History of Periodontics by Dr. Neelam Das.pptx
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Periodontal diseases have afflicted humans since the dawn of his tory. Oral hygiene is practiced since ancient times. Sushruta Samhita contains numerous descriptions of severe periodontal disease with loose teeth and purulent discharge from gingiva. Our understanding of the causes of periodontal disease have changed greatly over time. The past inabilities of generalists to pinpoint systemic causes are being overcome with the application of modern epidemiologic and clinical research approaches.
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Age of onset
Rapid rate of disease progression
Nature & composition of the associated subgingival micro flora
Alterations in the host’s immune response
Familial aggregation of the disease
Types of Aggressive Periodontitis
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Diffuse atrophy of the alveolar bone (Gottlieb-1923)
Deep cementopathia (Gottlieb-1928)
Parodontitis marginalis progressiva(Wannenmacher- 1938)
Periodontosis (world workshop in periodontics -1966)
Juvenile periodontitis (Chaput etal-1971)
Localized Juvenile periodontitis (world workshop in periodontics- 1989)
Localized aggressive periodontitis (International workshop by american academy of periodontology – 1999)
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Possible reasons for limitation of the destruction
After initial colonization of the first permanent teeth( first molars & incisors) Aa evades the host defenses by different mechanisms they are –
-PMN chemotaxis inhibiting factors
-Endotoxin
-Collagenases
-Leukotoxin
After this initial attack adequate immune defenses are stimulated to produce opsonic antibodies to enhance the clearance & phagocytosis of invading bacteria & neutralize leukotoxic activity there by colonization of other sites may be prevented
Bacteria antagonistic to Aa may colonize the periodontal tissues & inhibit Aa from further colonization of periodontal sites in the mouth ,hence Aa infection & tissue destruction is localized
Aa may lose its leukotoxin producing ability for unknown reasons
A defect in cementum formation may be responsible for the localization of the lesions
Clinical features of LAP
Age of onset –puberty & around 20 years of age
It affects both male & female
There will be a lack of clinical inflammation despite the presence of deep periodontal pockets & advanced bone loss
The amount of plaque is minimal & is rarely mineralizes to calculus
Plaque Contains elevated levels of Aa & Pg
The Rate of boneloss is about 3 to 4 times faster than in chronic periodontitis
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Distolabial migration of the maxillary incisors with concomitant diastema formation
Increasing mobility of the maxillary & mandibular incisors & first molars
Sensitivity of denuded root surfaces to thermal & tactile stimuli
Deep dull radiating pain during mastication
Robust antibody response to pathogens
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2) Diagnosing endo-perio lesions can be complicated, as they involve both pulp and periodontal components. Clinical findings, radiographs, vitality tests, and probing are used.
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Aggressive periodontitis is distinguished from chronic periodontitis with respect to,
Age of onset
Rapid rate of disease progression
Nature & composition of the associated subgingival micro flora
Alterations in the host’s immune response
Familial aggregation of the disease
Types of Aggressive Periodontitis
Localized Aggressive Periodontitis-LAP
Generalized Aggressive Periodontitis-GAP
Localized aggressive periodontitis
Historical background,
Diffuse atrophy of the alveolar bone (Gottlieb-1923)
Deep cementopathia (Gottlieb-1928)
Parodontitis marginalis progressiva(Wannenmacher- 1938)
Periodontosis (world workshop in periodontics -1966)
Juvenile periodontitis (Chaput etal-1971)
Localized Juvenile periodontitis (world workshop in periodontics- 1989)
Localized aggressive periodontitis (International workshop by american academy of periodontology – 1999)
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LAP is localized to first molar or incisor with interproximal attachment loss on at least two permanent teeth ,one of which is a first molar & involving no more than two teeth other than first molars & incisors.
Possible reasons for limitation of the destruction
After initial colonization of the first permanent teeth( first molars & incisors) Aa evades the host defenses by different mechanisms they are –
-PMN chemotaxis inhibiting factors
-Endotoxin
-Collagenases
-Leukotoxin
After this initial attack adequate immune defenses are stimulated to produce opsonic antibodies to enhance the clearance & phagocytosis of invading bacteria & neutralize leukotoxic activity there by colonization of other sites may be prevented
Bacteria antagonistic to Aa may colonize the periodontal tissues & inhibit Aa from further colonization of periodontal sites in the mouth ,hence Aa infection & tissue destruction is localized
Aa may lose its leukotoxin producing ability for unknown reasons
A defect in cementum formation may be responsible for the localization of the lesions
Clinical features of LAP
Age of onset –puberty & around 20 years of age
It affects both male & female
There will be a lack of clinical inflammation despite the presence of deep periodontal pockets & advanced bone loss
The amount of plaque is minimal & is rarely mineralizes to calculus
Plaque Contains elevated levels of Aa & Pg
The Rate of boneloss is about 3 to 4 times faster than in chronic periodontitis
Clinical features of LAP
Distolabial migration of the maxillary incisors with concomitant diastema formation
Increasing mobility of the maxillary & mandibular incisors & first molars
Sensitivity of denuded root surfaces to thermal & tactile stimuli
Deep dull radiating pain during mastication
Robust antibody response to pathogens
Radiographs reveal ‘arc shaped loss of alveolar bone extending from distal surface of the second premolar to the mesial surface of the second molar’
Localized Aggressive periodontitis
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clinical features of gingivitis.pdf
This document discusses gingivitis, including its classification, distribution, and causes of gingival bleeding. It notes that experimental studies show plaque accumulation on teeth leads to gingival inflammation. Chronic gingivitis is the most common form and involves red, swollen gingiva that bleeds easily. Gingivitis can be localized to certain areas or generalized throughout the mouth. Bleeding is often an early sign and results from damaged blood vessels in inflamed tissue. Systemic conditions like platelet or coagulation disorders can also cause bleeding. Various indices are used to assess bleeding during gingival exams.
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1. Motivational interviewing is an evidence-based counseling technique used to help patients overcome ambivalence about behavior change and develop intrinsic motivation to change.
2. Some key principles of motivational interviewing include expressing empathy, developing discrepancy between current behaviors and goals, rolling with resistance rather than arguing, and supporting self-efficacy.
3. Motivational interviewing uses open-ended questions, affirmation, reflective listening, and summarization to help patients explore and resolve ambivalence and develop their own reasons for change.Mast cells.ppt
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