class I : A depression that does not catch a curette or probe Class II : A furca deep enough to catch a curette or probe but does not contiguous with other furcae on the same tooth Class III : Through-and-through bone loss Standard probes can be used horizontally in buccal and lingual furcae. When combined with the determination of vertical probing depths, this approach is an accurate way to quantify bone loss. FURCATION INVOLVEMENT
Clinical probing: • In maxillary molars the mesial furcation entrance is located closer to the palatal than to the buccal surface.thus the mesial furcation should be probed from the palatal aspect. • The distal furcation entrance is present midway between the buccal and palatal surface hence this furcation could be probed from either the buccal or the palatal aspect. Palatal approach for mesial furcation in maxillary molar.
• Due to anatomic variations and limited access, the clinical assessment of furcation involvement in maxillary premolars is often difficult. Furcation in maxillary premolar
• Probing of the mandibular furcations is relatively easy because there are only buccal and lingual entrances,each located midway mesiodistally. • Vertical attachment loss on the adjacent roots should be probed at the furcation line angle of each root,angling the probe somewhat,to place the tip of the probe slightly into the furca. • Bone sounding or transgingival probing should be done to determine the bone contours associated with FI more accurately after anesthetizing the soft tissue.(Easley,Greenberg,Listgarten).
CLASSIFICATION Glickman classified FI into 4 grades Grade I: Pocket formation into the flute of the furcation,but the interradicular bone is intact. Grade II: Loss of interradicular bone and pocket formation of varying depths into the furcation but not completely probable to the opposite side of the tooth. Grade III: Complete loss of interradicular bone with pocket formation that is completely probable to the opposite side of the tooth. Grade IV: Loss of attachment and gingival recession that has made the entire furcation clearly visible to clinical examination.
Glickman’s classification of furcation involvement Goldman and Cohen have incorporated a descriptive classification of FI referring to Grade I incipient Grade II cul-de-sac Grade III through and through.
TOOTH MOBILITY: • Mobility is evaluated by placing an instrument on the facial and lingual surfaces and a finger on the appearance side of a tooth and applying pressure while rocking the tooth. If the tooth being tested has no adjacent tooth, the instruments and pressure should be applied obliquely and mesiodistally. A “normal” tooth has a minute amount of “give” to it (ie, is not ankylosed). (O Leary,1969) • All teeth have a slight degree of physiologic mobility. Varies for different teeth and at different times of the day. Increased mobility in morning & progressively decrease(O Leary,1963)
• NORMAL TOOTH MOBILITY-More during early mornings and progressively decreases – 4-12/100mm for 500g force applied(Muhleman,1954) • REDUCED TOOTH MOBILITY-Ankylosed teeth after failing replantation or autogenous bone grafts are placed in contact with detached root surface(Lindhe,1997) • ALTERED TOOTH MOBILITY-It represents transient or permanent change in mobility . – Increased or decreased as a result of therapy(Lindhe,1997)
• INCREASED or STATIC TOOTH MOBILITY-It is a form of stabilized mobility – Due to TFO but may be due to periodontal diseases. (Lindhe,1997) • HYPERMOBILITY(Residual Mobility)-Increased mobility persisting after completion of periodontal treatment – Developing Phase – Permanent Phase(Ramfjord S.P.,1981) • INCREASING/PROGRESSIVE MOBILITY-Progressive nature & can be identified anly through a series of repeated mobility measurements carried out over a period of several days or weeks(Lindhe,1997)
Tooth mobility occurs in 2 stages (Mulemann,1954) The Initial/Intrasocket stage :  Tooth moves within the confines of the periodontal ligament.  Associated with viscoelastic distortion of the ligament and redistribution of periodontal fluids, interbundle contact,fibers.). • The secondary stage :  Occurs gradually.  Entails elastic deformation of the alveolar bone in response to increased horizontal forces..
GRADING OF MOBILITY : The clincian can the use a modification of the Lindhe scale, as recommended by Fleszar et al Class 0 : Physiologic mobility, firm tooth Class I : Slightly increased mobility Class II : Definite to considerable increase in mobility, but no impairment of function Class III : Extreme mobility; a loose tooth that would be uncomfortable in function
Miller mobility index • A tooth that moves more than this minute amount but in a total arc of less than 1 mm has Class 1 mobility. • A tooth that moves in an arc of 1 mm or more but less than 2 mm has Class 2 mobility. • A tooth that moves in an arc of 2 mm or more and can be depressed into its socket has Class 3 mobility.
PHYSIOLOGIC CAUSES  Tooth mobility is increased in pregnancy. (Rateitschak,1967)  Circadian rhythm  Age(Wasserman,1973)  Higher in females and negroes (Wasserman,1973)  Menstrual cycle (Burdein,1970)  Oral contraceptives ( Knight,1967) PATHOLOGIC CAUSES  Also increased by hypofunction.  Mobility produced by TFO occurs initially as a result of resorption of cortical layer of bone leading to reduced fiber support, and later as an adaptation phenomenon resulting in a widened periodontal space.  Extension of inflammation from the gingiva/from the periapex into the periodontal ligament -. Eg.Periapical abscess in the absence of periodontal disease.  Periodontal surgery : Temporarily (Persson,1981)  Pathologic processes of the jaws that destroy the alveolar bone and /or roots of the teeth. Eg. Osteomyelitis and tumours
ADVANCES • More precise and objective measurement of tooth mobility has been pursued and includes mechanical, electronic and optical devices, and laser Doppler vibrometry. • Mobilometers-Elbrecht’s indicator,Werner’s oscillator. • Periotest-evaluates damping charecteristics of teeth
• The term traumatic occlusion was introduced by Stillman in 1917. • Later, in 1922, Stillman and McCaII stated, "Traumatic occlusion is an abnormal occlusal stress which is capable of producing or has produced an injury to the periodontium.” WHO in 1978 defined trauma form occlusion as “ the damage caused by stress on the teeth produced directly or indirectly by teeth of the opposing jaw.’’ Glossary of Periodontic terms, 1986 defined TFO as “ an injury to the attachment apparatus as a result of excessive occlusal force” . Carranza defined TFO as a condition when occlusal forces exceed the adaptive capacity of the tissues , tissue injury results and the resultant injury is termed as trauma form occlusion. TRAUMA FROM OCCLUSION
TFO is Classified as 1. Primary 2. Secondary Types of trauma from occlusion 1. Acute 2. Chronic
Clinical diagnosis of trauma from occlusion A clinical diagnosis of occlusal trauma can only be confirmed where progressive mobility can be identified through a series of repeated measurements over an extended period. This means that simple but reliable monitoring needs to be undertaken.
The common Clinical signs of occlusal trauma are: – Increasing tooth mobility and migration or drifting – Fremitus – Persistent discomfort on eating. - pathologic migration, especially of the anterior teeth
Fremitus (functional mobility) is the movement of teeth during function or parafunction. Fremitus can often be detected earlier than bidigital tooth mobility and has been associated, in the presence of inflammation, with increased bone and attachment loss (pocket formation) when compared with teeth without fremitus. The photograph shows testing for fremitus. The index finger is placed on the buccals surface of the maxillary teeth, and the patient is asked to grind in lateral and protrusive movements. Any movement seen or felt is termed fremitus. Class I: Mild vibration or movement felt Class II: Easily palpable, no visible movement Class III: Movement clearly visible TRAUMA FROM OCCLUSION
PROCEDURE 1. Set the patient upright with the head stabilized against the headrest 2. Press an index finger on each maxillary tooth at cervical third. 3. Request the patient to “click the back teeth” repeatedly. 4. Start with the most posterior maxillary tooth on one side and move index finger tooth by tooth around the arch 5. Record by tooth number the teeth vibration is felt and teeth where actual movement noted.
PATHOLOGIC MIGRATION OF THE TEETH:Change in tooth position that occurs when there is disruption of forces that maintain teeth in a normal relationship(Chasens A,1997)  Alterations in tooth position should be carefully noted.  Premature tooth contacts in posterior region that deflect the mandible anteriorly contribute to destruction of the periodontal of the maxillary anterior teeth  pathologic migration, premolar of anterior teeth in young person - sign of JP. ETIOLOGY •Destruction of periodontal supporting tissues(Martinez,1997) •Occlusal Factors •Posterior bite collapse •Arch Integrity •Class II MO •Occlusal Interferences •Anterior component of force •Protrusive pattern of mastication •Bruxism •Shortened dental arches
• Soft tissue pressure of the tongue ,cheek and lips(Profit W,1975) • Periodontal and Periapical inflammation (Hirschfeld,1933)-Pressure from granulation tissue • Extrusive forces • Habits DRIFTING OF TEETH-It does not results from destruction of periodontal tissues • It creates chances for periodontal diseases.
• SENSITIVITY TO PERCUSSION:  Is a feature of inflammation of the periodontal tissues..
DETERMINATION OF DISEASE ACTIVITY • Currently no sure method to determine disease activity. • Inactivate lesions may show little or no bleeding on probing & minimal amount of gingival fluid, the bacterial flora revealed by dark field microscopy consists of coccoid cells. • Active lesions bleed more readily on probing and have large amounts of fluid & exudate, their bacterial flora shows a greater no. of spirochetes & motile bacteria. • In patients with aggressive Periodontitis, progressing and non progressing sites may show no differences in bleeding on probing.
VARIATION IN SOFT TISSUE & BONE • SOFT TISSUE – High frenal attachment – Shallow vestibular depth • BONE – Exostoses – Tori-mandibular & maxillary tori
ALVEOLAR BONE LOSS • Evaluated by clinical and radiographic examination. • Probing is helpful for determining  The height and contour of the facial & lingual bones obscured on the radiograph by the dense roots.  The architecture of the interdental bone. • Transgingival probing performed after the area is anaesthetized, is a more accurate method of evaluation and provides additional information on bone architecture.(Greenberg,1976)
PALPATION • Palpating the oral mucosa in the lateral and apical areas of the tooth may help to locate the origin of radiating pain that the patient can not localize. • Infection deep in the periodontal tissues and the early stages of a periodontal abscess may also be detected by palpation.
SUPPURATION(Armitage GC,2004) • The presence of abundant no. of neutrophils in the gingival fluid transforms it into a purulent exudate.  It is not by itself a good indicator.  Clinically presence of pus is determined by placing the ball of the index finger along the lateral aspect of the marginal gingiva and applying pressure in a rolling motion toward the crown.  The purulent exudate is formed in the inner pocket wall and therefore the external appearance may give no indication of its presence. Pus formation does not occur in all periodontal pocket but digital pressure often reveals it in pockets where its presence is not suspected
LABORATORY TESTING OF PATIENTS WITH SYSTEMIC CONDITIONS IN PERIODONTAL PRACTICE • In addition to the diagnosis, laboratory tests are also extremely important in assisting in the management of the patient during treatment of the disease • When unusual gingival or periodontal problems are present and cannot be explained by local causes, the possibility of contributing systemic factors must be explored. • The dentist must understand the oral manifestations of systemic disease so that he or she can question the patient’s physician regarding the type of systemic disturbance that may be involved in individual cases.
Total WBC count 4500 – 10000/cm3 Differential WBC count Polymorphs: 55 – 70% adult 49 – 65% children Lymphocytes: 29 – 40% adult 30 – 60% children Eosinophil: 1 – 6% Monocytes: 2 – 10% Basophils: 0 – 1% Hemoglobin% - 14 – 16gm% for men; 12 – 14gm% for women Bleeding time – Duke’s Method < 5 minutes Clotting time – Wright’s Capillary Method -2 – 5 minutes ESR –Westergren mm/ first hour Males: 0-15mm Females 0-20mm Blood glucose – random 60 – 120 mg/dl Glycosylated hemoglobin: 4 - 5.9%
EFFICACY OF DIAGNOSTIC TESTS (Greenstein,1995) • There are a few principal concepts that must be under stood by practitioners when they use diagnostic tests. The most basic of these concepts are: 1. Gold standard 2. Accuracy 3. Sensitivity 4. Specificity 5. Positive predictive value 6. Negative predictive value
• a gold standard measure is obtained from an independent definitive diagnosis of disease presence or absence, which is usually provided by histopathologic examination of the tissues. • The basic method used to compare the diagnostic test with the gold standard is the decision matrix.
DECISION MATRIX - GOLD STANDARD Test Result Disease Present Disease Absent Total (D+) (D-) Positive (T+) Negative (T-) TP FP TP+FP FN TN FN+TN Total TP+FN FP+TN • Here test results (test positive and test negative) tells us whether disease is truly present or absent. • This is called the accuracy of the test and is calculated as TP + TN/all tests conducted, i.e., the proportion or percentage of times that the test gives accurate results.
SENSITIVITY (the true-positive ratio) TP/TP+FN. represents the proportion or percentage of times that the tests results help correctly identify patients with disease. SPECIFICITY (the true-negative ratio) TN/FP + TN. specificity represents the proportion or percentage of times that the test results help correctly identify patients who do not have disease.
THE DECISION MATRIX IN A HORIZONTAL DIMENSION, CALCULATE TWO TYPES OF PREDICTIVE VALUES. POSITIVE PREDICTIVE VALUE TP/TP + FP The proportion or percentage of true-positive results of all positive results. In other words, when the test result is positive, what is the probability that the patient (or site) really has disease? NEGATIVE PREDICTIVE VALUE TN/FN + TN The proportion or % of true-negative test results of all negative test results. That is what percent do not have the disease
• It is important to understand that both the positive predictive value and the negative predictive value are affected by disease prevalence in the population being tested • Diagnostic testing should be considered an aid to the diagnostic process—not a device or procedure that provides the diagnosis.
THRESHOLD FOR DISEASE • When do we actually label the process being observed as Periodontal disease? • Unfortunately, in many patients there is no clear demarcation between disease and no disease. • Periodontal disease presents throughout a range from incipient to severe. • Hence it may be reasonable for practitioners to consider more than one threshold of disease at which the test result is determined to be positive to get a sense of the magnitude of risk taken when making this decision one way or the other.
THE EXAMINATION OF PATIENTS CONSIDERED FOR IMPLANTS • Examination of patients - considered for implants includes both clinical evaluation of soft tissues and a radiographic evaluation.. • Probing around implants is difficult (Bragger U,1997) (1) the prosthetic construction may need to be removed for access (2) standard metal instruments are unsuitable. • Instead, plastic or titanium probe tips should be used to avoid damage of the implant / tissue interface. • If automatic probing is considered, the Florida Probe is available with a titanium tip that will not hurt the implant ; also, the Interprobe system comes with disposable plastic tips.
CLINICAL EVALUATION OF DENTAL IMPLANT TREATMENT • Diagnostic procedure prior to implant placement 1. Competent treatment planning is a key to long term success of implant therapy. Indications & contraindications must carefully be balanced & optional treatments must be taken into the decision making process in each individual patient eligible for implant therapy 2. Diagnosis 3. Medical history
4. Dental history- 5. Intra / Extra Oral examination – Oral hygiene – Parafunctional activities eg: bruxism – Salivary flow – Soft tissue condition – Periodontal health 6. Study casts 7. Anatomical limits for fixture placement
8. Radiographic examination – Periapical radiographs – Orthopantomographs – Computed tomogram – Combination . etc 9. Fabrication of radiographic splint 10. Additional bone evaluation 11. Designs for dentulous/ edentulous patient treatment 12. Consultation
DIAGNOSTIC PROCEDURE BETWEEN IMPLANT PLACEMENT AND INITIATION OF PROSTHESIS FABRICATION & MAINTENANCE • Evaluation during the phase of tissue integration • Measurement of insertion torque as well as assessments of bone implant damping reactions (e.g. damping & resonance frequency analysis) are used to determine the initial stability of the newly placed implants. • PERIOTEST- (Schultz,1983) Resonance frequency analysis (RFA)- method based on steady state , swept frequency technique – non invasive , easy to use & capable of eliciting quantitative information on implant stability & stiffness
• Soft tissue integration –BOP , Suppuration, probing depth • Radiographs – For correct placement of implant – Position , sink depth , & angulation • Healing – 6 weeks-12 months
PERIODONTAL DIAGNOSIS: a) Components of a periodontal diagnosis b)Establishing a diagnosis in treated periodontal disease c) Chronic versus Aggressive periodontitis
COMPONENTS OF A PERIODONTAL DIAGNOSIS Before arriving at a periodontal diagnosis the clinician must answer 3 basic questions: 1. What periodontal disease or condition does the patient have? 2. How severe is the problem? 3. Is the disease or condition localized or generalized?
ESTABLISHING A DIAGNOSIS IN TREATED PATIENTS Treatment of plaque-induced periodontal diseases often results in the resolution of the patient’s periodontal infection. It is important to note that periodontal therapy can change the pre-treatment diagnosis to a more favorable post-treatment diagnosis. For example, effective treatment routinely converts plaque-induced gingivitis into a state of periodontal health (i.e. a Gingivitis to Periodontal Health shift.)
Successful treatment of plaque-induced periodontitis is often converted to a state of periodontal health with a reduced periodontium. In such cases, damage persists from the previous periodontitis in the form of gingival recession. An interesting diagnostic problem arises when successfully treated patients who once had periodontitis subsequently develop gingival inflammation during the maintenance phase of therapy.
Do such patients have gingivitis superimposed on a reduced periodontium or do they have a recurrence of periodontitis? At a single evaluation visit one cannot determine if previously treated periodontitis is recurring. Data collected during multiple maintenance visits are required to make this determination.
SUMMARY
CLASSIFICATION OF GINGIVAL DISEASES PLAQUE INDUCED GINGIVAL LESIONS 1. Gingivitis associated with dental plaque only 2. Gingival diseases modified by systemic factors Associated with endocrine system Associated with blood dyscrasias 3. Gingival diseases modified by medications 4. Gingival diseases modified by malnutrition
CLASSIFICATION OF GINGIVAL DISEASES NON-PLAQUE INDUCED GINGIVAL LESIONS 1. Gingival diseases of specific bacterial origin 2. Gingival diseases of viral origin 3. Gingival diseases of fungal origin 4. Gingival diseases of genetic origin 5. Gingival manifestations of systemic conditions 6. Traumatic lesions 7. Foreign body reactions
CLASSIFICATION OF PERIODONTITIS • 1. Chronic Periodontitis* – Localized – Generalized • 2. Aggressive Periodontitis – Localized – Generalized • 3. Periodontitis Associated with Systemic Diseases • 4. Necrotizing Periodontal Diseases • 5. Abscesses of the Periodontium • 6. Periodontal Diseases associated with Endodontic Lesions • 7. Developmental or Acquired Deformities and Conditions • *Can be further classified on basis of extent and severity
DISEASE/CONDITION CLINICAL FEATURES DIFFERENTIAL DIAGNOSIS Gingivitis associated with dental plaque •Gingival bleeding •Colour •Acute-Reddish •Chronic-Deep blue •Consistency-Soft and edematous or fibrotic •Stippling -absent •Inflammation with pocket depth restricted to gingival tissues. Desquamative gingivitis Atrophic Gingivitis Gingival diseases modified by systemic factors: 1. Diabetes Mellitus 2. Leukemia •Diffuse inflammation with increased bleeding & increase gingival inflammatory reaction to plaque •Extensive bone loss •Increased tooth mobility •Supperation •Multiple abscess formation •red.boggy,edematous gingiva that bleeds persistently on slight provocation or spontaneosly •gingiva is hypertrophic and shows a typical intragingival hemorrhage. Abscess Ascorbic acid dificiency Plasma Cell Wegners Gingival enlargement Gingival Diseases modified by medications: 1. DIGO •Bead like enlargement of IDP extends into facial and lingual gingival margin •Marginal and papillary enlargement unite to form massive tissue folds covering crown and interfering with occlusion. •Pale pink,mulberry shaped,firm and resilient,lobulated surface and no bleeding in absence of inflammation •Inflammation-reddish coloured ,incresed bleeding& size. •Idiopathic gingival enlargment
DISEASE/CONDITION CLINICAL FEATURES D D Gingival diseases of specific bacterial origin: 1. ANUG 1. Lesions are painful 2. Lesions are gingival ulcers, punched-out crater-like, of interdental papilla and may involve marginal gingiva 3. Gingival ulcers bleed spontaneously or readily Gonococcal Stomatitis Vincent’s Angina Desquamative Gingivitis Gingival diseases of specific viral origin: 1. Primary Herpetic Gingivostomatitis 1. Diffuse gingivitis 2. Vesiculoulcerative eruption-discrete sherical grey vesicles that rupture in 24hrs to form ulcers with red elevated margins and depressed yellow grayish central core 3. In children ANUG Erythema multifome Steven’s Johnson Syndrome Lichen Planus Aphthous Stomatitis Desquamative gingivitis Gingival diseases of specific fungal origin: 1. Candidiasis 1. acute pseudo- membranous candidiasis (thrush),white lesions that can be lifted off the gingiva. 2. acute atrophic (eythematous) gingival candidiasis. Leukoplakia Lichen Planus Carcinoma Erythema multiforme Gingival diseases of specific genetic origin: 1. Hereditary gingival fibromatosis 1. Attached,marginal gingiva & IDP-Diffuse enlargement 2. Gingiva is pink firm and leathery in consistency with Pebbled surface 3. Enlargement projects into vestibule- distortion of jaw DIGO Fibroma Gingival manifestations of systemic conditions: 1. Lichen Planus 1. Mimics gingivitis 2. Reticulated,hypertrophic ,keratotic lesion Leukoplakia Aphthous White sponge nevus
DISEASE/CONDITI ON CLINICAL FEATURES D D Gingival manifestations of systemic conditions: 1. Lichen Planus 1. Allergic Reaction:Tooth Paste 1. Mimics gingivitis 2. Reticulated,hypertrophic ,keratotic lesion 3. gingival inflammation and pain 4. lace like white lesions of gingiva, tongue and cheek.ulcerations may be present. 5. Reticular,Atrophic,Bullous,Erosive 6. herbal compound sanguinaria were shown to produce gingivo-vestibular reactions characterized by leukoplakia Leukoplakia Aphthous White sponge nevus Leukoplakia Lichen planus Chronic Periodontitis •Amount of destruction consistent with local factors •Subgingival calculus present •Slow to moderate rate of progression, but may have periods of rapid progression • Can be associated with local predisposing factors (e.g., tooth related or iatrogenic factors) • May be modified by and / or associated with systemic diseases (e.g., diabetes mellitus) • Can be modified by factors other than systemic disease such as cigarette smoking and emotional stress Aggressive Periodontitis Desquamative Gingivitis Aggressive Periodontitis 1. Except for the presence of periodontitis, patients are otherwise clinically healthy 2. Rapid attachment loss and bone destruction 3. Familial aggregation 4. Distolabial movement of anterior teeth Chronic Periodontitis Desquamative Gingivitis
DISEASE/CONDITION CLINICAL FEATURES D D DIAGNOSIS OF ACUTE PERIODONTAL LESIONS : 1. NUG 2. NUP 1.Lesions are painful 2.Lesions are gingival ulcers, punched-out crater-like, of interdental papilla and may involve marginal gingiva 3.Gingival ulcers bleed spontaneously or readily 1.Deep interproximal craters with denudation of interdental alveolar bone 2.Sequestration of interdental, and possibly buccal and/or lingual, alveolar bone Gonococcal Stomatitis Vincent’s Angina Desquamative Gingivitis ACUTE PERIODONTAL ABSCESSES Gingival abscess Periodontal Abscess Periapical Abscess confined to marginal gingival tissues, often at previously non-diseased sites.. offending foreign material is, thus, often diagnostic. history of 1–2 days of pain and very localized gingival swelling red, shiny swelling confined to marginal gingival tissues. Smooth, shiny swelling of the gingiva Painful, tender to palpation Purulent exudate Increased probing depth Mobile and/or percussion sensitive Tooth usually vital Sinus tract opens via keratinized gingiva Non-vital tooth Caries No pocket Apical radiolucency No or minimal mobility Percussion sensitivity Sinus tract opens via alveolar mucosa •Lateral periapical cyst, •Vertical root fracture, •Endo-periodontal abscess, •Postoperative infection
DISEASE/CONDITION CLINICAL FEATURES D D Periodontal Diseases associated with Endodontic Lesions 1. Swelling caused by endodontic infections occur in the mucobuccal fold and periodontal infections occur in the attached gingiva . 2. Teeth are examined for any caries, defective restoration, erosions, abrasions, cracks, fractures and discolorations. 3. Increased bleeding,pocket depth,mobility may be associated 4. Radiographs are required to confirm diagnosis Periodontal Abscess Periapical Abscess Developmental or Acquired Deformities and Conditions 1. Gingival soft tissue recession 2. Lack of keratinized gingiva • inadequate band of keratinized gingiva, excessive muscle pull and too vigorous tooth brushing. • lack of keratinized gingiva together with muscle pull can cause on-going gingival recession. Shallow vestibule Recession
Developmental or Acquired Deformities and Conditions
REFERENCES: • Clinical periodontology: Glickman, Carranza, 10th edition • Diagnostics: Perio 2000, vol. 34, 2004 • Fundamentals of periodontics: 2cnd edition, K.S. Kornman, K.J. Wilson • Diagnosis and risk prediction of periodontal diseases: vol. 3, 2002: Per Axelsson • Clinical Periodontology and Implant Dentistry: 5th ed, Jan Lindhe • Periodontal Medicine: Rose, Cohen, Genco, Mealey, 2000 • Position paper: Diagnosis of Periodontal diseases- J Periodontol 2003 • Clinical practice of the dental hygienist ,9 th edition by Esther M . Wilkins
REFERENCES: • Critical Decisions in Periodontology 4th edition: Walter B. Hall • Dwight E. Mcleod: A Practical Approach To The Diagnosis And Treatment Of Periodontal Disease. JADA, Vol. 131, April 2000. • Gary C. Armitage: Periodontal Diseases: Diagnosis. Annals of Periodontology, 1996 • John O .Grippo et al : Attrition, Abrasion, Corrosion and abfraction revisited. A new perspective on tooth surface lesions. JADA, VOL 135, AUG 2004 • Vivien Kwok, Jack Caton: Prognosis revisited: A system for assigning periodontal prognosis. J Periodontol 2007;78 • Dental hygiene theory and practice: Darby and Walsh. 2cnd edition • The Periodontal- Endodontic controversy: Harrington, Steiner, Ammons.Periodontology 2000, Vol. 30, 2002, 123–130
THANK YOU

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CLINICAL DIAGNOSIS M.pptx

  • 1. C L I N I C A L D I A G N O S I S O F P E R I O D O N T A L D I S E A S E PRESENTED BY: AKANKSHA GROVER IInd YEAR PG
  • 2. CONTENTS  Introduction  What is diagnosis?  Categories of periodontal diseases.  The gingival diseases  Various types of periodontitis  Periodontal manifestation of systemic diseases.  First visit  Second visit  Clinical examination  Extra oral  Intra oral  Oral hygiene  Caries  Wasting disease of teeth  Dental Stains  Halitosis  Quality and quantity of saliva  Soft tissue examination
  • 3.  Examination of periodontium  Introduction  Gingiva  Mucogingival Junction  Width of attached gingiva  Plaque and calculus  Periodontal probing  Furcation  Tooth mobility  TFO  Pathologic tooth migration  Determination of disease activity Variations in soft tissue & Bone  Alveolar bone loss  Palpation  Suppuration  Lab tests  Efficacy of diagnostic tests  Summary
  • 4. INTRODUCTION • Diagnosis” is the ability and skill of the clinician to detect, recognize, and know the nature of the disease process • DIAGNOSIS: The correct determination, discriminative estimation, and logical appraisal of the conditions found during examination as evidenced by signs and symptoms of health and disease. • WHO Definition: It is the art of chronological organization and critical evaluation of the information obtained of patients’ history, lab investigations, clinical examination so as to identify the disease type and etiology. PRINCIPLES OF DIAGNOSIS: • SPECIFICITY: The ability of a test or observation to clearly differentiate one disease from another. • SENSITIVITY: The ability of a test or observation to detect the disease whenever it is present. • PREDICTIVE VALUE: The probability that the test result (ie. the proportion of true positive results and true negative results combined) agrees with the disease status.
  • 5. • In general diseases that can afflict the periodontium fall into 3 broad categories. The gingival diseases The various types of periodontitis The periodontal manifestation of systemic diseases
  • 6. Classified by AAP World Workshop in Clinical Periodontics (1989). • Adult Periodontitis. • Early Onset Periodontitis – -Prepubertal -Juvenile -Rapidly progressive. • Necrotizing Ulcerative Periodontitis. • Refractory Periodontitis.
  • 7. CLASSIFIED BY AAP INTERNATIONAL WORKSHOP FOR PERIODONTAL DISEASES (1999).
  • 8. CLASSIFICATION OF GINGIVAL DISEASES PLAQUE INDUCED GINGIVAL LESIONS 1. Gingivitis associated with dental plaque only 2. Gingival diseases modified by systemic factors Associated with endocrine system Associated with blood dyscrasias 3. Gingival diseases modified by medications 4. Gingival diseases modified by malnutrition
  • 9. CLASSIFICATION OF GINGIVAL DISEASES NON-PLAQUE INDUCED GINGIVAL LESIONS 1. Gingival diseases of specific bacterial origin 2. Gingival diseases of viral origin 3. Gingival diseases of fungal origin 4. Gingival diseases of genetic origin 5. Gingival manifestations of systemic conditions 6. Traumatic lesions 7. Foreign body reactions
  • 10. CLASSIFICATION OF PERIODONTITIS • 1. Chronic Periodontitis* – Localized – Generalized • 2. Aggressive Periodontitis – Localized – Generalized • 3. Periodontitis Associated with Systemic Diseases • 4. Necrotizing Periodontal Diseases • 5. Abscesses of the Periodontium • 6. Periodontal Diseases associated with Endodontic Lesions • 7. Developmental or Acquired Deformities and Conditions • *Can be further classified on basis of extent and severity
  • 11. PROPER DIAGNOSIS -BASIS • Proper evaluation of history of the disease process • Signs & symptoms present • Laboratory data • Special tests & radiographs • The value of establishing a diagnosis is to provide a logical basis for treatment & prognosis
  • 12. • Periodontal diagnosis should first determine whether disease is present, then identify its type, extent, distribution & severity and finally provide an understanding of the underlying pathologic process and its cause.
  • 13. RECOMMENDED SEQUENCE FOR DIAGNOSIS 1ST VISIT - OVERALL APPRAISAL OF PATIENT - MEDICAL HISTORY - DENTAL HISTORY - INTRAORAL R/G SURVEY - CASTS - CLINICAL PHOTOGRAPHS - REVIEW OF INITIAL EXAMINATION
  • 14. FIRST VISIT: OVERALL APPRAISAL OF THE PATIENT: • Consideration of the patients mental and emotional status • Temperament • Attitude • Physiologic age
  • 15. Observation of patient’s general health and appearance Commences when the patient enters the dental office • Body weight: recent weight loss may indicate serious underlying pathology e.g. cancer Excessive weight may suggest risk of heart attack or stroke, type 2 diabetes mellitus • Awkward gait: degenerative joint disease, a nervous system disorder such as multiple sclerosis • Complexion: pallor with anemia, yellow with jaundice • Breathlessness with minor exertion may indicate cardiac or lung disease
  • 16. PERSONAL INFORMATION NAME-  Full name includes pt’s name, father’s or husband’s name and surname  For - Record Communication Certification. AGE-  Recorded in years  In case of periodontal disease helps in diagnosis of puberty gingivitis, ANUG, Prepubertal periodontitis, Juvenile periodontitis and Adult periodontitis. SEX  Hormonal disturbances during puberty, menstrual period & pregnancy modifies tissue response to local irritation in females.  Certain systemic conditions also seen with significant sex difference( e.g. hemophilia in male)also affects overall condition.
  • 17. RESIDENCE-  This should be noted in details mentioning the house number,street, society, city or village, pincode and district. Previous visit or residency also noted.  Due to high fluoride content in water fluorosis is more common in certain regions.  Also gives information about convenience of patient for recall visits. OCCUPATION-  Both the present and past occupations should be noted.  Erosion is commonly seen in persons associated with acid fume works  Some occupational habits (e.g. holding nails by anterior teeth in carpenters, shoe makers and tailors.) causes notching of incisal edges of maxillary incisors.
  • 18. HISTORY OF PERIODONTAL PATIENTS • The history of the patient is a revealing document as a basis for comprehensive treatment planning and understanding of the patient’s needs, social and economic situation, as well as general medical conditions. • The assessment of the patient’s history required an evaluation of the following six aspects: – Chief complaint – Social and family history – Dental history – Oral hygiene habits – Smoking history – Medical history and medications
  • 19. CHIEF COMPLAINT The presenting problem of the patient Has to be recorded in the patients own words Obtained by asking the patient to describe the problem for which help is being sought or reason for visit It is essential to realise the patient’s needs and desires for treatment. If a patient has been referred for specific treatment, the extent of the desired treatment has to be defined and the referring dentist should be informed of the intentions for treatment.
  • 20. • Patients reporting independently, however, usually have specific desires and expectations regarding treatment outcomes. • These may not be congruent with the true assessment of a professional with respect to the clinical situation. • Optimal treatment results may only be achieved if the patient’s demands are in balance with the objective evaluation of the disease and the projected treatment outcomes. Therefore, the patient’s expectations have to be taken seriously and must be incorporated in the evaluation in harmony with the clinical situation.
  • 21. History of the present illness: Elaboration of the chief complaint In case of pain:  Mode of onset  Duration  Type of pain  Radiation or localization of the pain  Severity  Aggravating and relieving factors  Whether the patient has taken any medication or has consulted a doctor
  • 22. In case of lesion: When was the lesion first observed Mode of development Symptoms Previous treatment Bleeding gums: Time of onset Spontaneous/ on brushing/ while eating Duration of bleeding Manner of stopping
  • 23. • In case of mobility – History of trauma – Time duration – Pain – Pre treatment • In case of Recession – Time duration – Tooth brushing – hypesensitivity
  • 24. • In case of Hypersensitivity – On cold or hot stimulus – Timing – Generalized or localized • In case of Food Impaction – Area – Use tooth pick or pin-area of use – On eating what food items
  • 25. • In case of Supperation – Time duration – Swelling – Pain • In case of Bad Breath – Time duration – Timing – Association with burps
  • 26. MEDICAL HISTORY(Armitage ,2004) • Most of the medical history is obtained at the first visit. Health history can be obtained verbally by the questioning of the patient. • Importance of medical history should be explained to the patient. • Medical history will aid the clinician in diagnosis of oral manifestations of systemic disease, detection of systemic conditions that may be affecting the periodontal tissue response to local factors that require special precautions and or modifications in treatment procedures.
  • 27. Medical history should include reference to the following  Whether the patient is under the care of a physician. Name,address, telephone no. of the physician should be recorded.  Hospitalization and operations: Kind of operation, untoward effects such as anesthesia, hemorrhagic, infectious complications.  All medications being taken : Special inequity should be made regarding the dosage and duration of therapy with anticoagulant and cortico steroids.  History of all medical problems :Cardiovascular,hematologic, endocrine etc. Infectious diseases, sexually transmitted diseases, AIDS.  Possibility of occupational disease
  • 28. Medical history should include reference to the following • Abnormal bleeding tendencies : Nose bleeds, prolonged bleeding from minor cuts, spontaneous echymosis, tendency towards excessive bruxism, excessive menstrual bleeding. • History of allergy including : Hay fever, asthma, sensitivity of foods, sensitivity to drugs - Aspirin, Codeine, Barbiturates, Sulfonamides, Antibiotics, Procaine, Laxatives. Sensitivity to dental materials – Eugenol /Acrylic resin. • Information regarding the onset of puberty : Menopause, menstrual disorders, hysterectomy, pregnancies, miscarriages. • Family medical history, including bleeding disorders and diabetes.
  • 29.
  • 30. • Relevant dental history A list of dental visits, recent visit, nature of treatment and oral prophylaxis or cleaning by a dentist or hygienist including frequency & date of most recent cleaning. • Patient’s oral hygiene regimen – Toothbrushing frequency. – Method of brushing. – Time of day. – Type of toothbrush or datun – – Type of dentifrice – Interval at which brushes are replaced. – Other aids.
  • 31. • Previous tooth loss due to caries or periodontal lesion may change the treatment plan. • Any orthodontic treatment including duration and approximate date of termination. • Pain -Whether in teeth or gum -Manner by which provoked -Manner in which relieved -Nature and duration.
  • 32. Bleeding gums- • Since what time • Spontaneously, on brushing or eating. • At night or with regular periodicity whether associated with menstrual period or other specific factors • Duration of bleeding • Manner in which it is stopped. Bad taste and areas of food impaction. Tooth mobility-If teeth feel loose or insecure -Difficulty in chewing
  • 33. • Habits -grinding or clenching during day or night -Unilateral chewing -Mouth breathing -Tobacco smoking or chewing -Nail biting or foreign objects. • Previous periodontal problems -Nature & condition -If treated, type of treatment and approximate period of termination of treatment. -In the patient’s opinion present problem is recurrence of previous disease.
  • 34. FAMILY HISTORY History of any hereditary linked problems Diabetes Hemophilia Hypertension Is taken to determine if there is a familial predisposition to disease or if there are diseases in which inheritance is an important factor. e.g. diabetes mellitus. A patient with a strong history of diabetes mellitus and no apparent signs or symptoms should be evaluated periodically since clinical features may appear later in life.
  • 35. PERSONAL HISTORY • May assist in determining the patient’s response to the demands and conflicts of modern society. It explains the untoward incidence of patients to health problems and to therapeutic recommendations. DIET SMOKING/ TOBACCO USE: • Cigarette smoking has been documented to be the second most important risk factor after inadequate plaque control (Kinane et al, 2006) in the etiology and pathogenesis of periodontal disease. DRUG USE BRUSHING HABITS PARAFUNCTIONAL HABITS
  • 36.
  • 37. EXAMINATION OF THE PATIENT 1. Observation of patient’s general health and appearance 2. Extraoral examination 3. Intraoral examination
  • 38. EXTRAORAL EXAMINATION Is carried out using the principles of inspection, palpation. Thus it includes: 1. Head, face and neck • Swelling • Space infection 2. Eyes, nose • Icterus ,pallor 3. Skin • Skin allergy or infection 4. Lips • Angular chielitis • Infection-Herpes labialis STRESS STRESS
  • 39. 1. Lymph nodes • Palpable-infection,malignancy 2. TMJ • Dislocation,clicking 3. Salivary glands • Tumour,genetic disease,sialolithiasis 4. Nails • Clubbing,infection 5. Masticatory apparatus • Hypertrophy of muscles
  • 40. RADIOGRAPHIC EVALUATION •Radiographs are an indispensable aid in identifying the presence of pathogenesis and the conditions that affect the prognosis and treatment of periodontal diseases. •Proper angulation of the film and of the head of the x-ray machine minimizes distortion. •For periodontal purposes, it is useful to position bite-wing radiographs vertically so that both maxillary and mandibular bone crests are visible. •Individual periapical radiographs are superior in detail to panoramic radiographs and preferred for a more accurate analysis.
  • 41.
  • 42. THE RADIOGRAPH IS A VALUABLE AID IN THE: 1. Diagnosis of periodontal disease. 2. Determination of prognosis. 3. Evaluation of the outcome of treatment Radiograph is only an adjunct to the clinical examination, not a substitute for it.
  • 43. INTRAORAL RADIOGRAPHIC SURVEY -Minimum of 14 intraoral films and 4 posterior bitewing films. -Panaromic radiographs more convenient. -Provides information of distribution and severity of bone destruction in periodontal disease.
  • 44. EXTRAORAL RADIOGRAPHY •Panoramic radiography •Digital radiography •Digital subtraction radiography (DSR) •Tuned aperture tomography (TACT) •Computed tomography (CT)
  • 45. CASTS Casts from dental impressions are extremely useful adjuncts in the oral examination. Casts indicate : • the position of the gingival margins and • the position and the inclination of the teeth, • proximal contact relationships and • food impaction areas. • Developmental deformities in teeth • lingual-cuspal relationships
  • 46. • visual aids in discussions with the patient • pre-treatment and post-treatment comparisons. • Reference at checkup visits • Wear facets • Plunger cusp • Vestibular depth • Implants-Bucco-lingual width
  • 47. CLINICAL PHOTOGRAPH • Not essential but useful for recording before and after treatment tissue appearance • Can not always be relied on for comparing color changes in gingiva but they depict gingival morphologic changes • Record keeping for mucogingival problems like – Areas of gingival recession – Frenum involvment – Papilla loss
  • 48. REVIEW OF INITIAL EXAMINATION • If no emergency care is required the patient is dismissed and instructed when to report for 2nd visit. • Before second visit, a correlated examination is made of the radiographs and casts to relate the radiographic changes to unfavorable condition represented on the casts. • Casts should be checked for-Abnormal wear -Plunger cusps or ridges -Malposed teeth -Cross bite. • Such areas are marked for future reference. • The radiographs and casts are valuable diagnostic aids. However, clinical findings constitute the basis for diagnosis.
  • 49. SECOND VISIT Clinical examination Intra oral Oral hygiene • The cleanliness of the oral cavity is appraised in term of the extent of  Accumulated food debris  Materia alba  Tooth surface stains  Plaque - detected well by disclosing solutions. - Quality rather than quantity decides - severity of periodontal destruction
  • 50. EXAMINATION OF TEETH –should note for  caries  developmental defects  wasting diseases of teeth  proximal contact relationship
  • 51. WASTING DISEASE OF THE TEETH • Loss of tooth structure may occur through noncarious processes. Regressive alterations may vary in etiology, extent and clinical presentation among individuals and may be associated with physiologic or pathologic processes. • Traditionally, those entities have been classified as attrition, erosion, and abrasion . Attrition is defined as the physiologic loss of tooth structure as a result of the masticatory processes. • Erosion is the chemical dissolution of structure that does not involve the carious process; and Abrasion is the mechanical wearing away of structure.
  • 52. FORMS OF WASTING ARE Erosion : •Tooth surface loss caused by chemical or electrochemical action is termed 'corrosion.' (John O,2004) •Cupping of occlusal surfaces(incisal grooving)with dentin exposure •Broad concavities with smooth surface enamel , Increased incisal translucency •Sources of Erosion 1) Endogenous sources of Erosion 2) Exogenous sources of Erosion
  • 53. Endogenous sources of Erosion Bulimia produces a unique pattern of enamel loss. The corrosion, called perimolysis, is most marked on the palatal surfaces of maxillary anterior teeth and, in more severe cases, on the buccal surfaces of posterior teeth. This pattern is consistent with the head's position while vomiting. The forcefully directed movement of the vomitus, which has a mean pH of 3.8, determines the site and extent of dental Erosion
  • 54. Exogenous sources of Erosion. It has been reported that any food substance with a critical pH value of less than 5.5 can become a eroded and demineralize teeth. This may occur as a result of consuming and/or mulling highly acidic foods and beverages such as mangoes and other citrus fruits, drinking carbonated soft drinks and sucking sour candies.
  • 55. ABRASION : • The pathological wearing away of tooth structure resulting from direct frictional forces between the tooth and the external objects or from frictional forces between contacting teeth components in the presence of an abrasive medium. • Forms of dental abrasion may be related to habit or occupation. • Tooth brushing is the most common cause.(Kitchen PC,1941) • Notching of incisal edges may be caused by pipe smoking, nut and seed cracking, nail biting, and hairpin biting. • The appearance is commonly described as saucer shaped or wedge shaped indentations with a smooth and shiny surface • If teeth are worn on their occlusal surfaces, incisal surfaces or both by friction from the food bolus,this wear is termed “masticatory abrasion”(John O,2004) • The teeth most commonly affected are premolars and canines.
  • 56. ATTRITION : • The physiological wearing away of the tooth structure as a result of tooth to tooth contact as in mastication of abrasive foods or Para functional activity such as bruxism. • This is an age-related process that can occur at the incisal or occlusal surfaces and sometimes on the proximal surfaces. • Clinically, the first manifestation is the appearance of a small polished facet on a cusp tip or ridge or an incisal edge. • Shiny ,smooth and curviplanar facets.In severe attrition- cuneiform occlusal surface. • Occlusal and incisal attrition can occur during deglutition and clenching; (Kydd WL,1957) • Proximal attrition (which occurs at contact areas) can cause a reduction of the dental arch(Murphy TR,1964) • Severe attrition may lead to dentinal exposure, which may increase the rate of wear.
  • 57. ABFRACTION : • Abfraction is the microstructural loss of tooth substance in areas of stress concentration.(Grippo JO,2004) • This occurs most commonly in the cervical region of teeth, where flexure may lead to a breaking away of the extremely thin layer of enamel rods, as well as microfracture of cementum and dentin. • These lesions, which appear to result from occlusal loading forces, frequently have a crescent form along the cervical line, where this brittle and fragile enamel layer exists. (Lee WC,1984) • This is believed to cause V-shaped depressions on the side under tension and C-shaped depressions on the side under compression. • Mechanical microcracks on cementum and dentin may act as the initial contributor to the formation of cervical defects. • Abfraction has a possibility of being the initial factor and the dominant progressive modifying factor in producing cervical lesions. CERVICAL ABFRACTION ON THE MANDIBULAR LEFT INCISOR
  • 58.
  • 59. ABRASION EROSION ABFRACTION The pathological wearing away of tooth structure resulting from direct frictional forces between the tooth and the external objects or from frictional forces between contacting teeth components in the presence of an abrasive medium. The loss of tooth structure by a chemical dissolution without the involvement known of bacteria (corrosion or physico-chemical wear). Abfraction is the microstructural loss of tooth substance in areas of stress concentration. CAUSE-faulty tooth brushing with highly abrasive tooth pastes CAUSE-Acidic beverages,GERD CAUSE-cervical tensile stress under cuspal loading. Loss of enamel can lead to exposed dentin •Wedge shaped ditch Usually located at the cervical areas of the teeth. The exposed dentin appears highly polished. •Lesions are more wide than deep •Cupping of occlusal surfaces(incisal grooving )with dentin exposure •Broad concavities with smooth surface enamel •Increased incisal translucency •Wear on non occluding surfaces •Loss of surface characteristics of enamel in young children •Deep, narrow V shaped notch Premolars and cuspids Palatal surface of upper anteriors single teeth with eccentric occlusal loads
  • 60. CAUSE OF DENTAL STAINS • Oral cavity is subjected to many exogenous and endogenous substances that stains the teeth. • Also the oral flora contains many type of chromogenic deposits which also causes stain deposit. • Intrinsic stains are seen in porphyria, erythroblastosis fetalis and tetracycline therapy. DENTAL STAINS : •Pigmented deposits on the teeth. Carefully examined to determine their origin.
  • 61. Types of dental stains & Physical characteristics • Extrinsic stains:(Harris, 1991). Discoloration include brown, black, gray, green, orange, and yellow. The scratch test is usually used to distinguish between extrinsic and intrinsic discoloration. • Intrinsic stains: (Shafer et al, 1983) Discoloration colours include brown, black, gray, green, orange, and yellow. Unlike extrinsic discoloration, teeth with intrinsic discoloration may be red or pink. Under ultraviolet light, teeth with tetracycline staining and congenital porphyria may fluoresce yellow or red, respectively. Intrinsic discoloration cannot be removed by using the scratch test.
  • 62. EXTRINSIC STAINS Predisposing factors • Certain factors predispose children and adults to extrinsic stains, include – enamel defects - accumulation of stain-producing food, beverages, tobacco, and other topical agents. – salivary dysfunction- decreased removal of food debris and dental plaque from the outer and interproximal tooth surfaces, – poor oral hygiene. • Deposition of tannins found in tea, coffee cause brown stains . • Tobacco stains -dark brown and black stains • Pan chewing - red-black stain on the teeth, gingiva, and oral mucosal surfaces. • Metallic compounds -Industrial exposure to iron, manganese, and silver –black stain. Mercury and lead dust - blue-green stain.(Gaffar et al., 1977).
  • 63. Contd… • Chromogenic bacteria cause stains, typically at the gingival margin of the tooth. – black stain caused by Actinomyces species. – Green stains are attributed to fluorescent bacteria and fungi such as Penicillium and Aspergillus species. – Orange stain is caused by chromogenic bacteria such as Flavobacterium lutescens. • Topical medications cause staining. – Chlorhexidine rinse causes brown staining after several weeks of use (Solheim et al, 1980), – Iron-containing oral solutions used for treatment of iron deficiency anaemia cause black stains. – Potassium permanganate mouthwash (violet-black stain), – silver nitrate (black stain), – stannous fluoride (brown stain) – systemic medications (e.g. minocycline, doxycycline) can also cause extrinsic staining.
  • 64. Red extrinsic stain at gingival margin and interproximal and incisal region-habit of chewing pan. Sever tobacco stain
  • 65. Causes of intrinsic dental stains • Numerous causes for intrinsic tooth discoloration exist. • Stain distribution varies from localized (e.g. 1 or 2 teeth) to a regional or generalized involvement of primary and secondary teeth. • Following are some of the causes of intrinsic stains. • Dental restoration (Feinman et al., 1987) • Amalgam restorations can generate corrosion products leaving a gray-black colour in the tooth • Composites, and glass ionomer and acrylic restorations gradually can leave a gray hue in the tooth adjacent to the material. • Other dental materials that cause intrinsic discoloration include eugenol, root canal sealers, and polyantimicrobial pastes. – The erosion of enamel can lead to a yellow tooth discoloration. – Caries
  • 66. – Trauma can cause intrapulpal hemorrhagic and iron sulfide deposition along the dentinal tubules, producing a bluish black cast. – Periapical odontogenic infections, maternal rubella or cytomegalovirus infection and toxaemia of pregnancy and Systemic postnatal infections (e.g. measles, chicken pox, streptococcal infections, scarlet fever) can also cause enamel hypoplasia – MEDICATION- (McEvoy, 1989a) • Tetracyclin-When the affected teeth first erupt, they have a bright-yellow band like appearance that fluoresces under ultraviolet light, although upon exposure to sunlight, the color gradually changes to gray or brown • Minocyclin- a green-gray or blue-gray colour • Doxycycline – Flourosis – Genetic defects in enamel or dentin formation include amelogenesis imperfecta , dentinogenesis imperfecta , and dentinal dysplasia . (Shafer et al., 1983)
  • 67. Intrinsic dental discoloration caused by trauma to the mandibular incisors that led to pulpal necrosis. Tetracycline staining of mandibular teeth caused by the ingestion of tetracycline when the patient was aged 3 years. Severe fluorosis of the teeth.
  • 68. HYPERSENSITIVITY : DIAGNOSIS- Root surfaces exposed by gingival recession may be hypersensitive to thermal changes/tactile stimulation located by gentle exploration with a probe/cold air. EVALUATION •MECHANICAL STIMULATION •CHEMICAL(ELECTRICAL) STIMULATION •DEHYDRATING(EVAPORATIVE) STIMULI •THERMAL STIMULATION
  • 69. OBJECTIVE EVALUATION  MECHANICAL STIMULATION-(Tactile stimuli) Pader M 1998 • Sharp Dental explorer or Yeaple probe is used to identify regions of sensitive dentin. • Subjects will then evaluate their level of tactile sensitivity using a Verbal Rating Scale (VRS). 0 - no discomfort 1 - mild discomfort 2 - marked discomfort 3 - marked discomfort that lasted more than 10 sec DEHYDRATING(EVAPORATIVE) STIMULI(Kleinberg et al,1990) • Evaporation of fluids from dentin is seen when relatively dry air is directed at a tooth. The time is within a second. The direction of air blast should be 90 degrees to dentin.
  • 70. CHEMICAL(OSMOTIC) STIMULATION • This requires the use of very HYPERTONIC solution to induce enough fluid movement to cause pain. • A cotton pellet saturated with the solution(Sucrose or Calcium chloride) is placed on the suspected area. ELECTRICAL STIMULATION • Directly stimulates pulpal nerves. • Evaluates only the presence or absence of pulp vitality. THERMAL STIMULATION • In using cold water, each tooth is isolated with a rubber dam and then water at known temperature is slowly flowed on exposed dentin surfaces for a maximum of 3 sec.
  • 71. FOOD IMPACTION • FOOD IMPACTION-Forceful wedging of food into the periodontium by occlusal forces • CAUSE(Hirschfeld,1930) – Uneven occlusal wear – Light or open proximal contact – Extrusion – Congenital morphologic abnormalities – Faulty restorations – Excessive anterior open bite – Plunger cusp • PLUNGER CUSP-Cusps that tend to wedge food forcibly into interproximal embrasures – As teeth wear down ,their originally convex proximal surfaces become flattened and wedging effect of the opposing cusp is exagerrated – Missing teeth are not replaced and the relationship between proximal contacts of adjacent teeth is altered
  • 72. PROXIMAL CONTACT RELATIONS: •Slightly open contacts - permit food impaction. •Tightness of contacts - Checked by means of clinical observation & with Dentalfloss •Abnormal contact relationships may also initiate occlusal changes.Such as: Shift in the median line between incisors. Labial version of the maxillary canine Buccal/lingual displacement of the posterior teeth Uneven relationship of the marginal ridges
  • 73. OPEN BITE RELATIONSHIPS(Hirschfeld,1930)  Abnormal vertical spaces exist between the maxillary and mandibular teeth.  Accumulation debris, calculus formation,  Mechanical cleansing by the passage of the food.  Most often occurs in anterior region. Posterior open bite is occasionally seen.  Mouth breathing habit-marginal & papillary gingivitis- maxillary anterior region  No effect on prevalence or extent of gingivitis except when large amounts of calculus is present  Crowding of teeth aggravates (Alexander A,1970)
  • 74. • Most frequently in the anterior region may cause . Impingement of the teeth on the gingiva, food Impacation. • Attachment loss ,gingival inflammation, gingival enlargement and pocket formation. • Food impaction on the lingual surface of maxillary anterior teeth and facial surface of opposing mandibular teeth Excessive Overbite :(Hirschfeld,1930)
  • 75. CROSSBITE : Normal relationship of the mandibular teeth to the maxillary teeth is reversed. Maxillary teeth being lingual to the mandibular teeth. Crossbite may be unilateral/bilateral. Leads to: TFO, Food impaction, Flaring of the mandibular teeth, associated gingival and periodontal disturbances. Check for Functional Occlusal Relationships : Important part of the diagnostic procedure. Dentitions that appear normal when the jaws are closed may present marked functional abnormalities.
  • 76. MOUTH ODORS INTRODUCTION • Also termed as fetor exore, fetor oris and oral malodor, bad breath. • Common complain of adult population .Prevalence may be as high as 50%, in most cases originate from oral cavity. • In many studies but not all, periodontal disease related parameters have been found to be associated with bad breath levels. • DEFINITION – “It is foul or offensive odor emanating from the oral cavity.” – First described by howe in 1874.
  • 77. ETIOLOGY MULTIFACTORIAL ETIOLOGY 1. Local factors of pathologic origin  -Poor oral hygiene  -Extensive caries  -Gingivitis and Periodontitis  -Open contact which allows food impaction -Vincent’s disease -Hairy or coated fissured tongue -Dry socket  -Necrotic tissue from ulceration  -Cyst with fistula draining in oral cavity • 2. Local factors of non pathologic origin  In the morning due to lack of cheek and tongue movement,(Collins,1987)  Smoking.  Denture traps food debris and causes denture breath.
  • 78. EXTRAORAL SOURCES OF MOUTH ODOUR  ENT(Rosenberg,1996)  Bronchial and lung(Lorber,1975)  Gastro intestinal tract (Norfleet,1993)  Liver-liver insufficiency(cirrhosis)-sweetish amine odour(Chen S,1970)  Alcoholics- Alcoholic breath  Systemic metabolic disease-Diabetes- Acetone odor  Kidney dysfunction- Ureamic breath  Halitosis due to xerostomia (Kleinberg,1995)  Hormonal –increase in progestrone level during menstrual cycle  Medications-metronidazole, antineoplastic agents ,diuretics,etc  Eucalyptus containing medication  Arsenic smells of rotten eggs
  • 79. PATHOGENESIS • The most common cause of mouth odor is being local causes. • Sulphur compounds such as indole & volatile sulfur compounds hydrogen sulphide, methylmercapten and dimethyl sulphide (Tonzetich,1977)
  • 80. Diagnosis of halitosis through  Medical history  Clinical / laboratory examination  Self examination  Organoleptic Rating  Specific character of breath odor  Portable volatile sulfide monitor  Gas chromatography  field or phase contrast microscopy  Saliva incubation test  Electronic nose
  • 81. SALIVARY GLANDS • These are exocrine glands that are responsible for the secretion of saliva • The salivary glands are categorized as major and minor • The major salivary glands are the parotid, submandibular and sublingual glands • Minor glands that produce saliva are located in the lower lip, tongue, palate, cheeks and pharynx
  • 82. • The major salivary glands contribute to maximum saliva production. The average daily flow of saliva is between 1 to 1.5 liters in healthy individuals. Percentage contribution from different salivary glands are as follows: • Parotid gland: 20% • Submandibular:65% • Sublingual: 7 to 8% • Minor salivary glands: 10% These percentages are described for unstimulated whole saliva. Stimulated high flow rates change the percentage contribution from different salivary glands with the maximum from parotid gland:50%(serous)
  • 83. SALIVA FLOW • There is a great variability in salivary flow rates in different persons • The accepted flow rate of unstimulated saliva is anything above.1 ml per minute. For stimulated saliva, the accepted norm is .2 ml per minute. Salivary flow is highly individualized and should be recorded. • On an average, the flow rate for unstimulated saliva is .3 ml per minute. With the average total of 16 hours of unstimulated flow being 300 ml. (Fox et al,1987) • Stimulated flow of saliva is 7 ml per minute on an average. Stimulated saliva is supposed to contribute as much as 80 to 90 % of the daily secretion.(Daniel et al,1984)
  • 84. Quality and quantity of saliva Protective and maintain oral soft tissue in a physiologic state •Plaque is mechanically cleansed by saliva from oral surfaces. •By buffering acids produced by bacteria. •Controlling bacterial activity. Antibacterial factors Salivary antibodies • Preponderant Ig A. (secretary) • Lesser amount Ig G and Ig M. Salivary secretion decreases in certain conditions causing xerostomia Salivary secretion increases whenever local irritation in oral cavity & in certain gingival disease states
  • 85. QUANTITY OF SALIVA Physiological Causes • In the same individual, salivary flow has a circadian rhythm • Salivary flow is minimum to zero in the night and peaks during the day • In the year low salivary flow rates occur in summer and peak in winter • In the mouth, there are areas with high and low flow. The mandibular lingual areas have high flow while maxillary anteriors have a low flow rate Pathological Changes Xerostomia(Fox et al,1987) • Medications - – Antihypertensives, antidepressants, analgesics, tranquilizers, diuretics and antihistamines – Cancer Therapy - Chemotherapeutic drugs can change the flow and composition of the saliva. – Radiation treatment that is focused on or near the salivary gland • Sjogren's syndrome - An autoimmune disease, • Other conditions -such as bone marrow transplants, endocrine disorders, stress, anxiety, depression, and nutritional deficiencies may cause xerostomia. • Nerve Damage - Trauma to the head and neck area from surgery or wounds can damage the nerves that supply sensation to the mouth.
  • 86. Ptyalism • Medications – central nervous system depressants such as barbiturates, anticholinergics such as belladonna alkaloid. (Van Dinter MC,1991) • During pregnancy • Oral infections-abscesses,Respiratory diseases,gastrointestinal,cardiovascular causes • Neoplasia • Pain
  • 87. Quality of Saliva • Systemic Diseases(hereditary, autoimmune, malignancy, and infectious) – congenital adrenal hyperplasia – Cystic fibrosis – Sjögren's syndrome • Viral diseases – Herpes virus,HIV,CMV,EB virus • Medications – Antipyrine – Caffeine – Carbamazepine
  • 88. • patient’s response to a health questionnaire and the outcome of clinical evaluation as the basis for identification and assessment of dry mouth. For example, “yes” responses to the following four questions have been significantly associated with salivary gland hypofunction: – Does the amount of saliva in your mouth seem too little? – Does your mouth feel dry when eating a meal? – Do you have difficulty swallowing any food? – Do you sip liquids to aid in swallowing dry food?(Fox PC,1987) • Visual Analogue scale, an ordinal scale based on rank-ordered categories (for example, I have no/slight/severe/ annoying feeling of dry mouth) or both to assess salivary gland function. • Objective measurements of qualitative or quantitative changesin saliva are best captured by collecting saliva from individual glands or from all that contribute to whole saliva. (avazesh M, 1982) • Commonlyused stimulants include – gum base, paraffin wax, rubber bandsand citric acid. Secretagogues such as pilocarpine and cevimeline hydrochloride ( Chambers MS, 2007) – mechanical stimuli such as a transcutaneous electrical nerve stimulator and powered toothbrushes have been used to stimulate salivary flow. (Hargitai IA,2005) DIAGNOSIS
  • 89.
  • 90. SOFT TISSUE EXAMINATION • Floor of mouth • Oropharyngeal region • Tongue • Lips
  • 91. • Soft tissue should be examined for o -Keratotic or nonkeratotic white lesions o -Ulcerative lesions o -Vesiculobullous lesions o -Precancerous lesions Particularly in case of desquamative gingivitis, oral soft tissue examination is very important.
  • 92. PLAQUE AND CALCULUS : • Many methods for assessing plaque and calculus accumulation. • Supragingival plaque and calculus  Directly observed  amount measured with a calibrated probe. • Sub gingival calculus :  Each tooth surface is carefully checked to the level of the gingival attachment with a sharp explorer no. #17or #3A explorer.  For Visualization of the Calculus : • Warm air may be used to deflect the gingiva
  • 93. EXAMINATION OF PERIODONTIUM GINGIVA • Color • Generally described as coral pink, produced by • Vascular supply • Thickness and degree of keratinization • Presence of pigment containing cells(Dummett,1946)
  • 95. CONTOUR AND FORM • Is related to teeth, underlying bone and presence or absence of disease. • Normal gingiva: tissue fills interdental space and gingival margin ends in a knife like edge coronal to CEJ and interdental papilla are tucked beneath contact points. • Depends on -Shape of teeth. -Alignment in the arch. -Location & size of the area of proximal contact. -Dimensions of facial & lingual embrasures. -Caries • The marginal gingiva follows scalloped outline on the facial and lingual surfaces. • Gingival contour changes with gingival enlargement such changes may also occur in other conditions. e.g. Stillman’s cleft ,Mc call’s festoons.
  • 96. • Marginal gingiva in diastema-Flat or saddle shaped • In disease- • Marginal gingiva-Rounded or rolled out • IDP- – Bulbous – Flattened – Blunted – Cratered
  • 97. • STILMAN’S CLEFT(Stilman PR,1921) – Apostrophe shaped indentations exteding from and into gingival margin for varying distance – Triangular shaped gingival recession-Common on the facial surface – Cause-occlusal trauma • Clefts are divided into – Simple Clefts – Compound clefts • MCCALL’S FESTOONS – Liver shaped enlargements of the marginal gingiva – Canines and premolar
  • 98. CONSISTENCY • It is firm and resilient with the exception of the movable free margin,tightly bound to underlying bone. • In chronic gingivitis it may be destructive with edematous soft consistency and reparative with fibrotic changes. • In case of acute gingivitis diffuse puffiness, softening, eroded surface and vesicle formation can be seen. • .
  • 99. DIAGNOSIS • DIAGNOSIS-Gently pressure ongingiva with the side of the periodontal probe. – Soft & edematous- Pits on pressure – Fibrotic,Firm & leathery- No imprint left on gingiva
  • 100. SIZE • Sum total of bulk of cellular & intercellular elements and their vascular supply. • Alteration in size is a common feature of gingival disease.
  • 101. ACUTE GINGIVAL DISEASES CHRONIC GINGIVAL DISEASES DIGO Gingival abscess-marginal gingiva or IDP Slight ballooning of IDP & marginal gingiva then to attached gingiva Bead like enlargement of IDP extending to facial and lingual margins Periodontal abscess- involves supportive periodontal tissues with gingiva Gingival abscess DIAGNOSIS
  • 102. SURFACE TEXTURE • Stipples are small regularly spaced depressions in the surface of the attached gingiva that give it an ‘orange peel’ appearance.(owings ,1969, orbans, 1948). • The absence of stippling is not a sign of disease, and conversely its presence is not necessarily a sign of gingival health.(greene,1962.) • Best viewed by drying the gingiva • Attached gingiva and center of interdental papilla is stippled. • Microscopically produced by alternate rounded protuberances and depressions in the gingival surface. The papillary layer of connective tissue projects into the elevations and the elevated & depressed areas covered by epithelium.
  • 103. DIAGNOSIS - Best viewed by drying the gingiva Healthy gingiva- small regularly spaced depressions in the surface of the attached gingiva that give it an ‘orange peel’ appearance PHYSIOLOGIC • Stippling varies with age. Absent in infancy, appears in some children at about 5 years of age, • Increases until adulthood and • Begins to disappear in old age. PATHOLOGIC • Loss of surface stippling is an early sign of gingivitis. • In chronic inflammation -the surface is either smooth & shiny or firm & nodular, depending on whether the dominant changes are exudative or fibrotic. • In atrophic gingivitis- gingival atrophy is seen • In desquamative gingivitis- peeling of surface • Drug induced gingival overgrowth- nodular surface and leathery
  • 104. Magnified model of the outer surface of the oral epithelium of the attached gingiva. The surface exhibits minute depressions. Subsurface of epithelium characterised by the presence of ridges.
  • 105. POSITION • Refers to the level at which the gingival margin attached to the tooth. when the tooth errupts in the oral cavity the margin and the sulcus are at the tip of the crown, as the erruption progresses, they are seen closer to the tooth. • The position of the gingiva on the surface of the tooth changes with time. • When the tooth first reaches the plane of occlusion one third to the one fourth of the enamel still remains covered by the gingiva. • Actual position is the level of epithelial attachment on the tooth. • Apparent position is the level of the crest of the gingival margin. • Visible gingival recession- clinically observed • Hidden recession- detected by periodontal probes
  • 107. Gingival recession Gingival recession is the exposure of the root surface by an apical shift in the position of the gingiva. •Recession is often of major concern to patients since it is a readily visible manifestation of periodontal damage and can cause esthetic problems when it occurs around anterior teeth. •Indeed, many patients have a chief complaint of ‘receeding gums’. Therefore, at the initial examination it is important to record the amount and location of gingival recession.
  • 108. Etiology: • Anatomy of the buccal plate of alveolar bone. • Periodontal disease • Frenum pulls • Overzealous tooth brushing • Dentifrice Abrasivity • Non surgical procedures (Root planing) and surgical periodontal Procedures • Orthodontic movement of teeth or roots outside the alveolar housing • Root prominence in the presence of thin mucosa • Chronic use of fingernails , toothpick or placement of tongue or lip jewellery and studs.
  • 109. • Classification of Recession-By Sullivan & Atkins Four morphologic categories –shallow narrow –shallow wide –deep narrow –deep wide
  • 110. BY P.D.MILLER(1985) Class-I This includes marginal tissue recession that does not extend to the mucogingival junction. There is no loss of bone or soft tissue in the interdental area. This type of recession can be narrow or wide. Class-II Consists of marginal tissue recession that extends to or beyond mucogingival junction. There is no loss of bone or soft tissue in the interdental area. Sub classified into wide and narrow. Class-III There is marginal tissue recession that extend to or beyond the mucogingival junction in addition there is bone &/or soft tissue loss interdentally or there is malpositioning of teeth. Class-IV There is marginal tissue recession that extend to or beyond the mucogingival junction with severe bone and soft tissue loss interdentally &/or severe tooth malposition.
  • 111. FRENUM • A frenum is a fold of mucous membrane, usually with enclosed muscle fibers, that attaches lips and cheeks to the alveolar mucosa &/or gingiva and underlying periosteum. Tension test • A frenum becomes problem if the attachment is too close to the marginal gingiva. Tension on the frenum may pull the gingival margin away from the tooth. This condition may be conductive to plaque accumulation an inhibit proper brushing of teeth.
  • 112. Classification of Frenum(Placek et al,1974) • Mucosal • Gingival • Papillary • Papilla penetrating DIAGNOSIS- • PULL TEST-Lip is stretched-gingival margin or papilla is moved awaynfrom the tooth • BLANCHING TEST-On stretching frenum blanching is produced at the base of the frenum.
  • 113. ANKYLOGLOSSIA • CLASSIFICATION 1. Clinically acceptable,normal range of free tongue:greater than 16mm 2. CLASS I:Mild ankyloglossia:12 -16mm 3. CLASS II:Moderate ankyloglossia:8-11mm 4. CLASS III: Severe ankyloglossia:5-7mm 5. CLASS IV:Complete ankyloglossia:less than 3mm
  • 114. DIAGNOSIS • Tip of the tongue should:(Ayer F,1977) – protrudes outside mouth without clefting – Sweep the upper and lower lip,without straining – Normal swallowing pattern – Speech difficulties
  • 115. Mucogingival junction • The apical boundary of the attached gingiva is located at the mucogingival junction where the cornified epithelium merges abruptly with the non cornified epithelium of the alveolar mucosa (Schroeder et al) • Stable landmark probably genetically predetermined.(Ainamo et al.)
  • 116. Methods to identify mucogingival junction • Jiggling Method (Roll Method) Place the blunt end of an instrument over the alveolar mucosa and roll or jiggle coronally, the alveolar mucosa will bulge at the mucogingival junction
  • 117. Anatomical method By distinguishing between color of attached gingiva and alveolar mucosa
  • 118. Schiller’s Iodine solution Stains the alveolar mucosa and thus demarcates the mucogingival junction Local Anesthesia Inject LA into alveolar mucosa ; it swells up (elastic fibers)
  • 119. ALVEOLAR MUCOSA – Darker red. – Apical to Mucogingival junction – Loosely bound to the underlying bone. – Epithelium-Thin non keratinised stratified squamous epithelium – Mucosa –short papilla,Elastic fibres and capillary loops. – Lamina propria and submucosa of alveolar mucosa contain numerous elastic fibres.
  • 120. WIDTH OF ATTACHED GINGIVA • “Distance between the mucogingival junction and the projection on the external surface of the bottom of the gingival sulcus or periodontal pocket.” • Adequate amount of attached gingiva is detected by a positive or a negative tension test. . Adequacy of attached gingiva is important in maintenance of proper cleanliness around that particular tooth. . Inadequacy = increased alveolar mucosa which usually gets hurt during brushing so patients avoid cleaning that area. • Greatest in incisors – Maxilla -3.5 to 4.5mm, – Mandible -3.3 to 3.9mm. • Least in first premolar – Maxilla -1.9mm, – Mandible -1.8mm. • Width of attached gingiva increases with age and in supraerupted teeth. .(Ainamo et al.)
  • 121.
  • 122. The horizontal probe has located the mucogingival junction (the most apical area where nonmovable tissue is found), while other probes measure the probing depth (2 mm) and the width of the keratinized gingiva (7 mm). In this example, the amount of attached gingiva is 5 mm. The amount of attached gingiva can be recorded on the chart, or the relative amount, no attached gingiva (NAG), or minimal attached gingiva (MAG) can be indicated.
  • 123. VESTIBULAR DEPTH • Measured from gingival margin to the depth of vestibule. • ETIOLOGY for reduced vestibular depth – Physiological – Gingival recession • Reduced vestibular depth –oral hygiene measures jeopardized – Placement of removable prosthesis
  • 124. EXUDATE ON DIGITAL PRESSURE • At times found in gingivitis but most often in chronic periodontitis • PUS-Neutrophil rich exudate • Presence-Site is inflamed and infected • Not a good stand alone predictor of the progression of chronic periodontitis(Armitage GC,1996) • Seen in large amount in periodontal abscess  Clinically presence of pus is determined by placing the ball of the index finger along the lateral aspect of the marginal gingiva and applying pressure in a rolling motion toward the crown.
  • 125. BLEEDING ON PROBING • The insertion of a probe to the bottom of the pocket elicits bleeding if the gingiva is inflamed and the pocket epithelium is atrophic or ulcerated. • Objective sign of gingival inflammation.It is an earlier sign than color changes. • Depending on the severity of the inflammation bleeding can vary from a tenuous red line along the gingival sulcus to profuse bleeding.
  • 126. BLEEDING ON PROBING • Bleeding on probing is not a good diagnostic predictor for CAL.Absence of gingival bleeding –low risk of future attachment loss(long et al,1990) • When to probe For diagnosis Monitoring course of treatment Monitoring maintenance • Probing around implants To prevent scratching of the implant surface, plastic probes should be used instead of steel probes. • At the initial examination the percentage of sites that exhibit bleeding on probing prior to treatment is a clinically useful piece of information since it provides a full mouth pre treatment assessment of the extent of gingival inflammation
  • 127.
  • 129. FACTORS TO CONSIDER EVALUATING AT THE INITIAL PERIODONTAL EXAMINATION Medical Periodontal Radiographic Systemic diseases Gingival status Appropriate and diagnostic radiographs Medications Gingival recession Pattern of bone loss Medical consultations Periodontal probing Accretion Prophylactic antibiotics Loss of attachment Root caries Risk factors Mobility Crown-to-root ratio Family history Furcation involvement Periapical pathology Age Mucogingival defect Widened periodontal ligament Halitosis Food impactions Overhanging restorations Mental status Poor margins on restorations Root proximity Physical and dexterity statuses Occlusal examination Root trunk length TMD*/Parafunctional habits Restorative rehabilitation *TMD: Temporomandibular joint disorder. Some clinical information on TMD may be gathered at the initial periodontal examination, but a comprehensive evaluation of the Temporomandibular joint requires radiographs
  • 130. PROBING Periodontitis is characterized clinically by loss of attachment (LOA) and the formation of pockets and osseous defects. The documentation of LOA is essential in establishing baseline data, monitoring treatment results, and determining periodontal stability. Probes vary in design by length, thickness, and millimeter markings.
  • 131.
  • 132. The probe is inserted gently into the gingival sulcus and stepped around the tooth at about 1 mm increments. The probe should be kept as close as possible to the axial direction of the tooth while the tip remains in contact with the root surface. Measurements are made from the gingival margin for pocket depth and from the cementoenamel junction (CEJ), or a similar fixed point, to the gingival margin for recession. PROBE WALKING
  • 133. • Characteristics of a good periodontal probe include a thin shaft with a rounded tip, durable markings that are easily read, and ease of sterilization. Commonly, six measurements are recorded per tooth. • Special attention should be directed to detecting the presence of interdental craters and furcation involvement. • Naber’s probe is used specially for easier and more accurate exploration of the horizontal component of furcation lesions. • The probing depth and recession measurements added together determine the LOA. • Factors such as the health of the surrounding gingiva, probing force applied by the operator, and discomfort tolerance of the patient can make a difference of 1 to 2 mm in probe readings.
  • 134.
  • 135. PERIODONTAL POCKET • It is a pathologically deepened gingival sulcus. • Classification – Gingival pocket- Pseudo pocket . – Periodontal pocket • Two types – Suprabony (Supracrestal /Supraalveolar) – Intrabony (Infrabony /Subcrestal or Intra alveolar) • According to involved tooth surfaces it may be classified as – Simple pocket – Compound pocket – Complex pocket
  • 136. • Signs -Color changes to bluish red -Rolled edge of gingival margin -Edematous gingiva -Presence of bleeding -Suppuration -Loose extruded tooth. • Symptoms -generally painless or localized or dull radiating pain. -sensation of pressure after eating. -foul taste in localized area. -sensitivity to hot and cold. -toothache in absence of caries.
  • 137. DETECTION OF POCKETS(Armitage,2004) •The only accurate method of detecting and measuring periodontal pockets is careful exploration with a periodontal probe. •Gutta purcha points or calibrated silver points can be used with the radiograph to assist in determining the level of periodontal pockets.
  • 138. POCKET DEPTH • The biologic depth is the distance between the gingival margin and the base of the pocket, measured only in carefully prepared & adequately oriented histologic sections. • The probing depth is the distance to which an ad hoc instrument (probe) penetrates into the pocket. • Depth of penetration depends on - Size of the probe - Force with which it is introduced - condition of gingival tissue - angulation of the probe • The probing forces have been explored by several investigators, forces of 0.75N have been found to be well tolerated.
  • 139. TRANSGINGIVAL PROBING Introduced by Laser & Listgarten (1976) Transgingival probing or sounding, under local anesthesia confirms the extent and configuration of the intra bony component of the pocket or furcation defect.
  • 140. Prior to surgical therapy it is highly desirable to have an accurate assessment of bony defect morphology. This allows development of a surgical treatment plan that best addresses the degree of existing periodontal destruction. Revert et al (1981) found a mean difference of 0.3mm between transgingival probing and surgically determined bone level. Ursell (1989) reported a mean difference of 0.12mm intra bony defects it was found to be less accurate than horizontal defects.
  • 141. To obtain the most accurate manual readings, use a thin probe positioned as parallel to the long axis of the tooth as possible PROBING OF POCKETS
  • 142. LEVEL OF ATTACHMENT VERSUS POCKET DEPTH POCKET DEPTH • It is the distance between the base of pocket and the gingival margin. LEVEL OF ATTACHMENT • The distance between the base of the pocket and the cementoenamel junction. • It is a better indication because changes in the level of attachment can only be due to gain or loss of attachment and periodontal destruction.
  • 143.
  • 144. DETERMINING THE LEVEL OF ATTACHMENT • Gingival margin on anatomic crown-Level of attachment = pocket depth - distance from gingival margin to C-Ejunction. • Gingival margin coincides with C-E junction - Loss of attachment = pocket depth • Gingival margin apical to C-E junction-Loss of attachment = pocket depth + distance between the C-E junction and gingival margin.
  • 145. Advances in measurement of periodontal attachment loss 1)Tolerance method to determine thresholds for probing measurements This method uses two replicate measurements of each site which are made for each subject. Their standard deviation is then calculated.. Thus using this method any change below 3mm is considered to be unreliable and this makes it possible to measure small changes of attachment using manual probing. 2) Computer linked electronic constant pressure probes currently available includes: The Florida probe incorporates constant force, precise electronic measurement and constant storage of data. The Interprobe which has an optical encoder transduction element. The Birek probe which works by constant air pressure and uses the occlusal surface as its reference point . The Jeffcoat probe automatically detects CEJ.
  • 146. FURCATION INVOLVMENT •In treating molar teeth, it is essential to differentiate furcation involvement on the basis of severity and to keep a record of the observed data and the treatment decisions involved. •In general, a furcation is a common site for active bone loss accompanying periodontitis. •Some studies report that the most common sites of recurrent periodontitis are the distal furcations on the maxillary first molars. (Larato,1970) •Problems with plaque control in involved furcations may be explained by these differences.
  • 147. Facial furcations for a maxillary (A) and a mandibular (B) first molar. The portion of the furcation facing apicaily or toward the bone is the vault (vt), or roof. The vertical concavity on the common root trunk is the flute (fl). FURCATION FLUTES
  • 148.
  • 149. NABER’S probes are useful for mesial and distal furcae of maxillary molars and interproximal furcae of maxillary premolars. The furcae can be classified in one of the following manners: Approach 1 Class I : A depression that does not catch a curette or probe Class II : A furca deep enough to catch a curette or probe but does not contiguous with other furcae on the same tooth Class III : Through-and-through bone loss Standard probes can be used horizontally in buccal and lingual furcae. When combined with the determination of vertical probing depths, this approach is an accurate way to quantify bone loss. FURCATION INVOLVEMENT
  • 150. Clinical probing: • In maxillary molars the mesial furcation entrance is located closer to the palatal than to the buccal surface.thus the mesial furcation should be probed from the palatal aspect. • The distal furcation entrance is present midway between the buccal and palatal surface hence this furcation could be probed from either the buccal or the palatal aspect. Palatal approach for mesial furcation in maxillary molar.
  • 151. • Due to anatomic variations and limited access, the clinical assessment of furcation involvement in maxillary premolars is often difficult. Furcation in maxillary premolar
  • 152. • Probing of the mandibular furcations is relatively easy because there are only buccal and lingual entrances,each located midway mesiodistally. • Vertical attachment loss on the adjacent roots should be probed at the furcation line angle of each root,angling the probe somewhat,to place the tip of the probe slightly into the furca. • Bone sounding or transgingival probing should be done to determine the bone contours associated with FI more accurately after anesthetizing the soft tissue.(Easley,Greenberg,Listgarten).
  • 153. CLASSIFICATION Glickman classified FI into 4 grades Grade I: Pocket formation into the flute of the furcation,but the interradicular bone is intact. Grade II: Loss of interradicular bone and pocket formation of varying depths into the furcation but not completely probable to the opposite side of the tooth. Grade III: Complete loss of interradicular bone with pocket formation that is completely probable to the opposite side of the tooth. Grade IV: Loss of attachment and gingival recession that has made the entire furcation clearly visible to clinical examination.
  • 154. Glickman’s classification of furcation involvement Goldman and Cohen have incorporated a descriptive classification of FI referring to Grade I incipient Grade II cul-de-sac Grade III through and through.
  • 155. TOOTH MOBILITY: • Mobility is evaluated by placing an instrument on the facial and lingual surfaces and a finger on the appearance side of a tooth and applying pressure while rocking the tooth. If the tooth being tested has no adjacent tooth, the instruments and pressure should be applied obliquely and mesiodistally. A “normal” tooth has a minute amount of “give” to it (ie, is not ankylosed). (O Leary,1969) • All teeth have a slight degree of physiologic mobility. Varies for different teeth and at different times of the day. Increased mobility in morning & progressively decrease(O Leary,1963)
  • 156.
  • 157. • NORMAL TOOTH MOBILITY-More during early mornings and progressively decreases – 4-12/100mm for 500g force applied(Muhleman,1954) • REDUCED TOOTH MOBILITY-Ankylosed teeth after failing replantation or autogenous bone grafts are placed in contact with detached root surface(Lindhe,1997) • ALTERED TOOTH MOBILITY-It represents transient or permanent change in mobility . – Increased or decreased as a result of therapy(Lindhe,1997)
  • 158. • INCREASED or STATIC TOOTH MOBILITY-It is a form of stabilized mobility – Due to TFO but may be due to periodontal diseases. (Lindhe,1997) • HYPERMOBILITY(Residual Mobility)-Increased mobility persisting after completion of periodontal treatment – Developing Phase – Permanent Phase(Ramfjord S.P.,1981) • INCREASING/PROGRESSIVE MOBILITY-Progressive nature & can be identified anly through a series of repeated mobility measurements carried out over a period of several days or weeks(Lindhe,1997)
  • 159. Tooth mobility occurs in 2 stages (Mulemann,1954) The Initial/Intrasocket stage :  Tooth moves within the confines of the periodontal ligament.  Associated with viscoelastic distortion of the ligament and redistribution of periodontal fluids, interbundle contact,fibers.). • The secondary stage :  Occurs gradually.  Entails elastic deformation of the alveolar bone in response to increased horizontal forces..
  • 160.
  • 161. GRADING OF MOBILITY : The clincian can the use a modification of the Lindhe scale, as recommended by Fleszar et al Class 0 : Physiologic mobility, firm tooth Class I : Slightly increased mobility Class II : Definite to considerable increase in mobility, but no impairment of function Class III : Extreme mobility; a loose tooth that would be uncomfortable in function
  • 162. Miller mobility index • A tooth that moves more than this minute amount but in a total arc of less than 1 mm has Class 1 mobility. • A tooth that moves in an arc of 1 mm or more but less than 2 mm has Class 2 mobility. • A tooth that moves in an arc of 2 mm or more and can be depressed into its socket has Class 3 mobility.
  • 163. PHYSIOLOGIC CAUSES  Tooth mobility is increased in pregnancy. (Rateitschak,1967)  Circadian rhythm  Age(Wasserman,1973)  Higher in females and negroes (Wasserman,1973)  Menstrual cycle (Burdein,1970)  Oral contraceptives ( Knight,1967) PATHOLOGIC CAUSES  Also increased by hypofunction.  Mobility produced by TFO occurs initially as a result of resorption of cortical layer of bone leading to reduced fiber support, and later as an adaptation phenomenon resulting in a widened periodontal space.  Extension of inflammation from the gingiva/from the periapex into the periodontal ligament -. Eg.Periapical abscess in the absence of periodontal disease.  Periodontal surgery : Temporarily (Persson,1981)  Pathologic processes of the jaws that destroy the alveolar bone and /or roots of the teeth. Eg. Osteomyelitis and tumours
  • 164. ADVANCES • More precise and objective measurement of tooth mobility has been pursued and includes mechanical, electronic and optical devices, and laser Doppler vibrometry. • Mobilometers-Elbrecht’s indicator,Werner’s oscillator. • Periotest-evaluates damping charecteristics of teeth
  • 165. • The term traumatic occlusion was introduced by Stillman in 1917. • Later, in 1922, Stillman and McCaII stated, "Traumatic occlusion is an abnormal occlusal stress which is capable of producing or has produced an injury to the periodontium.” WHO in 1978 defined trauma form occlusion as “ the damage caused by stress on the teeth produced directly or indirectly by teeth of the opposing jaw.’’ Glossary of Periodontic terms, 1986 defined TFO as “ an injury to the attachment apparatus as a result of excessive occlusal force” . Carranza defined TFO as a condition when occlusal forces exceed the adaptive capacity of the tissues , tissue injury results and the resultant injury is termed as trauma form occlusion. TRAUMA FROM OCCLUSION
  • 166. TFO is Classified as 1. Primary 2. Secondary Types of trauma from occlusion 1. Acute 2. Chronic
  • 167. Clinical diagnosis of trauma from occlusion A clinical diagnosis of occlusal trauma can only be confirmed where progressive mobility can be identified through a series of repeated measurements over an extended period. This means that simple but reliable monitoring needs to be undertaken.
  • 168. The common Clinical signs of occlusal trauma are: – Increasing tooth mobility and migration or drifting – Fremitus – Persistent discomfort on eating. - pathologic migration, especially of the anterior teeth
  • 169.
  • 170. Fremitus (functional mobility) is the movement of teeth during function or parafunction. Fremitus can often be detected earlier than bidigital tooth mobility and has been associated, in the presence of inflammation, with increased bone and attachment loss (pocket formation) when compared with teeth without fremitus. The photograph shows testing for fremitus. The index finger is placed on the buccals surface of the maxillary teeth, and the patient is asked to grind in lateral and protrusive movements. Any movement seen or felt is termed fremitus. Class I: Mild vibration or movement felt Class II: Easily palpable, no visible movement Class III: Movement clearly visible TRAUMA FROM OCCLUSION
  • 171. PROCEDURE 1. Set the patient upright with the head stabilized against the headrest 2. Press an index finger on each maxillary tooth at cervical third. 3. Request the patient to “click the back teeth” repeatedly. 4. Start with the most posterior maxillary tooth on one side and move index finger tooth by tooth around the arch 5. Record by tooth number the teeth vibration is felt and teeth where actual movement noted.
  • 172. PATHOLOGIC MIGRATION OF THE TEETH:Change in tooth position that occurs when there is disruption of forces that maintain teeth in a normal relationship(Chasens A,1997)  Alterations in tooth position should be carefully noted.  Premature tooth contacts in posterior region that deflect the mandible anteriorly contribute to destruction of the periodontal of the maxillary anterior teeth  pathologic migration, premolar of anterior teeth in young person - sign of JP. ETIOLOGY •Destruction of periodontal supporting tissues(Martinez,1997) •Occlusal Factors •Posterior bite collapse •Arch Integrity •Class II MO •Occlusal Interferences •Anterior component of force •Protrusive pattern of mastication •Bruxism •Shortened dental arches
  • 173. • Soft tissue pressure of the tongue ,cheek and lips(Profit W,1975) • Periodontal and Periapical inflammation (Hirschfeld,1933)-Pressure from granulation tissue • Extrusive forces • Habits DRIFTING OF TEETH-It does not results from destruction of periodontal tissues • It creates chances for periodontal diseases.
  • 174. • SENSITIVITY TO PERCUSSION:  Is a feature of inflammation of the periodontal tissues..
  • 175. DETERMINATION OF DISEASE ACTIVITY • Currently no sure method to determine disease activity. • Inactivate lesions may show little or no bleeding on probing & minimal amount of gingival fluid, the bacterial flora revealed by dark field microscopy consists of coccoid cells. • Active lesions bleed more readily on probing and have large amounts of fluid & exudate, their bacterial flora shows a greater no. of spirochetes & motile bacteria. • In patients with aggressive Periodontitis, progressing and non progressing sites may show no differences in bleeding on probing.
  • 176. VARIATION IN SOFT TISSUE & BONE • SOFT TISSUE – High frenal attachment – Shallow vestibular depth • BONE – Exostoses – Tori-mandibular & maxillary tori
  • 177. ALVEOLAR BONE LOSS • Evaluated by clinical and radiographic examination. • Probing is helpful for determining  The height and contour of the facial & lingual bones obscured on the radiograph by the dense roots.  The architecture of the interdental bone. • Transgingival probing performed after the area is anaesthetized, is a more accurate method of evaluation and provides additional information on bone architecture.(Greenberg,1976)
  • 178. PALPATION • Palpating the oral mucosa in the lateral and apical areas of the tooth may help to locate the origin of radiating pain that the patient can not localize. • Infection deep in the periodontal tissues and the early stages of a periodontal abscess may also be detected by palpation.
  • 179. SUPPURATION(Armitage GC,2004) • The presence of abundant no. of neutrophils in the gingival fluid transforms it into a purulent exudate.  It is not by itself a good indicator.  Clinically presence of pus is determined by placing the ball of the index finger along the lateral aspect of the marginal gingiva and applying pressure in a rolling motion toward the crown.  The purulent exudate is formed in the inner pocket wall and therefore the external appearance may give no indication of its presence. Pus formation does not occur in all periodontal pocket but digital pressure often reveals it in pockets where its presence is not suspected
  • 180. LABORATORY TESTING OF PATIENTS WITH SYSTEMIC CONDITIONS IN PERIODONTAL PRACTICE • In addition to the diagnosis, laboratory tests are also extremely important in assisting in the management of the patient during treatment of the disease • When unusual gingival or periodontal problems are present and cannot be explained by local causes, the possibility of contributing systemic factors must be explored. • The dentist must understand the oral manifestations of systemic disease so that he or she can question the patient’s physician regarding the type of systemic disturbance that may be involved in individual cases.
  • 181. Total WBC count 4500 – 10000/cm3 Differential WBC count Polymorphs: 55 – 70% adult 49 – 65% children Lymphocytes: 29 – 40% adult 30 – 60% children Eosinophil: 1 – 6% Monocytes: 2 – 10% Basophils: 0 – 1% Hemoglobin% - 14 – 16gm% for men; 12 – 14gm% for women Bleeding time – Duke’s Method < 5 minutes Clotting time – Wright’s Capillary Method -2 – 5 minutes ESR –Westergren mm/ first hour Males: 0-15mm Females 0-20mm Blood glucose – random 60 – 120 mg/dl Glycosylated hemoglobin: 4 - 5.9%
  • 182. EFFICACY OF DIAGNOSTIC TESTS (Greenstein,1995) • There are a few principal concepts that must be under stood by practitioners when they use diagnostic tests. The most basic of these concepts are: 1. Gold standard 2. Accuracy 3. Sensitivity 4. Specificity 5. Positive predictive value 6. Negative predictive value
  • 183. • a gold standard measure is obtained from an independent definitive diagnosis of disease presence or absence, which is usually provided by histopathologic examination of the tissues. • The basic method used to compare the diagnostic test with the gold standard is the decision matrix.
  • 184. DECISION MATRIX - GOLD STANDARD Test Result Disease Present Disease Absent Total (D+) (D-) Positive (T+) Negative (T-) TP FP TP+FP FN TN FN+TN Total TP+FN FP+TN • Here test results (test positive and test negative) tells us whether disease is truly present or absent. • This is called the accuracy of the test and is calculated as TP + TN/all tests conducted, i.e., the proportion or percentage of times that the test gives accurate results.
  • 185. SENSITIVITY (the true-positive ratio) TP/TP+FN. represents the proportion or percentage of times that the tests results help correctly identify patients with disease. SPECIFICITY (the true-negative ratio) TN/FP + TN. specificity represents the proportion or percentage of times that the test results help correctly identify patients who do not have disease.
  • 186. THE DECISION MATRIX IN A HORIZONTAL DIMENSION, CALCULATE TWO TYPES OF PREDICTIVE VALUES. POSITIVE PREDICTIVE VALUE TP/TP + FP The proportion or percentage of true-positive results of all positive results. In other words, when the test result is positive, what is the probability that the patient (or site) really has disease? NEGATIVE PREDICTIVE VALUE TN/FN + TN The proportion or % of true-negative test results of all negative test results. That is what percent do not have the disease
  • 187. • It is important to understand that both the positive predictive value and the negative predictive value are affected by disease prevalence in the population being tested • Diagnostic testing should be considered an aid to the diagnostic process—not a device or procedure that provides the diagnosis.
  • 188. THRESHOLD FOR DISEASE • When do we actually label the process being observed as Periodontal disease? • Unfortunately, in many patients there is no clear demarcation between disease and no disease. • Periodontal disease presents throughout a range from incipient to severe. • Hence it may be reasonable for practitioners to consider more than one threshold of disease at which the test result is determined to be positive to get a sense of the magnitude of risk taken when making this decision one way or the other.
  • 189. THE EXAMINATION OF PATIENTS CONSIDERED FOR IMPLANTS • Examination of patients - considered for implants includes both clinical evaluation of soft tissues and a radiographic evaluation.. • Probing around implants is difficult (Bragger U,1997) (1) the prosthetic construction may need to be removed for access (2) standard metal instruments are unsuitable. • Instead, plastic or titanium probe tips should be used to avoid damage of the implant / tissue interface. • If automatic probing is considered, the Florida Probe is available with a titanium tip that will not hurt the implant ; also, the Interprobe system comes with disposable plastic tips.
  • 190. CLINICAL EVALUATION OF DENTAL IMPLANT TREATMENT • Diagnostic procedure prior to implant placement 1. Competent treatment planning is a key to long term success of implant therapy. Indications & contraindications must carefully be balanced & optional treatments must be taken into the decision making process in each individual patient eligible for implant therapy 2. Diagnosis 3. Medical history
  • 191. 4. Dental history- 5. Intra / Extra Oral examination – Oral hygiene – Parafunctional activities eg: bruxism – Salivary flow – Soft tissue condition – Periodontal health 6. Study casts 7. Anatomical limits for fixture placement
  • 192. 8. Radiographic examination – Periapical radiographs – Orthopantomographs – Computed tomogram – Combination . etc 9. Fabrication of radiographic splint 10. Additional bone evaluation 11. Designs for dentulous/ edentulous patient treatment 12. Consultation
  • 193. DIAGNOSTIC PROCEDURE BETWEEN IMPLANT PLACEMENT AND INITIATION OF PROSTHESIS FABRICATION & MAINTENANCE • Evaluation during the phase of tissue integration • Measurement of insertion torque as well as assessments of bone implant damping reactions (e.g. damping & resonance frequency analysis) are used to determine the initial stability of the newly placed implants. • PERIOTEST- (Schultz,1983) Resonance frequency analysis (RFA)- method based on steady state , swept frequency technique – non invasive , easy to use & capable of eliciting quantitative information on implant stability & stiffness
  • 194. • Soft tissue integration –BOP , Suppuration, probing depth • Radiographs – For correct placement of implant – Position , sink depth , & angulation • Healing – 6 weeks-12 months
  • 195. PERIODONTAL DIAGNOSIS: a) Components of a periodontal diagnosis b)Establishing a diagnosis in treated periodontal disease c) Chronic versus Aggressive periodontitis
  • 196. COMPONENTS OF A PERIODONTAL DIAGNOSIS Before arriving at a periodontal diagnosis the clinician must answer 3 basic questions: 1. What periodontal disease or condition does the patient have? 2. How severe is the problem? 3. Is the disease or condition localized or generalized?
  • 197. ESTABLISHING A DIAGNOSIS IN TREATED PATIENTS Treatment of plaque-induced periodontal diseases often results in the resolution of the patient’s periodontal infection. It is important to note that periodontal therapy can change the pre-treatment diagnosis to a more favorable post-treatment diagnosis. For example, effective treatment routinely converts plaque-induced gingivitis into a state of periodontal health (i.e. a Gingivitis to Periodontal Health shift.)
  • 198. Successful treatment of plaque-induced periodontitis is often converted to a state of periodontal health with a reduced periodontium. In such cases, damage persists from the previous periodontitis in the form of gingival recession. An interesting diagnostic problem arises when successfully treated patients who once had periodontitis subsequently develop gingival inflammation during the maintenance phase of therapy.
  • 199. Do such patients have gingivitis superimposed on a reduced periodontium or do they have a recurrence of periodontitis? At a single evaluation visit one cannot determine if previously treated periodontitis is recurring. Data collected during multiple maintenance visits are required to make this determination.
  • 201. CLASSIFICATION OF GINGIVAL DISEASES PLAQUE INDUCED GINGIVAL LESIONS 1. Gingivitis associated with dental plaque only 2. Gingival diseases modified by systemic factors Associated with endocrine system Associated with blood dyscrasias 3. Gingival diseases modified by medications 4. Gingival diseases modified by malnutrition
  • 202. CLASSIFICATION OF GINGIVAL DISEASES NON-PLAQUE INDUCED GINGIVAL LESIONS 1. Gingival diseases of specific bacterial origin 2. Gingival diseases of viral origin 3. Gingival diseases of fungal origin 4. Gingival diseases of genetic origin 5. Gingival manifestations of systemic conditions 6. Traumatic lesions 7. Foreign body reactions
  • 203. CLASSIFICATION OF PERIODONTITIS • 1. Chronic Periodontitis* – Localized – Generalized • 2. Aggressive Periodontitis – Localized – Generalized • 3. Periodontitis Associated with Systemic Diseases • 4. Necrotizing Periodontal Diseases • 5. Abscesses of the Periodontium • 6. Periodontal Diseases associated with Endodontic Lesions • 7. Developmental or Acquired Deformities and Conditions • *Can be further classified on basis of extent and severity
  • 204. DISEASE/CONDITION CLINICAL FEATURES DIFFERENTIAL DIAGNOSIS Gingivitis associated with dental plaque •Gingival bleeding •Colour •Acute-Reddish •Chronic-Deep blue •Consistency-Soft and edematous or fibrotic •Stippling -absent •Inflammation with pocket depth restricted to gingival tissues. Desquamative gingivitis Atrophic Gingivitis Gingival diseases modified by systemic factors: 1. Diabetes Mellitus 2. Leukemia •Diffuse inflammation with increased bleeding & increase gingival inflammatory reaction to plaque •Extensive bone loss •Increased tooth mobility •Supperation •Multiple abscess formation •red.boggy,edematous gingiva that bleeds persistently on slight provocation or spontaneosly •gingiva is hypertrophic and shows a typical intragingival hemorrhage. Abscess Ascorbic acid dificiency Plasma Cell Wegners Gingival enlargement Gingival Diseases modified by medications: 1. DIGO •Bead like enlargement of IDP extends into facial and lingual gingival margin •Marginal and papillary enlargement unite to form massive tissue folds covering crown and interfering with occlusion. •Pale pink,mulberry shaped,firm and resilient,lobulated surface and no bleeding in absence of inflammation •Inflammation-reddish coloured ,incresed bleeding& size. •Idiopathic gingival enlargment
  • 205. DISEASE/CONDITION CLINICAL FEATURES D D Gingival diseases of specific bacterial origin: 1. ANUG 1. Lesions are painful 2. Lesions are gingival ulcers, punched-out crater-like, of interdental papilla and may involve marginal gingiva 3. Gingival ulcers bleed spontaneously or readily Gonococcal Stomatitis Vincent’s Angina Desquamative Gingivitis Gingival diseases of specific viral origin: 1. Primary Herpetic Gingivostomatitis 1. Diffuse gingivitis 2. Vesiculoulcerative eruption-discrete sherical grey vesicles that rupture in 24hrs to form ulcers with red elevated margins and depressed yellow grayish central core 3. In children ANUG Erythema multifome Steven’s Johnson Syndrome Lichen Planus Aphthous Stomatitis Desquamative gingivitis Gingival diseases of specific fungal origin: 1. Candidiasis 1. acute pseudo- membranous candidiasis (thrush),white lesions that can be lifted off the gingiva. 2. acute atrophic (eythematous) gingival candidiasis. Leukoplakia Lichen Planus Carcinoma Erythema multiforme Gingival diseases of specific genetic origin: 1. Hereditary gingival fibromatosis 1. Attached,marginal gingiva & IDP-Diffuse enlargement 2. Gingiva is pink firm and leathery in consistency with Pebbled surface 3. Enlargement projects into vestibule- distortion of jaw DIGO Fibroma Gingival manifestations of systemic conditions: 1. Lichen Planus 1. Mimics gingivitis 2. Reticulated,hypertrophic ,keratotic lesion Leukoplakia Aphthous White sponge nevus
  • 206. DISEASE/CONDITI ON CLINICAL FEATURES D D Gingival manifestations of systemic conditions: 1. Lichen Planus 1. Allergic Reaction:Tooth Paste 1. Mimics gingivitis 2. Reticulated,hypertrophic ,keratotic lesion 3. gingival inflammation and pain 4. lace like white lesions of gingiva, tongue and cheek.ulcerations may be present. 5. Reticular,Atrophic,Bullous,Erosive 6. herbal compound sanguinaria were shown to produce gingivo-vestibular reactions characterized by leukoplakia Leukoplakia Aphthous White sponge nevus Leukoplakia Lichen planus Chronic Periodontitis •Amount of destruction consistent with local factors •Subgingival calculus present •Slow to moderate rate of progression, but may have periods of rapid progression • Can be associated with local predisposing factors (e.g., tooth related or iatrogenic factors) • May be modified by and / or associated with systemic diseases (e.g., diabetes mellitus) • Can be modified by factors other than systemic disease such as cigarette smoking and emotional stress Aggressive Periodontitis Desquamative Gingivitis Aggressive Periodontitis 1. Except for the presence of periodontitis, patients are otherwise clinically healthy 2. Rapid attachment loss and bone destruction 3. Familial aggregation 4. Distolabial movement of anterior teeth Chronic Periodontitis Desquamative Gingivitis
  • 207. DISEASE/CONDITION CLINICAL FEATURES D D DIAGNOSIS OF ACUTE PERIODONTAL LESIONS : 1. NUG 2. NUP 1.Lesions are painful 2.Lesions are gingival ulcers, punched-out crater-like, of interdental papilla and may involve marginal gingiva 3.Gingival ulcers bleed spontaneously or readily 1.Deep interproximal craters with denudation of interdental alveolar bone 2.Sequestration of interdental, and possibly buccal and/or lingual, alveolar bone Gonococcal Stomatitis Vincent’s Angina Desquamative Gingivitis ACUTE PERIODONTAL ABSCESSES Gingival abscess Periodontal Abscess Periapical Abscess confined to marginal gingival tissues, often at previously non-diseased sites.. offending foreign material is, thus, often diagnostic. history of 1–2 days of pain and very localized gingival swelling red, shiny swelling confined to marginal gingival tissues. Smooth, shiny swelling of the gingiva Painful, tender to palpation Purulent exudate Increased probing depth Mobile and/or percussion sensitive Tooth usually vital Sinus tract opens via keratinized gingiva Non-vital tooth Caries No pocket Apical radiolucency No or minimal mobility Percussion sensitivity Sinus tract opens via alveolar mucosa •Lateral periapical cyst, •Vertical root fracture, •Endo-periodontal abscess, •Postoperative infection
  • 208. DISEASE/CONDITION CLINICAL FEATURES D D Periodontal Diseases associated with Endodontic Lesions 1. Swelling caused by endodontic infections occur in the mucobuccal fold and periodontal infections occur in the attached gingiva . 2. Teeth are examined for any caries, defective restoration, erosions, abrasions, cracks, fractures and discolorations. 3. Increased bleeding,pocket depth,mobility may be associated 4. Radiographs are required to confirm diagnosis Periodontal Abscess Periapical Abscess Developmental or Acquired Deformities and Conditions 1. Gingival soft tissue recession 2. Lack of keratinized gingiva • inadequate band of keratinized gingiva, excessive muscle pull and too vigorous tooth brushing. • lack of keratinized gingiva together with muscle pull can cause on-going gingival recession. Shallow vestibule Recession
  • 209. Developmental or Acquired Deformities and Conditions
  • 210. REFERENCES: • Clinical periodontology: Glickman, Carranza, 10th edition • Diagnostics: Perio 2000, vol. 34, 2004 • Fundamentals of periodontics: 2cnd edition, K.S. Kornman, K.J. Wilson • Diagnosis and risk prediction of periodontal diseases: vol. 3, 2002: Per Axelsson • Clinical Periodontology and Implant Dentistry: 5th ed, Jan Lindhe • Periodontal Medicine: Rose, Cohen, Genco, Mealey, 2000 • Position paper: Diagnosis of Periodontal diseases- J Periodontol 2003 • Clinical practice of the dental hygienist ,9 th edition by Esther M . Wilkins
  • 211. REFERENCES: • Critical Decisions in Periodontology 4th edition: Walter B. Hall • Dwight E. Mcleod: A Practical Approach To The Diagnosis And Treatment Of Periodontal Disease. JADA, Vol. 131, April 2000. • Gary C. Armitage: Periodontal Diseases: Diagnosis. Annals of Periodontology, 1996 • John O .Grippo et al : Attrition, Abrasion, Corrosion and abfraction revisited. A new perspective on tooth surface lesions. JADA, VOL 135, AUG 2004 • Vivien Kwok, Jack Caton: Prognosis revisited: A system for assigning periodontal prognosis. J Periodontol 2007;78 • Dental hygiene theory and practice: Darby and Walsh. 2cnd edition • The Periodontal- Endodontic controversy: Harrington, Steiner, Ammons.Periodontology 2000, Vol. 30, 2002, 123–130