The presentation describe the influence of systemic disease on periodontum such as:
nutritional,endocrine,Haemotologic, psycosomatic, immunodeficiency disorders
This document discusses the clinical features of gingivitis. It begins by defining gingivitis as inflammation of the gingiva and describes how plaque bacteria can damage gingival tissues. It then covers the different types of gingivitis based on duration and distribution. Key signs of gingivitis that are discussed include gingival bleeding, color changes, changes in consistency, size, surface texture, position and contour. Specific conditions like gingival recession are also explained in terms of definition, classification, etiology and clinical significance.
This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.
Localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP) are forms of periodontitis that primarily affect younger individuals. LAP typically affects the first molars and incisors, causing rapid attachment loss and bone destruction. GAP affects at least three teeth besides molars and incisors, with periods of destruction followed by remission. Both involve familial factors and bacterial pathogens like P. gingivalis and A. actinomycetemcomitans. Treatment involves non-surgical and surgical therapies along with systemic antibiotics. Frequent maintenance is important for managing the diseases.
This document provides a classification system for periodontal pathology, dividing it into gingival diseases and periodontitis. It describes various forms of gingival disease including those induced by dental plaque, modified by systemic factors like pregnancy or diabetes, drug-induced forms from medications like phenytoin, and non-plaque induced lesions from conditions such as linear gingival erythema. It also outlines different types of periodontitis including chronic, aggressive, periodontitis associated with systemic diseases, necrotizing forms, abscesses, and lesions associated with endodontic problems. Developed deformities and occlusal trauma are additionally discussed.
Clinical features of gingivitis include:
1. The gingiva appears red, swollen, and bleeds easily when probed due to inflammatory cell infiltration and increased vascularity.
2. Interdental papillae become blunted and bulbous as they bulge out between teeth.
3. Histopathology shows inflammatory cell infiltration, ulceration of sulcular epithelium, edema, and fibrosis in long-standing cases.
Treatment involves thorough scaling, removing local irritants, improving plaque control, and oral hygiene instruction. The prognosis is generally excellent.
The document discusses the defense mechanisms of the gingiva that help it withstand various adverse environmental conditions. There are nonspecific and specific defense mechanisms. Nonspecific mechanisms include the anatomical structure of the gingiva, the mucous barrier formed by saliva and gingival crevicular fluid, and tissue resistance. Specific mechanisms include the host-microbial symbiosis provided by beneficial commensal bacteria and the local inflammatory response. Saliva plays an important role through its antibacterial factors such as antibodies, enzymes, and buffers that help maintain pH and protect against pathogens. The gingival crevicular fluid also acts as a permeable barrier, with its production increased during inflammation. These defense mechanisms work together to keep the
BASIC CONCEPTS OF INFLAMMATION-STAGES OF INFLAMMATION-ALL ABOUT GINGIVAL INFLAMMATION-CLINICAL FEATURES AND STAGES OF GINGIVITIS-HOW TO MANAGE-ALL IN ONE-FOR B.D.S LEVEL PROJECTS AND SEMINARS
This document provides an overview of the clinical features of gingivitis. It discusses gingival bleeding on probing as a key clinical sign of gingivitis. Local factors like plaque, calculus and trauma as well as systemic factors like certain medications and diseases can cause gingival bleeding. The color of inflamed gingiva changes from normal coral pink to red or bluish-red due to increased vascularization and reduced keratinization. Types of gingivitis are classified based on duration, distribution, and description. Chronic gingivitis is the most common form characterized by a slow onset and long duration without pain.
This document discusses the clinical features of gingivitis. It begins by defining gingivitis as inflammation of the gingiva and describes how plaque bacteria can damage gingival tissues. It then covers the different types of gingivitis based on duration and distribution. Key signs of gingivitis that are discussed include gingival bleeding, color changes, changes in consistency, size, surface texture, position and contour. Specific conditions like gingival recession are also explained in terms of definition, classification, etiology and clinical significance.
This document discusses gingival inflammation and gingivitis. It begins by defining inflammation and describing the cardinal signs. It then outlines the stages of gingivitis from initial to established to advanced/periodontitis. Microorganisms attached to teeth secrete enzymes that damage tissues and widen junctional epithelium, allowing bacterial products to access connective tissue and activate immune cells. Studies showed that not practicing oral hygiene led to plaque buildup and gingivitis within 10-21 days. Gingivitis is characterized by redness, swelling, bleeding and is prevalent worldwide. The document discusses features, course, distribution and systemic influences of gingival inflammation.
Localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP) are forms of periodontitis that primarily affect younger individuals. LAP typically affects the first molars and incisors, causing rapid attachment loss and bone destruction. GAP affects at least three teeth besides molars and incisors, with periods of destruction followed by remission. Both involve familial factors and bacterial pathogens like P. gingivalis and A. actinomycetemcomitans. Treatment involves non-surgical and surgical therapies along with systemic antibiotics. Frequent maintenance is important for managing the diseases.
This document provides a classification system for periodontal pathology, dividing it into gingival diseases and periodontitis. It describes various forms of gingival disease including those induced by dental plaque, modified by systemic factors like pregnancy or diabetes, drug-induced forms from medications like phenytoin, and non-plaque induced lesions from conditions such as linear gingival erythema. It also outlines different types of periodontitis including chronic, aggressive, periodontitis associated with systemic diseases, necrotizing forms, abscesses, and lesions associated with endodontic problems. Developed deformities and occlusal trauma are additionally discussed.
Clinical features of gingivitis include:
1. The gingiva appears red, swollen, and bleeds easily when probed due to inflammatory cell infiltration and increased vascularity.
2. Interdental papillae become blunted and bulbous as they bulge out between teeth.
3. Histopathology shows inflammatory cell infiltration, ulceration of sulcular epithelium, edema, and fibrosis in long-standing cases.
Treatment involves thorough scaling, removing local irritants, improving plaque control, and oral hygiene instruction. The prognosis is generally excellent.
The document discusses the defense mechanisms of the gingiva that help it withstand various adverse environmental conditions. There are nonspecific and specific defense mechanisms. Nonspecific mechanisms include the anatomical structure of the gingiva, the mucous barrier formed by saliva and gingival crevicular fluid, and tissue resistance. Specific mechanisms include the host-microbial symbiosis provided by beneficial commensal bacteria and the local inflammatory response. Saliva plays an important role through its antibacterial factors such as antibodies, enzymes, and buffers that help maintain pH and protect against pathogens. The gingival crevicular fluid also acts as a permeable barrier, with its production increased during inflammation. These defense mechanisms work together to keep the
BASIC CONCEPTS OF INFLAMMATION-STAGES OF INFLAMMATION-ALL ABOUT GINGIVAL INFLAMMATION-CLINICAL FEATURES AND STAGES OF GINGIVITIS-HOW TO MANAGE-ALL IN ONE-FOR B.D.S LEVEL PROJECTS AND SEMINARS
This document provides an overview of the clinical features of gingivitis. It discusses gingival bleeding on probing as a key clinical sign of gingivitis. Local factors like plaque, calculus and trauma as well as systemic factors like certain medications and diseases can cause gingival bleeding. The color of inflamed gingiva changes from normal coral pink to red or bluish-red due to increased vascularization and reduced keratinization. Types of gingivitis are classified based on duration, distribution, and description. Chronic gingivitis is the most common form characterized by a slow onset and long duration without pain.
Localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP) are severe forms of periodontitis that primarily affect younger individuals. LAP is characterized by localized periodontal bone loss around the first molars and incisors. GAP affects multiple teeth and involves periods of rapid bone destruction followed by periods of quiescence. Both are associated with small amounts of plaque harboring bacteria like P. gingivalis and A. actinomycetemcomitans. Genetic and immune factors also contribute to disease risk. Treatment involves scaling, root planing, surgery and systemic antibiotics like tetracycline to eliminate pathogenic bacteria from tissues and prevent reinfection.
This document discusses drug-induced gingival enlargement, which occurs as a side effect of certain medications including anti-convulsants, immunosuppressants, and calcium channel blockers. It provides details on the pathogenesis, clinical features, and histological features of enlargement caused by specific drugs like phenytoin, cyclosporine, and nifedipine. Management involves improving plaque control, modifying the medication regimen, and periodontal surgical procedures like gingivectomy if needed to remove excess tissue.
Described here are the clinical features of gingiva, the various stages of gingivitis and the clinical features associated with them. The microscopic features have been described on a different slide presentation.
Gingivitis is defined as the inflammation of gingival tissue.Gingival inflammation has two components: the acute
inflammatory component, with vasodilation, edema, and
polymorphonuclear infiltration, and the chronic inflammatory
component, with B and T lymphocytes and capillary
proliferation forming a granulomatous response.
The document discusses the classification and features of periodontal disease. It covers topics such as marginal periodontitis, juvenile periodontitis, trauma from occlusion, and periodontal atrophy. It also describes the periodontal pocket in detail, including its pathogenesis, morphology, contents, and relationship to bone loss. The extension of inflammation from the gingiva to the supporting periodontal tissues is discussed as well.
This document discusses aggressive periodontitis, a serious gum infection that can destroy the tissues and bone supporting teeth and potentially lead to tooth loss. It defines aggressive periodontitis and differentiates it from chronic periodontitis. It describes the characteristics of aggressive periodontitis such as rapid attachment and bone loss, familial aggregation, and an inconsistent amount of plaque. The document classifies aggressive periodontitis into localized and generalized forms and discusses causes such as plaque, smoking, heredity, and certain microorganisms. It also briefly mentions juvenile periodontitis and Papillon-Lefevre syndrome, a rare genetic disorder associated with early onset periodontitis.
This document summarizes various gingival and periodontal diseases. It describes diseases caused by dental plaque, such as gingivitis, and modified by factors like medications, malnutrition, and systemic diseases. It also discusses periodontitis and other conditions like necrotizing gingivitis/periodontitis, endo-perio lesions, and developmental deformities that can affect the gingiva and periodontium. Diagnostic methods and typical treatments are mentioned for several conditions.
Gingival enlargement, also known as gingival hyperplasia or hypertrophy, is an increase in the volume of gingival tissue that can be caused by various local and systemic factors. Common causes include plaque accumulation resulting in inflammation, certain medications like phenytoin and cyclosporine, pregnancy, and rare hereditary conditions. Left untreated, gingival enlargement can negatively impact oral health, function, and aesthetics. Treatment options depend on the underlying cause but may involve improved plaque control, changing medications, surgery to remove excess tissue, or resolving systemic conditions.
Hormonal changes in female patients and periodontal diseasesPerio Files
Hormonal fluctuations in females can impact periodontal disease. Puberty, menstruation, pregnancy, menopause, and oral contraceptive use can all influence the gingival tissues and affect susceptibility to periodontal disease. Pregnancy in particular increases sex hormone levels like estrogen and progesterone, which can directly impact the periodontium and immune response, resulting in conditions like pregnancy gingivitis. Periodontal disease has also been associated with adverse pregnancy outcomes like preterm birth and preeclampsia. Proper oral hygiene and treatment during stages of hormonal change in females can help reduce risks to oral and overall health.
AGGRESSIVE PERIODONTITIS
PRESENTER
DR. REBICCA RANJIT
DEPT. OF PERIODONTOLOGY & ORAL IMPLANTOLOGY
Why is there localisation of disease to 1st molars and incisors in LAP?
Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis).
Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP.
Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke.
IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.
This document discusses gingivitis and abnormal gingival bleeding. It describes the types and characteristics of acute, subacute, chronic, recurrent, localized, generalized, marginal and papillary gingivitis. Bleeding is an early sign of gingivitis and occurs due to dilation of blood vessels and thinning of epithelium. Bleeding can be provoked by trauma from brushing or biting and indicates more inflamed tissue. Some systemic conditions can also cause abnormal bleeding. Color changes in chronic gingivitis are due to vascular proliferation and reduced keratinization under inflamed tissue.
This document discusses different types of necrotizing ulcerative periodontitis including non-AIDS type and AIDS-associated type. It also discusses refractory periodontitis caused by abnormal host response, resistant bacteria, failure to remove plaque, and smoking. Microbial complexes associated with refractory periodontitis include Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Treatment involves antimicrobial therapy and local drug delivery. The document also discusses periodontitis caused by systemic diseases that impair neutrophil function such as Papillon-Lefèvre syndrome, Chédiak-Higashi syndrome, and Down syndrome.
This document discusses gingivitis, including its classification, clinical features, etiology, and management. Gingivitis can be classified based on its course (acute, recurrent, chronic) or distribution (localized or generalized). Clinical features include bleeding, color changes, consistency changes, and position changes in the gums. Gingivitis is caused by factors like plaque, genetics, medications, and systemic diseases. Management involves treating symptoms, diagnosing through examination, preventing further issues through proper oral hygiene like brushing and flossing, and treating existing inflammation.
This document provides an overview of the pathogenesis of periodontal disease. It begins with definitions of pathogenesis and periodontitis. Key points include: plaque bacteria initiate inflammatory responses leading to tissue damage; the host immune response determines susceptibility; and the transition from gingivitis to periodontitis involves a shift from localized to widespread inflammation and bone/tissue loss. Histopathological changes are described at each disease stage. The roles of bacterial virulence factors and host inflammatory mediators such as cytokines are discussed.
Juvenile periodontitis is a type of periodontitis that occurs in otherwise healthy individuals under 30 years old. It is characterized by rapid attachment and bone loss. There are two types: localized juvenile periodontitis, which is destructive to the first molars and incisors, and generalized juvenile periodontitis, which affects at least three teeth besides the first molars and incisors. Both types are caused by specific microorganisms like Actinobacillus actinomycetemcomitans and have features like deep pockets despite minimal plaque. Treatment involves scaling, root planing, antibiotics, and sometimes surgery.
Periodontitis is an inflammatory disease of the supporting tissues of teeth caused by specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone. Localized aggressive periodontitis (LAP) generally affects systemically healthy individuals under 30 years of age and is characterized by rapid progression and localized attachment loss on first molars and incisors. Generalized aggressive periodontitis (GAP) also affects individuals under 30 but produces a poor antibody response to pathogens and results in generalized interproximal attachment loss affecting at least 3 teeth. Both LAP and GAP can progress rapidly and result in bone loss despite minimal plaque.
Periodontal disease is a chronic inflammatory disease of the gums and tissues surrounding the teeth. It is caused by plaque bacteria, including Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans. Left untreated, it can lead to tooth loss. Symptoms include red, swollen, bleeding gums; bad breath; and loose teeth. It is diagnosed through examination of the gums and bone measurements. Treatment involves deep cleaning or surgery to remove bacterial infection. Daily brushing and flossing is the best prevention method.
The document discusses the classification of periodontal diseases. It provides an overview of how periodontal diseases were previously classified, noting that the classification system was heavily based on age. It then summarizes the updated 1999 classification system, which introduced categories for gingival diseases and refined the categories for periodontal diseases. The key changes were introducing gingival disease categories, replacing terms like "adult periodontitis" with "chronic periodontitis", and expanding definitions of systemic diseases and their implications for periodontal health.
This document summarizes the medical history, examination findings, diagnosis, and treatment plan for a 42-year-old Filipino female patient presenting with carious teeth. The patient has a history of rheumatoid arthritis, hypothyroidism, and inflammatory lymphadenitis. Clinical examination revealed a pigmented lesion on the buccal mucosa consistent with oral lichen planus. Laboratory tests were within normal limits. The patient was diagnosed with asymptomatic oral lichen planus and prescribed topical corticosteroids with follow up every 6 months to 1 year.
This study investigated the biodegradation of the antifungal drug griseofulvin by Bacillus subtilis isolated from expired pharmaceutical raw materials. Key findings include:
1) B. subtilis was able to degrade griseofulvin as detected by TLC, IR and HPLC analysis of degradation products but not physical/chemical tests.
2) The degradation enzyme was purified using column chromatography and identified to have a molecular weight of 5.3439 kDa.
3) Gas chromatography-mass spectrometry identified diethyl phthalate and carbon dioxide as biodegradation products, indicating B. subtilis' ability to metabolize griseofulvin.
4
Localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP) are severe forms of periodontitis that primarily affect younger individuals. LAP is characterized by localized periodontal bone loss around the first molars and incisors. GAP affects multiple teeth and involves periods of rapid bone destruction followed by periods of quiescence. Both are associated with small amounts of plaque harboring bacteria like P. gingivalis and A. actinomycetemcomitans. Genetic and immune factors also contribute to disease risk. Treatment involves scaling, root planing, surgery and systemic antibiotics like tetracycline to eliminate pathogenic bacteria from tissues and prevent reinfection.
This document discusses drug-induced gingival enlargement, which occurs as a side effect of certain medications including anti-convulsants, immunosuppressants, and calcium channel blockers. It provides details on the pathogenesis, clinical features, and histological features of enlargement caused by specific drugs like phenytoin, cyclosporine, and nifedipine. Management involves improving plaque control, modifying the medication regimen, and periodontal surgical procedures like gingivectomy if needed to remove excess tissue.
Described here are the clinical features of gingiva, the various stages of gingivitis and the clinical features associated with them. The microscopic features have been described on a different slide presentation.
Gingivitis is defined as the inflammation of gingival tissue.Gingival inflammation has two components: the acute
inflammatory component, with vasodilation, edema, and
polymorphonuclear infiltration, and the chronic inflammatory
component, with B and T lymphocytes and capillary
proliferation forming a granulomatous response.
The document discusses the classification and features of periodontal disease. It covers topics such as marginal periodontitis, juvenile periodontitis, trauma from occlusion, and periodontal atrophy. It also describes the periodontal pocket in detail, including its pathogenesis, morphology, contents, and relationship to bone loss. The extension of inflammation from the gingiva to the supporting periodontal tissues is discussed as well.
This document discusses aggressive periodontitis, a serious gum infection that can destroy the tissues and bone supporting teeth and potentially lead to tooth loss. It defines aggressive periodontitis and differentiates it from chronic periodontitis. It describes the characteristics of aggressive periodontitis such as rapid attachment and bone loss, familial aggregation, and an inconsistent amount of plaque. The document classifies aggressive periodontitis into localized and generalized forms and discusses causes such as plaque, smoking, heredity, and certain microorganisms. It also briefly mentions juvenile periodontitis and Papillon-Lefevre syndrome, a rare genetic disorder associated with early onset periodontitis.
This document summarizes various gingival and periodontal diseases. It describes diseases caused by dental plaque, such as gingivitis, and modified by factors like medications, malnutrition, and systemic diseases. It also discusses periodontitis and other conditions like necrotizing gingivitis/periodontitis, endo-perio lesions, and developmental deformities that can affect the gingiva and periodontium. Diagnostic methods and typical treatments are mentioned for several conditions.
Gingival enlargement, also known as gingival hyperplasia or hypertrophy, is an increase in the volume of gingival tissue that can be caused by various local and systemic factors. Common causes include plaque accumulation resulting in inflammation, certain medications like phenytoin and cyclosporine, pregnancy, and rare hereditary conditions. Left untreated, gingival enlargement can negatively impact oral health, function, and aesthetics. Treatment options depend on the underlying cause but may involve improved plaque control, changing medications, surgery to remove excess tissue, or resolving systemic conditions.
Hormonal changes in female patients and periodontal diseasesPerio Files
Hormonal fluctuations in females can impact periodontal disease. Puberty, menstruation, pregnancy, menopause, and oral contraceptive use can all influence the gingival tissues and affect susceptibility to periodontal disease. Pregnancy in particular increases sex hormone levels like estrogen and progesterone, which can directly impact the periodontium and immune response, resulting in conditions like pregnancy gingivitis. Periodontal disease has also been associated with adverse pregnancy outcomes like preterm birth and preeclampsia. Proper oral hygiene and treatment during stages of hormonal change in females can help reduce risks to oral and overall health.
AGGRESSIVE PERIODONTITIS
PRESENTER
DR. REBICCA RANJIT
DEPT. OF PERIODONTOLOGY & ORAL IMPLANTOLOGY
Why is there localisation of disease to 1st molars and incisors in LAP?
Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis).
Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP.
Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke.
IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.
This document discusses gingivitis and abnormal gingival bleeding. It describes the types and characteristics of acute, subacute, chronic, recurrent, localized, generalized, marginal and papillary gingivitis. Bleeding is an early sign of gingivitis and occurs due to dilation of blood vessels and thinning of epithelium. Bleeding can be provoked by trauma from brushing or biting and indicates more inflamed tissue. Some systemic conditions can also cause abnormal bleeding. Color changes in chronic gingivitis are due to vascular proliferation and reduced keratinization under inflamed tissue.
This document discusses different types of necrotizing ulcerative periodontitis including non-AIDS type and AIDS-associated type. It also discusses refractory periodontitis caused by abnormal host response, resistant bacteria, failure to remove plaque, and smoking. Microbial complexes associated with refractory periodontitis include Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Treatment involves antimicrobial therapy and local drug delivery. The document also discusses periodontitis caused by systemic diseases that impair neutrophil function such as Papillon-Lefèvre syndrome, Chédiak-Higashi syndrome, and Down syndrome.
This document discusses gingivitis, including its classification, clinical features, etiology, and management. Gingivitis can be classified based on its course (acute, recurrent, chronic) or distribution (localized or generalized). Clinical features include bleeding, color changes, consistency changes, and position changes in the gums. Gingivitis is caused by factors like plaque, genetics, medications, and systemic diseases. Management involves treating symptoms, diagnosing through examination, preventing further issues through proper oral hygiene like brushing and flossing, and treating existing inflammation.
This document provides an overview of the pathogenesis of periodontal disease. It begins with definitions of pathogenesis and periodontitis. Key points include: plaque bacteria initiate inflammatory responses leading to tissue damage; the host immune response determines susceptibility; and the transition from gingivitis to periodontitis involves a shift from localized to widespread inflammation and bone/tissue loss. Histopathological changes are described at each disease stage. The roles of bacterial virulence factors and host inflammatory mediators such as cytokines are discussed.
Juvenile periodontitis is a type of periodontitis that occurs in otherwise healthy individuals under 30 years old. It is characterized by rapid attachment and bone loss. There are two types: localized juvenile periodontitis, which is destructive to the first molars and incisors, and generalized juvenile periodontitis, which affects at least three teeth besides the first molars and incisors. Both types are caused by specific microorganisms like Actinobacillus actinomycetemcomitans and have features like deep pockets despite minimal plaque. Treatment involves scaling, root planing, antibiotics, and sometimes surgery.
Periodontitis is an inflammatory disease of the supporting tissues of teeth caused by specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone. Localized aggressive periodontitis (LAP) generally affects systemically healthy individuals under 30 years of age and is characterized by rapid progression and localized attachment loss on first molars and incisors. Generalized aggressive periodontitis (GAP) also affects individuals under 30 but produces a poor antibody response to pathogens and results in generalized interproximal attachment loss affecting at least 3 teeth. Both LAP and GAP can progress rapidly and result in bone loss despite minimal plaque.
Periodontal disease is a chronic inflammatory disease of the gums and tissues surrounding the teeth. It is caused by plaque bacteria, including Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans. Left untreated, it can lead to tooth loss. Symptoms include red, swollen, bleeding gums; bad breath; and loose teeth. It is diagnosed through examination of the gums and bone measurements. Treatment involves deep cleaning or surgery to remove bacterial infection. Daily brushing and flossing is the best prevention method.
The document discusses the classification of periodontal diseases. It provides an overview of how periodontal diseases were previously classified, noting that the classification system was heavily based on age. It then summarizes the updated 1999 classification system, which introduced categories for gingival diseases and refined the categories for periodontal diseases. The key changes were introducing gingival disease categories, replacing terms like "adult periodontitis" with "chronic periodontitis", and expanding definitions of systemic diseases and their implications for periodontal health.
This document summarizes the medical history, examination findings, diagnosis, and treatment plan for a 42-year-old Filipino female patient presenting with carious teeth. The patient has a history of rheumatoid arthritis, hypothyroidism, and inflammatory lymphadenitis. Clinical examination revealed a pigmented lesion on the buccal mucosa consistent with oral lichen planus. Laboratory tests were within normal limits. The patient was diagnosed with asymptomatic oral lichen planus and prescribed topical corticosteroids with follow up every 6 months to 1 year.
This study investigated the biodegradation of the antifungal drug griseofulvin by Bacillus subtilis isolated from expired pharmaceutical raw materials. Key findings include:
1) B. subtilis was able to degrade griseofulvin as detected by TLC, IR and HPLC analysis of degradation products but not physical/chemical tests.
2) The degradation enzyme was purified using column chromatography and identified to have a molecular weight of 5.3439 kDa.
3) Gas chromatography-mass spectrometry identified diethyl phthalate and carbon dioxide as biodegradation products, indicating B. subtilis' ability to metabolize griseofulvin.
4
The document discusses various conditions that can affect the tongue coating and papillae, including atrophy and increased coating. Atrophy can be caused by nutrient deficiencies, vascular disease, or medications. Increased coating is due to lack of removal factors from medications, illness, or mouth breathing. Other conditions mentioned include geographic tongue, hairy tongue from antibiotics, papillitis from dental factors, and glossodynia which can have local, systemic, or psychogenic causes.
This document discusses clinical features of gingivitis and chronic periodontitis. It describes the signs and symptoms of gingivitis such as color changes, consistency changes, and bleeding. It also discusses the progression of inflammation from the gingiva to the supporting periodontal tissues. Finally, it outlines the characteristics, disease distribution, risk factors, and prevalence of chronic periodontitis.
The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.
This document discusses gingivitis and periodontal disease. It defines gingivitis as inflammation of the gums that does not affect the underlying tooth structures. Periodontitis is defined as inflammation that extends below the gumline and can cause bone and tissue loss. The document outlines the signs and symptoms, causes, and types of both gingivitis and periodontitis.
013.systemic diseases in the etiology of periodontal diseaseDr.Jaffar Raza BDS
The document discusses various systemic diseases and conditions that can affect the periodontium. It covers topics like nutritional deficiencies (such as scurvy from vitamin C deficiency), hematological disorders like leukemia which can cause gingival enlargement and bleeding, and metabolic conditions such as diabetes that increase periodontal disease risk. The document also discusses effects of medications, toxins, and diseases like HIV/AIDS on the periodontal tissues and considerations for treatment.
Gingivitis refers to inflammation of the gums. The main cause is plaque-induced microorganisms that release enzymes damaging epithelial and connective tissues. This destroys barriers between gum cells allowing bacterial products or bacteria into tissues. Untreated gingivitis can progress to periodontitis. Symptoms of gingivitis include red, swollen, bleeding gums and changes in texture or consistency. The severity and ease of bleeding provides clues to the integrity of the inflammatory process. Localized or generalized inflammation depends on distribution. Chronic inflammation is usually painless while acute cases can be painful.
This document provides definitions and information about premalignant lesions and conditions of the oral cavity. It discusses leukoplakia, erythroplakia, lichen planus, oral submucous fibrosis, candidiasis, and smoker's palate. For each condition, it describes the etiology, clinical features, diagnosis, and treatment options. The document aims to educate about potentially pre-cancerous lesions in the mouth.
Oral manifestations of gastrointestinal disordersThilanka Umesh
This document discusses various oral manifestations of gastrointestinal disorders, including:
1. Gastroesophageal reflux disease, which can cause tooth erosion from stomach acid contact. Enamel is lost in a smooth, shiny pattern.
2. Crohn's disease and ulcerative colitis, which can cause oral ulcers and lesions related to nutritional deficiencies from inflammation and malabsorption.
3. Orofacial granulomatosis, characterized by non-caseating granulomatous inflammation affecting the lips and oral tissues, causing swelling. Corticosteroids are a first-line treatment but relapses are common.
This document discusses clinical and microscopic changes that occur in gingivitis. It notes that gingivitis is characterized by inflammation of the gingiva caused by plaque bacteria. Key signs include redness, bleeding, changes in consistency from firm to soggy. Microscopically, there is thinning of sulcular epithelium and dilation of blood vessels. The document also outlines factors that can affect gingival features like color, contour, size, surface texture and position in health and disease.
This document discusses gingival enlargement and recession. It covers various causes of gingival enlargement including inflammatory, drug-induced, disease-related, and neoplastic enlargement. Drug-induced enlargement can be caused by medications like phenytoin and cyclosporine. Treatment involves improving oral hygiene and potentially substituting medications. For persistent enlargement, gingivectomy is recommended. Gingival recession has classifications based on depth and width. Causes include plaque, tooth malposition, trauma, and aging. Recession increases sensitivity and caries risk. Treatment focuses on eliminating causes and using surgery to reposition or graft tissues.
Stress and nutritional factors on periodontal disease april 12013Dr Saif khan
Stress and nutritional deficiencies can impact the periodontium both directly and indirectly. Chronic stress can lead to poor oral hygiene habits and suppressed immunity, increasing risk for periodontal disease. Certain vitamin deficiencies like vitamins C and D are associated with impaired wound healing and bone health, worsening the effects of plaque on the gingiva. Protein deficiency weakens periodontal tissues, making them more vulnerable to breakdown from bacteria. Certain systemic diseases involving cyanosis from congenital heart defects or metal intoxication can also directly impact the gingiva through discoloration or tissue damage.
This document discusses gingivitis, including its classification, clinical features, causes, diagnosis, treatment, and prevention. Gingivitis can be classified based on its course (acute, recurrent, chronic) or distribution in the mouth (localized or generalized). Clinical signs include red, swollen gums that bleed easily. Gingivitis is usually caused by plaque buildup and can be prevented through regular brushing, flossing, and dental cleanings. The key to treatment and management is proper oral hygiene and professional dental care.
Burkitt's lymphoma is an undifferentiated B-cell lymphoma that commonly affects the jaws of children, particularly the maxilla. Histopathology shows sheets of small round tumor cells with prominent nuclei and minimal cytoplasm, giving a starry-sky appearance. Hyperparathyroidism is caused by increased PTH secretion or calcium demand, resulting in bone and joint issues. Primary hyperparathyroidism is due to parathyroid hyperplasia while secondary involves chronic renal disease. Mucous membrane pemphigoid is a rare autoimmune blistering disease of the mouth, eyes, and other mucosal surfaces causing blisters, erosions and vision impairment. Treatment requires systemic immunosuppression.
This document discusses protein-energy malnutrition (PEM) in infants and children. It defines malnutrition and the specific forms of PEM, including marasmus and kwashiorkor. For kwashiorkor, it covers the pathophysiology, etiology, clinical signs and symptoms, laboratory findings, and complications. For marasmus it discusses the definition, etiology, clinical assessment, and differences from kwashiorkor. The document also outlines the WHO's 10 steps for recovery from malnutrition and provides a nursing care plan to address malnutrition through dietary interventions and maintaining appropriate body temperature.
Many systemic diseases are reflected in the oral mucosa, maxilla, and mandible.
Mucosal changes may include ulceration or mucosal bleeding.
Immunodeficiency can lead to opportunistic diseases such as infection and neoplasia.
Bone disease can affect the maxilla and mandible.
Systemic disease can cause dental and periodontal changes.
Drugs prescribed for a systemic disease can affect oral tissue.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
etiology of malocclusion for general practitioners.docxDr.Mohammed Alruby
Etiology of Malocclusion
For general practitioners
Prepared by
Dr. M Alruby
Etiology in orthodontics is the study of actual causes of dento – facial abnormalities.
Malocclusion is the condition where there is a deviation from the usual or accepted relationship, dental malocclusion exists when the individual teeth within one or both jaws are abnormally related to each other, this condition may be limited to a couple of teeth or involving the majority of teeth present.
Development of normal dentition and occlusion depends on a number of interrelated factors that include the dento alveolar, skeletal and the neuromuscular factors. Thus localization of the possible etiology may be a very difficult task.
A- Extrinsic factors:
1- Evolution:
With evolution, the jaws become smaller, reduction in the number and size of teeth and diminution of jaw projection together with increased in vertical height of the face and there is retrognathic tendency in man as he ascends the evolutionary scale.
2- Heredity:
Transmission of dento facial characteristic through generation by genes. The child is a product of parents who have dissimilar genetic material. Thus the child may inherit conflicting traits from both the parents resulting in abnormalities of the dentofacial region. Another reason attributed for genetically determined malocclusion is the racial, ethnic and regional intermixer, which might have led to uncoordinated inheritance of teeth and jaws.
There are three types of transmission of malocclusion from the stand point of genetics:
1- Repetitive: the recurrence of single dentofacial deviation within the immediate family.
2- Discontinuous: a tendency for a malocclusion trait to reappear within the family over several generations.
3- Variable: the occurrence of different but related types of malocclusion within several generation of the same family.
Dental defect of genetic origin include the following:
= Crowding and spacing of teeth.
= Size and characteristic of soft tissue including muscles and frenum.
= Macrognathia and micrognathia.
= Macrodontia and microdontia.
= Oligodontia.
= Tooth shape variations.
= Median diastemas.
= upper face height, nose height, and bigonial width.
= Bimaxillary protrusion.
4- Congenital:
Those are deformities of hereditary or non-hereditary origin but exciting at birth.
The congenital abnormalities that cause malocclusion:
= Cleft lip and palate:
lack of fusion between the two palatal processes to each other. From one third to one half of all cleft palate children have familial history of this deformity.
As with the non-cleft child, palatal, pharyngeal and perioral musculature is well developed at birth to meet the demand of suckling, deglutition and mastication. While the complete unilateral or complete bilateral cleft break the continuity of the upper lip and disturbs the functional pattern and significantly reduce the restraining effect of the buccinators mechanism that pro
Gingivitis is the most common form of gingival disease and is caused by bacterial infection resulting in inflammation of the gingival tissue. The characteristics of gingivitis include redness, swelling, bleeding upon provocation, and a change in consistency but no loss of attachment or bone loss. Gingivitis can be classified as dental plaque-induced or non-plaque induced. Dental plaque-induced gingivitis can be modified by local factors, systemic factors, medications, or malnutrition. Non-plaque induced gingivitis can result from bacterial, viral, fungal infections or genetic conditions.
This document discusses the relationship between periodontal disease and various systemic conditions. It covers how diabetes, metabolic syndrome, hormonal factors like pregnancy, and hematologic/immune disorders can influence periodontal health. Specifically, it describes how these conditions can alter the host response and make individuals more susceptible to periodontal pathogens by impairing immune function or increasing inflammation. The document also discusses genetic disorders and stress/psychosomatic factors that predispose to periodontal disease.
This document discusses the influence of various systemic conditions on periodontal health. It covers topics like endocrine disorders and hormonal changes including diabetes mellitus, metabolic syndrome, and effects of puberty, pregnancy, and menopause. It also discusses hematological disorders and immune deficiencies such as leukocyte disorders, leukemia, and various types of anemia. Finally, it touches on genetic disorders, nutrition influences, stress, medication effects, and other systemic conditions and how they can impact periodontal health.
This document provides an overview of periodontal pockets, including:
- Definitions and classifications of periodontal pockets as gingival, periodontal, suprabony, or intrabony pockets.
- Clinical features such as signs of inflammation, bleeding, mobility, and symptoms like pain, sensitivity, and loose teeth.
- Pathogenesis involving the inflammatory response to bacteria, cytokine production, collagen degradation, and pocket formation through destruction of tissues.
- Histopathology showing features like edema, infiltration of leukocytes, epithelial proliferation and degeneration, and bacterial invasion along the pocket walls.
Similar to Influence of Seystemic Diseases on Periodontum (20)
This document discusses oroantral communications and fistulas. It defines them as abnormal connections between the oral and maxillary sinus cavities. Causes include tooth extraction, tumors, cysts, and trauma. Signs and symptoms may include unpleasant taste/odor, fluid/food reflux into the nose, and air leakage. Examination involves inspection, suctioning the socket, and radiographs. Management includes immediate closure attempts and antibiotics to prevent sinusitis. Surgical techniques like buccal and palatal flaps are used for larger defects or fistulas based on factors like location, size, and presence of infection.
Minimum intervention dentistry is a concept based on a better understanding of the caries process and development of the carious process and the development of new diagnostic technologies and adhesives, bioactive restorative materials.
The document discusses principles of wound closure through suturing. It describes various suturing instruments including needles, needle holders, forceps and scissors. It explains the principles of proper suturing technique such as bite size, tension, and knot tying distance from the wound. Different suture materials are also outlined, categorizing them based on absorbability, source, gauge and filament type. Common absorbable and non-absorbable suture materials are named and their properties and uses discussed.
The document discusses wound classification and the normal sequence of wound healing. It defines a wound and classifies wounds based on exposure to the external environment and risk of sepsis. There are two main types of wound healing: primary intention and secondary intention. Primary intention involves clean wounds where the edges are closed, leading to rapid healing. Secondary intention occurs when the edges are separated, requiring slower healing from the bottom up. The normal sequence of wound healing involves three phases - inflammation, proliferation, and remodeling - occurring over days to months.
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The document discusses the importance of preoperative assessment and preparation of patients prior to surgery. Key aspects of assessment include taking a thorough medical history, conducting a physical examination, evaluating nutritional status, ordering relevant investigations, and determining surgical risk. Important elements of preparation are obtaining informed consent, preventing cardiovascular and respiratory complications, reducing risk of aspiration, preparing the bowels if needed, and ensuring adequate sleep, skin preparation, catheterization and pre-medication when applicable. The goals are to identify risk factors, optimize the patient's health status, and reduce postoperative complications.
The lecture presents skills and requirements of the initial interview in dental clinic, how could dentist gain patient rapport and patient's required information to reach diagnosis also identifying pits and errors of initial interview
Local anesthesia complications can be divided into those associated with absorption of the anesthetic solution and those associated with needle insertion. Complications from solution absorption include toxicity from overdose, idiosyncrasy from abnormal reactions, allergy, and anaphylaxis. Toxicity symptoms involve early CNS stimulation and late CNS depression that can lead to respiratory depression and death if not treated. Prevention focuses on careful patient evaluation, using minimum effective doses, and monitoring after injection. Needle insertion complications involve issues like fainting, infection, and nerve injury.
The document discusses various mandibular anesthetic techniques including infiltration anesthesia of the anterior labial, anterior lingual, and long buccal regions as well as inferior alveolar and lingual nerve block. It describes the relevant anatomy, patient positioning, needle selection, injection sites, and steps for each technique. The goal is to effectively anesthetize the nerves supplying sensation to the mandibular teeth and surrounding tissues.
Retracts cheek
6. Inject 1.8 ml of LA solution slowly
7. Withdraw needle and apply pressure
8. Wait for 5 minutes
9. Check anesthesia
ELHAWARY
Maxillary Anesthetic Techniques
Posterior superior alv. N.B. Technique
alv.
Cont.
Advantages Disadvantages
- Anesthetizes the whole area of - Technically more difficult
the posterior maxilla - Risk of intravascular injection
- Longer duration of anesthesia - Risk of hematoma formation
- Less traumatic - Requires an assistant
- Suitable for multiple
The document discusses the preparation and procedures for dental injections. It covers taking a case history, examining the patient, grouping patients based on their health status, and performing sensitivity tests. It then describes the proper positioning of the patient and operator for different procedures. The document outlines the sterilization of equipment and infection control practices. It provides details on the types of syringes, needles, and local anesthetics used. Finally, it discusses the steps for preparing the injection site and properly inserting the needle.
This document discusses the anatomical considerations for local anesthesia, focusing on the trigeminal nerve, its branches (maxillary, mandibular), and associated structures like the sphenopalatine ganglion. It provides detailed descriptions and diagrams of the nerves that innervate the face and oral cavity, including their branches and sensory/motor functions. Key points covered include the branches and distributions of the maxillary and mandibular nerves, as well as the innervation of the maxillary teeth from structures like the posterior superior alveolar nerve.
The document discusses the pharmacology of local anesthesia, including the constituents of local anesthetic cartridges which contain a local anesthetic agent, vasoconstrictor, preservative, and vehicle. It describes the properties and mode of action of common local anesthetic drugs, which are classified as esters or amides, and how they are metabolized and excreted from the body. The document also compares the differences between ester and amide local anesthetics and lists some commonly used local anesthetic agents.
Innervation of the face
The nervvous system
Nerve transmission
Definition of Pain
Pain Receptors
Pain nerve fibers
Reaction to pain
Pain Pathway
Control of Pain
Mode of action of local anesthesia
This document discusses searching for evidence to practice evidence-based dentistry. It describes primary sources like original research articles and secondary sources like systematic reviews, synopses, guidelines, and evidence summaries. Popular secondary sources mentioned include Cochrane Library, DARE, EBD journal, CATs, textbooks like UpToDate, and clinical guidelines from NICE and NGC. The document emphasizes appraising the quality of evidence from different sources and searching efficiently using keywords and databases like PubMed. It notes that absence of evidence found does not mean absence of evidence overall.
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1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
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4. There are no nutritional diffeciences that by
themselves can cause gigivitis or periodontitis but it
can affect the condition of the priodontium &
aggrevate the injurious effect of local factors.
Physical character of the diet :
in experimental animals it was found that:
1- Soft diet ( nutritionally adequate ) plaque and
calculus formation.
2- Hard fibrous food surface cleaning action and
stimulation less plaque and calculus even if
nutritionally inadequate .
5. In humans effect of nutrition ort oral M.O.:
Dietry intake, influence the oral, bacteria as it form
the source of nutrition for bacteria . So, it influence:
Relative distribution of types of organisms.
Metabilic activity of the organisms.
Pathogenicity of organisms.
7. A ) fat soluble Vit.
(1) Vit. A Diffeciency
Function:
maintain the health of epithelial cells of the skin and
m.m.
responsible for re-epitheliazation as epithelial tissues
provide a protective barrier against invading micro-
organisms
Vitamin A diffeciency result in:
dermatologic , mucosal and accular manifestations .
degenerative changes in epithelial tissues
resulting in keratinizing metaplasia .
8. (2) Vit. D “calciferol”
Function:
absorption of calcium from GIT .
maintainer of calcium phosphorus balance
Vitamin D diffeciency result in:
Inexperimaental animals there will be :
1. Osteoprosis of alveolar bone .
2. Sever alveolar bone resorption Proliferation of
fibroblast that replace the bone and marrow New
bone formation around the remnant unresobed bony
trabiculae .
3. Radiographically :
• absence of lamina dura .
• decrease density of supporting bone
• loss of trabeculae.
9. (2) Vit. D "calciferol”
Function:
absorption of calcium from GIT .
maintainer of calcium phosphorus balance
10. (2) Vit. E
Function:
anticxiddant to limit the free radical reaction .
protect cells from peroxidation .
Effect of vit. E diffeciency
no relationship demonstrated between vit.E and oral
disease in humans .
11. B) Water soluble
Vitamins
(1 ) vit, B complex:
Thiamin.
Riboflavin.
Niacin.
Pyridoxine (B6).
Biotin.
Folic acid.
Cobalamin (B12).
12. oral diseases rarely accure due to diffeciency in one
component but diffeciency is generally multiple
Thamin Riboflwin Niacin Folic acid
Diffeciency Diffeciency Diffeciency Diffeciency
1- Beriberi: 1) Glossitis 1) Pellegra : • Macrocytic anemia
• paralysis. • Magenta discoloration •Dermatitis. with megaloplastic
• C.V. symptoms. and atrophy of tongue •GIT disturb. erythropiosis
• Edema . papillae. •Mental disturb.
• Loss of appetite • In mild cases there is •Glossitis. • Diarhea and GIT
patshy atrophy with •Gingivitis. malabsorption
2) orally : engorged fungi form •Stomatitis
• hypersensitwity of papillae. • In luimans :
oral mucosa • In severe cases the a. generalized
• Minute viscles on dorsum tongue is flat, dry stomatitis
• The B. mucosa, and fissured. b. ulcerated glossitis
under the tongue or c. cheihtis
on the palate. 2) Seborrheic
• Errosion of the oral • Dermatits
mucosa
3) Dangular cbeilitis
• Which is inflammation at
the lip commisures.
14. Ariboflavinosis, angular In folate deficiency angular
cheilitis, erythema, and cheilitis may be marked.
atrophy of tongue papillae.
15. (2) Vit. C
Vit. C deficiency lead to :
Scurvy which characterized by :
Haemorrhage lesion into the ms. Of extremities,
joints.
Petechial haemorrhage.
Increase susceptibility to infection around hair follicle
and delayed wound healing .
Bleeding and swollen gingiva.
Loosening of teeth
16. Relationship between vit. C & P. diseases :
Decrease vit. C deficiency influence the metabolism
of collagen in the P. tissues decrease ability of the
tissues to regenerate and repair themselves.
Decrease vit. C deficiency interfere with bone
formation due to failure of osteoblasts to form osteod
and decreased calcification o the osteod tissues
deficiency loss of the periodontal bone .
Increase vit. C deficiency enhance the chemotactic
and migratory action of leukocytes without affecting
their phagocyte activity.
Optimal level of vit. C is required to maintain the
integrity of periodontal microvasculature and wound
healing.
17. Vitamin C deficiency
(scurvy) The characteristic Scurvy, swelling and redness
oral change in scurvy is a of the gingiva.
gingivitis, the papillae being
swollen, with a purple tint and
are fragile.
18. II. protein
deficiency
cells and blood components are formed from protein .
19. Protein deficiency will
lead to
Muscular atrophy and weakness.
Weight loss.
Anemia.
Leukemia.
Edema.
Decrease resistance to infection.
Slaw wound healing.
Decrease ability to form hormones and enzyme.
23. insulin dependent diabetes.
Caused by cell mediated autoimmune
distinction of B. cell of the islets of
pancrease.
Type I
Not preceded by obesity.
Great tendency to coma & ketosis.
In young age & treatment by insulin
injection.
24. Non insulin dependent diabetes.
Caused by peripheral resistance to
insulin impaired insulin secretion and
increased glucose production by the
Type II liver.
Preceded by obesity
Coma and ketosis not common
Adult onset and treatment by diet control
or hypoglycemic agents
25. Gestational diabetes : diabetes associated with
pregnancy in 2% - 5% of women but it
disappear after delivery .
Diabetes associated with diseases involve
pancreas and cause destruction of insulin or
pancreateactomy .
26. Xerostomia .
Gingiva:
inflamed.
enlargement either localized or generalized.
sessile or peduncualted gingival p lips.
Gingival color is bright red dark red .
Alveolar bone destruction, deep periodontal pockets and
looseing of the teeth.
Increased susceptibility to infection due to diffceicncy in
Polymorophnuclear leukocytes impaired chemotactic
and phagocytosis.
27. Frequent abscess formation due to :
high glucose level which serve as bacterial substrate.
impaired chemotactic and phagocytosis of neutrophils.
Impaired wound healing due to and collagenitic activity
and decrease synthesis of collagen which is important for-
wound healing .
Alterations in the bacterial pathogenes and oral microbial
flora this is clue to higher glucose content of gingival
fluid and blood which in turn alter the environment of
microflora in ducing qualitivate changes in bacteria that
account for severity of periodontal disease .
28.
29.
30. 2- Hyper
parthyrodism
It will be lead to:
generalized demineralization of the skeleton .
increase osteoclasits with proliferation of C.T. in the
enlarged marrow spaces diffeciency bone cyst and giant
tumors ( osteitis fibrosa cystica )
oral changes include
Malocclusion and tooth mobility.
Widening of P.L. space.
Absence of lamina dura.
Cyst like space in the jaws, diffeciency filled with
fibrous tissues and haemosedrin laden macrophages
and giant cells ( brown tumors ).
32. 3- Sex
hormones
Gingival changes in puberty :
Exaggerated response of the gingiva to local factors.
Pronounced in flammation , bluish red discoloration ,
edema and enlargement .
Increased tendency for bleeding .
Gingival changes with menstrual cycle :
not-accompaneid with notable gingival change .
33. Gingival changes in pregnancy :
pregnancy itself does not cause gingivities.
pregnancy accentuate the gingival response lo plaque.
no notable change occure with absence of local factors.
Enlarged, edematous, discolored gingiva.
increased tooth mobility, pocket depth and gingival
fluids.
marginal and interdental gingiva are edematous, piton
pressure, appear smooth and shiny.
discrete tumor like masses (pregnancy tumor).
due to increase levels of progesterone hormons which
cause:
Dilatation and tortuosity of gingival microvasculary .
Circulatory stasis .
Susceptibility to mechanical irritation.
36. 1.Leukemia
Def. Malignant neoplasias of WBCs.
precursors characterized by :
replacement of the bone marrow with leukaemic cells.
abnormal no. and forms of immature W.B.Cs in the
blood.
wide spread infiltrate in the liver, spleen, L.N. and other
sites throughout the body.
In all types of leukaemia there is : -
decrease in R.B.Cs anemia.
decrease in platelet tlrombocytopenia.
37. Periodontium in leukaemic patients :
leukaemic gingival enlargement.
Bluish red and cyanotic gingiva.
Rounded tens gingival margin .
Bleeding in leukaemic patients:
pctechae, echymosis and spontaneous bleeding
commonly occur due to replacement of the bone marrow
cells by leukaemic cells and inhibition of normal stem
cells function by leukaemic cells or their infiltrate.
38. Oral ulceration and infections in leukaemic
patients:
granulocytopenia resulting from replacement of the
bone marrow by leukaemic cells decrease tissues
resistance to M.O. opportunistic infections
discrete, punched out ulcer penetrate deeply into
submucosa and covered by firmly attached white slough
in the palate or in B. mucosa along the line of occlusion.
Gingiva is bluish red in color, sponge like, friable and
bleed easily.
39. Acute myelomonocytic leukemia, Acute myelocytic leukemia,
severe gingival enlargement. marked gingival enlargement.
Chronic lymphocytic leukemia, Chronic lymphocytic leukemia,
ulcer on the palate. severe gingival enlargement.
40. 2. Anemia
Def. Deficiency in the quantity or quality of the blood
manifested by reduction in no. of erytluocytes and the
amount of haemoglobin.
Types:
1) Pernicious anemia :
Tongue atrophy red , smooth and shiny appearance .
pallor gingiva .
Pernicious anemia, smooth, red,
and shiny dorsum of the tongue.
41. 2) Sickle cell anemia :
generalized osteoprosi.s of the jaw.
pallor and yellowish discoloration of the oral mucosa.
periodontal in fection may precipitate sickle cell crisis.
pallor, jundice, weakness and reumatoid
manifestations.
42. 3) Iron deficiency anemia :
glossitis.
Ulceration of oral mucosa and oropharynx, inducing
dysphagia, (Plummer - Vinson syndrome).
Iron deficiency anemia, smooth Plummer-Vinson syndrome, redness and
dorsal surface of the tongue. atrophy of tongue papillae associated
with angular cheilitis.
43. 4) Aplastie anemia :
occure due to failure of the bone marrow to produce
erythrocytes. As a result of toxic drugs .
• pale discoloration of the oral rnucosa.
• increased susceptibility to infection.
Aplastic anemia, ecchymoses
and ulcers on the tongue.
44. 3. Thrombocytopenia
Etiology:
• Idiopathic.
Effects :
• Spontaneous bleeding in the skin and m.m.
• petechae and haemorrhage vesicles in the palate,
tonsillar pillar and the buccal mucosa.
• the gingiva swollen, soft, friable, bleed easily and
difficult control the bleeding.
Idiopathic thrombo-cytopenic
purpura, petechiae and
ecchymoses of the buccal
mucosa.
46. It affect the oral cavity by :
1) development of habits that are injures to the
periodontium as grinding or clenching the teeth,
nibbing on foreign objects as pencils, nail biting of
excessive use of tobacco gingiaval recession and
periodontal diseases .
2) direct effect to the autonomic nervous system on the
psycologic tissue balance.
48. Leukocyte disorders :
Disorders that affect production or function of
leukocytes severe P. distinction.
Cyclic neutropenia, ulcer
on the labial mucosa
49. Agranulocytosis :
Characters:
reduction in the no. of circulating granulocytes.
Etiology:
occur due to drug idiosyncrasy which occur as acute
disease, but some items it may reappear in cyclic
episodes (Cyclic neutropenia).
Effects :
sever infections including ulcerative necroting lesions
of the oral mucosa skin, GIT and genitourinary tract .
Fever, malaise, general weakness and sore throat .
The mucosa exhibit isolated black to gray necrotic
patches that are sharply demarcated from the adjacent
uninvolved areas .
Gingival hemorrhage, necrosis, increased salivation and
fetid odor.
50. Agranulocytosis, ulcer on Agranulocytosis, severe
the tongue. periodontal destruction.
Agranulocytosis, mild
periodontal destruction.
51. AIDS:
Etiology :
• human Immuno deficiency virus .
Effects:
• Destruction of lymphocytes increase susceptibility to
opportunistic infections including destructive
periodontitis and malignancies .
53. Bismuth intoxication:
It will lead to
GIT disturbances, Nausea, Jaundice.
Lucrative gingivostomatitis with pigmentation.
Metallic taste.
Burning sensation of the mucosa .
Inflamed sore tongue .
Erythromatous eruptions of different types and hyrpes
zoster like eruptions of the skin and m.m.
Narrow bluish black discoloration of the gingiaval
margin due to precipitation of bismuth sulfide
associated with vascular changes in
inflammation of the gingiva .
54. Lead in toxication :
It will lead to :
pallar of face and lips .
GIT disturbances including nausea , vomiting , loss of
apetite and abdominal colic .
Peripheral neuritis, psycologic disorders and
encephalitis .
Excessive salivation .
Coated tongue .
Sweetish taste.
Gingival ulceration and pigmentation (Linear
pigmentation in burtonian line, Steel gray )
55. Mercury in toxication :
It will lead to :
Headache .
Isornnia .
C.V.S. sympioms .
Increase salivation .
Metallic taste .
Giugival pigmentation in liner pattern due to mercuric
sulfide.
Gingival ulceration and destruction of the underlying
bone.
56. Other chemicals :
Include :
Phosphorus .
Arsenic .
Chromium .
It will lead to :
Inflammation and ulceration of the gingiva .
Necrosis of alveolar bone and loosening of teeth .