This document discusses gingival and periodontal diseases in children. It begins with an introduction and overview, then discusses characteristics of the normal child periodontium compared to adults. It describes various gingival diseases that can occur in children such as gingivitis, nectrotizing ulcerative gingivitis, drug-induced gingival enlargements, and periodontitis. It also discusses how periodontal diseases can be associated with or exacerbated by certain systemic diseases and conditions in children. The document provides details on clinical features, causes, and treatment approaches for many of these pediatric oral diseases.
Taurodontism is a condition where the body of the tooth is enlarged at the expense of the root, resulting in an elongated tooth body and short roots. It is caused by a failure of the epithelial root sheath to invaginate properly during tooth development. Taurodontism can range from mild to severe and may affect deciduous or permanent molars either unilaterally or bilaterally. Radiographically, there is an extremely large pulp chamber that extends into the elongated tooth body and short, wide roots. Diagnosis is based on the characteristic rectangular tooth crown and large pulp chamber seen clinically or radiographically. No treatment is needed as taurodontism does not typically cause clinical problems.
The document defines a dental home as an ongoing relationship between a dentist and patient that provides comprehensive, accessible, and family-centered oral healthcare from infancy through adolescence. A dental home has characteristics like being accessible in the community, family-centered, providing unbiased information continuously, and being comprehensive, coordinated, and compassionate. When a parent or caregiver approaches a dental home, the dentist will take a history, do an examination, and do a risk assessment to enhance the dentist's ability to assist the child and family with optimal oral healthcare.
This document discusses the management of Class IV Ellis fractures, which involve trauma to teeth resulting in pulp involvement or loss of crown structure. It describes the emergency treatment, which may include reinserting an avulsed tooth. Intermediate treatment options for exposed or necrotic pulps include pulpectomy, apexification, or extraction. Pulpectomy involves conventional root canal treatment to eliminate infection, while apexification induces formation of new tissue at the root end in immature teeth. The document also discusses crown fractures involving enamel, dentin, or both, and the treatment options depending on the extent of injury and pulp involvement. These may include protective dressings, temporary crowns, or reattachment of fragments.
Pulpitis refers to inflammation of the dental pulp and can be acute or chronic. Acute pulpitis is reversible or irreversible, with irreversible pulpitis involving more severe pain. Chronic pulpitis presents with dull, continuous pain. Complications of pulpitis include periapical periodontitis, periapical abscess, periapical granuloma, and radicular cyst formation. Left untreated, pulpitis and its complications can spread and cause cellulitis or other severe infections.
The wasting diseases of teeth, namely attrition, abrasion and dental erosion have taken their toll in the population around the world due to the changing lifestyles, increase in the stress levels and many others factors that were persistent earlier but have suddenly increased drastically. This presentation brings to light the new factors that have attributed to this condition as well as discusses the previous ones.
Necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP) are microbial diseases caused by a mixed bacterial infection and impaired host response. NUG presents with crater-like ulcers and gray pseudomembrane on the gums, accompanied by pain and foul taste. If untreated, NUG can progress to NUP and involve bone loss. Treatment involves removing debris, using antiseptics like chlorhexidine, scaling, and antibiotics in severe cases. Prognosis is good with proper treatment and maintenance of oral hygiene.
This seminar includes features of the normal periodontium seen in children along with various gingival and periodontal diseases seen in children with updated classifications along with clinical features and treatment modalities and a note on clinical assessment of oral cleanliness and periodontal diseases
The document summarizes various abnormalities and diseases that can affect the dental pulp and periapical tissues, including:
1) Pulp calcification, which involves mineralization within the pulp chamber or root canals and can occur as denticles, pulp stones, or diffuse linear calcifications.
2) Resorption of teeth, which can be physiological for deciduous teeth but pathological for permanent teeth.
3) Diseases of periapical tissues including periapical abscesses, granulomas, radicular cysts, phoenix abscesses, and condensing osteitis. These conditions are responses to dental infection and inflammation and can develop from other lesions if left untreated.
Taurodontism is a condition where the body of the tooth is enlarged at the expense of the root, resulting in an elongated tooth body and short roots. It is caused by a failure of the epithelial root sheath to invaginate properly during tooth development. Taurodontism can range from mild to severe and may affect deciduous or permanent molars either unilaterally or bilaterally. Radiographically, there is an extremely large pulp chamber that extends into the elongated tooth body and short, wide roots. Diagnosis is based on the characteristic rectangular tooth crown and large pulp chamber seen clinically or radiographically. No treatment is needed as taurodontism does not typically cause clinical problems.
The document defines a dental home as an ongoing relationship between a dentist and patient that provides comprehensive, accessible, and family-centered oral healthcare from infancy through adolescence. A dental home has characteristics like being accessible in the community, family-centered, providing unbiased information continuously, and being comprehensive, coordinated, and compassionate. When a parent or caregiver approaches a dental home, the dentist will take a history, do an examination, and do a risk assessment to enhance the dentist's ability to assist the child and family with optimal oral healthcare.
This document discusses the management of Class IV Ellis fractures, which involve trauma to teeth resulting in pulp involvement or loss of crown structure. It describes the emergency treatment, which may include reinserting an avulsed tooth. Intermediate treatment options for exposed or necrotic pulps include pulpectomy, apexification, or extraction. Pulpectomy involves conventional root canal treatment to eliminate infection, while apexification induces formation of new tissue at the root end in immature teeth. The document also discusses crown fractures involving enamel, dentin, or both, and the treatment options depending on the extent of injury and pulp involvement. These may include protective dressings, temporary crowns, or reattachment of fragments.
Pulpitis refers to inflammation of the dental pulp and can be acute or chronic. Acute pulpitis is reversible or irreversible, with irreversible pulpitis involving more severe pain. Chronic pulpitis presents with dull, continuous pain. Complications of pulpitis include periapical periodontitis, periapical abscess, periapical granuloma, and radicular cyst formation. Left untreated, pulpitis and its complications can spread and cause cellulitis or other severe infections.
The wasting diseases of teeth, namely attrition, abrasion and dental erosion have taken their toll in the population around the world due to the changing lifestyles, increase in the stress levels and many others factors that were persistent earlier but have suddenly increased drastically. This presentation brings to light the new factors that have attributed to this condition as well as discusses the previous ones.
Necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP) are microbial diseases caused by a mixed bacterial infection and impaired host response. NUG presents with crater-like ulcers and gray pseudomembrane on the gums, accompanied by pain and foul taste. If untreated, NUG can progress to NUP and involve bone loss. Treatment involves removing debris, using antiseptics like chlorhexidine, scaling, and antibiotics in severe cases. Prognosis is good with proper treatment and maintenance of oral hygiene.
This seminar includes features of the normal periodontium seen in children along with various gingival and periodontal diseases seen in children with updated classifications along with clinical features and treatment modalities and a note on clinical assessment of oral cleanliness and periodontal diseases
The document summarizes various abnormalities and diseases that can affect the dental pulp and periapical tissues, including:
1) Pulp calcification, which involves mineralization within the pulp chamber or root canals and can occur as denticles, pulp stones, or diffuse linear calcifications.
2) Resorption of teeth, which can be physiological for deciduous teeth but pathological for permanent teeth.
3) Diseases of periapical tissues including periapical abscesses, granulomas, radicular cysts, phoenix abscesses, and condensing osteitis. These conditions are responses to dental infection and inflammation and can develop from other lesions if left untreated.
Dental erosion is the irreversible loss of tooth structure caused by chemical processes rather than bacteria. It occurs when teeth come into contact with acids from internal sources like reflux or vomiting, or external sources like acidic drinks. It results in cup-shaped lesions in enamel surrounded by raised dentin. Salivary flow rate, pH, and buffering capacity are related, with higher flow resulting in higher pH and buffering capacity to neutralize acids. Lower salivary flow and buffering from medications or diseases increase risk of erosion. Another form of tooth wear is abfraction, which causes wedge-shaped cervical lesions from flexing forces on teeth during biting.
Dentinogenesis imperfecta is a hereditary condition that affects the formation of dentin in both primary and permanent teeth. It is classified into two main types - dentinogenesis imperfecta type 1 and type 2. Type 1 is caused by mutations in the DSPP gene and affects only the teeth. Type 2 may be caused by mutations in two tightly linked genes and is characterized by multiple pulp exposures and shell-like teeth. Treatment aims to prevent wear of enamel and dentin through full coverage restorations.
Tooth resorption is the progressive loss of dentine and cementum by the action of osteoclasts. This is a physiological process in the exfoliation of the primary dentition, caused by osteoclast differentiation due to pressure exerted by the erupting permanent tooth
This document discusses several conditions related to abnormalities in dentin formation, including dentinogenesis imperfecta and dentin dysplasia. It describes the genetic basis, clinical and radiographic features, classifications, and histopathological characteristics of these inherited disorders. The key features include opalescent or discolored teeth, bulbous crowns, thin dentin, enlarged pulp chambers, shortened roots, and premature tooth loss. Classification systems include those proposed by Shields and Witkop. Treatment may involve extraction and dental prosthetics due to poor cosmetic outcomes and functional complications.
Definition of pulpitis, Factors causing injury to the pulp, aerodontalgia, classification of pulpitis, clinical features of various types of pulpitis, histopathology and its treatment are inlisted in this presentation.
This document discusses different types of periapical abscesses, including acute periapical abscesses, phoenix abscesses, and chronic alveolar abscesses. It describes the etiology, symptoms, diagnosis, and treatment of each. Bacteria entering the pulp through breaks in dentin are the most common cause of these periradicular tissue lesions. Acute periapical abscesses present with rapid onset pain and swelling, while chronic alveolar abscesses are generally asymptomatic but can be detected by sinus tracts or radiographs. Treatment involves drainage, antibiotics if needed, and resolving the pulpal infection through root canal treatment or extraction.
This document discusses various dental conditions including attrition, abrasion, erosion, abfraction, fractures, enamel hypoplasia, and discoloration. It provides details on the causes, clinical features, and characteristics of each condition. Attrition is defined as wear from tooth-to-tooth contact, while abrasion is caused by direct friction from external objects. Erosion involves chemical dissolution of tooth structure from acids. Abfraction results from biomechanical forces causing flexure and fatigue away from the point of loading. Enamel hypoplasia occurs when enamel formation is disrupted, resulting in pits or grooves in the enamel surface.
1. Gingival recession is the exposure of root surface caused by an apical shift in gingival position. It can be classified as visible, hidden, localized, or generalized.
2. Miller and Atkin & Sullivan classified gingival recession defects based on their location and amount of bone loss. Common causes of recession include age, faulty brushing technique, tooth malposition, gingival inflammation, abnormal frenal attachment, and masochistic habits.
3. Recession can be treated non-surgically through modifying risks or surgically through pedicle or free soft tissue grafts to cover exposed root surfaces and reduce sensitivity.
Ankylosis is the fusion of a tooth root to the alveolar bone due to lack of periodontal ligament space. It occurs most commonly in deciduous teeth, especially the mandibular second molar, as a result of root resorption followed by fusion to the bone. This prevents normal exfoliation of deciduous teeth and impaction of the permanent successor. Ankylosis can be caused by local metabolic changes, trauma, infection or abnormal tongue pressure. Clinically, ankylosed teeth appear sunken, lack mobility, and percussion elicits a solid sound. Radiographically, there is partial or complete absence of the periodontal ligament space and lamina dura. Treatment depends on
This document discusses various classifications and types of periapical diseases including symptomatic and asymptomatic apical periodontitis, acute alveolar abscess, phoenix abscess, persistent apical periodontitis, chronic alveolar abscess, radicular cyst, condensing osteitis, and different types of external and internal root resorption. It provides definitions, causes, symptoms, diagnostic features and treatment options for each condition.
This document discusses various classifications of pulpal diseases. It describes classifications proposed by Grossman, Baume, Seltzer & Bender, Johnson, American Board of Endodontics, Reit et al., Walton & Torabinejad, Torabinejad & Shabahang, Tronstad, Ingle & Beveridge, Castelucci, Beer & Baumann, Abbott, and the World Health Organization. Many classifications divide pulpal diseases into categories such as normal pulp, reversible pulpitis, irreversible pulpitis, necrosis, hyperplastic pulpitis, and previously treated pulp. The classifications aim to help with treatment planning, prognosis determination, and assessing restorative needs based on the signs and symptoms of
Teeth don’t possess regenerative ability found in most other tissues. Therefore, once enamel & dentin are lost as a result of caries, trauma or wear, restorative material must be used, to reestablish form & function.
Teeth require preparation to receive restoration & these preparations must be based on fundamental principles, which are discussed in this presentation, from which basic criteria can be developed to help predict the success of prosthodontic treatment.
This document discusses Necrotizing Ulcerative Gingivitis (NUG), also known as trench mouth. It defines NUG as a microbial disease of the gingiva caused by an impaired host response. Key clinical features include necrosis of gingival tissue and pain. Diagnosis is based on these clinical findings and microscopic examination. Management involves reducing the microbial load, removing necrotic tissue, treating any systemic conditions, and supportive periodontal therapy. Prognosis is generally good with treatment but recurrence is possible without ongoing maintenance of oral hygiene.
This document describes the clinical features of the gingiva. It discusses the four main anatomical portions of the gingiva: the gingival sulcus, free gingiva, interdental gingiva, and attached gingiva. It provides details on the texture, color, contour, and size of healthy gingiva. Key anatomical landmarks are then described in more depth, including the gingival sulcus, marginal gingiva, attached gingiva, and interdental gingiva. Probings depths and widths of different regions are provided. Diagrams are included to illustrate features like the interdental col in different situations.
Dental caries leads to changes in the enamel and dentin, including tubular sclerosis, reactionary dentine, and dead tracts formation. Left untreated, dental caries can cause pulpitis, which involves inflammation of the pulp and can be reversible, acute, or chronic. Pulpitis and pulp necrosis can further lead to apical periodontitis, periapical abscess, osteomyelitis, or cellulitis as the infection spreads. Advanced stages include formation of a periapical cyst, bone destruction, and soft tissue infection.
Dental attrition is a type of tooth wear caused by tooth-to-tooth contact, resulting in loss of tooth tissue, usually starting at the incisal or occlusal surfaces. Tooth wear is a physiological process and is commonly seen as a normal part of aging.
This document discusses gingival diseases that can affect children. It begins by describing normal pediatric periodontium and then classifies and describes various gingival diseases including eruption gingivitis, dental plaque-induced gingivitis, acute conditions like herpes gingivostomatitis and recurrent aphthous ulcers, and gingival diseases modified by systemic factors. Treatment options are provided for each condition with an emphasis on prevention, improved oral hygiene and dental care, and management of predisposing factors.
This document discusses the anatomy and common conditions of the periodontium in children. It describes the features of the gingiva, periodontal ligament, cementum, and alveolar bone in children. Common gingival conditions in children mentioned include gingivitis, drug-induced gingival overgrowth, periodontal complications of orthodontic treatment, and early-onset aggressive periodontal disease. Specific conditions discussed in more detail include primary herpetic gingivostomatitis, acute necrotizing ulcerative gingivitis, chronic gingivitis, and Papillon-Lefevre Syndrome. The document emphasizes the importance of oral hygiene and prevention in children's oral health.
Dental erosion is the irreversible loss of tooth structure caused by chemical processes rather than bacteria. It occurs when teeth come into contact with acids from internal sources like reflux or vomiting, or external sources like acidic drinks. It results in cup-shaped lesions in enamel surrounded by raised dentin. Salivary flow rate, pH, and buffering capacity are related, with higher flow resulting in higher pH and buffering capacity to neutralize acids. Lower salivary flow and buffering from medications or diseases increase risk of erosion. Another form of tooth wear is abfraction, which causes wedge-shaped cervical lesions from flexing forces on teeth during biting.
Dentinogenesis imperfecta is a hereditary condition that affects the formation of dentin in both primary and permanent teeth. It is classified into two main types - dentinogenesis imperfecta type 1 and type 2. Type 1 is caused by mutations in the DSPP gene and affects only the teeth. Type 2 may be caused by mutations in two tightly linked genes and is characterized by multiple pulp exposures and shell-like teeth. Treatment aims to prevent wear of enamel and dentin through full coverage restorations.
Tooth resorption is the progressive loss of dentine and cementum by the action of osteoclasts. This is a physiological process in the exfoliation of the primary dentition, caused by osteoclast differentiation due to pressure exerted by the erupting permanent tooth
This document discusses several conditions related to abnormalities in dentin formation, including dentinogenesis imperfecta and dentin dysplasia. It describes the genetic basis, clinical and radiographic features, classifications, and histopathological characteristics of these inherited disorders. The key features include opalescent or discolored teeth, bulbous crowns, thin dentin, enlarged pulp chambers, shortened roots, and premature tooth loss. Classification systems include those proposed by Shields and Witkop. Treatment may involve extraction and dental prosthetics due to poor cosmetic outcomes and functional complications.
Definition of pulpitis, Factors causing injury to the pulp, aerodontalgia, classification of pulpitis, clinical features of various types of pulpitis, histopathology and its treatment are inlisted in this presentation.
This document discusses different types of periapical abscesses, including acute periapical abscesses, phoenix abscesses, and chronic alveolar abscesses. It describes the etiology, symptoms, diagnosis, and treatment of each. Bacteria entering the pulp through breaks in dentin are the most common cause of these periradicular tissue lesions. Acute periapical abscesses present with rapid onset pain and swelling, while chronic alveolar abscesses are generally asymptomatic but can be detected by sinus tracts or radiographs. Treatment involves drainage, antibiotics if needed, and resolving the pulpal infection through root canal treatment or extraction.
This document discusses various dental conditions including attrition, abrasion, erosion, abfraction, fractures, enamel hypoplasia, and discoloration. It provides details on the causes, clinical features, and characteristics of each condition. Attrition is defined as wear from tooth-to-tooth contact, while abrasion is caused by direct friction from external objects. Erosion involves chemical dissolution of tooth structure from acids. Abfraction results from biomechanical forces causing flexure and fatigue away from the point of loading. Enamel hypoplasia occurs when enamel formation is disrupted, resulting in pits or grooves in the enamel surface.
1. Gingival recession is the exposure of root surface caused by an apical shift in gingival position. It can be classified as visible, hidden, localized, or generalized.
2. Miller and Atkin & Sullivan classified gingival recession defects based on their location and amount of bone loss. Common causes of recession include age, faulty brushing technique, tooth malposition, gingival inflammation, abnormal frenal attachment, and masochistic habits.
3. Recession can be treated non-surgically through modifying risks or surgically through pedicle or free soft tissue grafts to cover exposed root surfaces and reduce sensitivity.
Ankylosis is the fusion of a tooth root to the alveolar bone due to lack of periodontal ligament space. It occurs most commonly in deciduous teeth, especially the mandibular second molar, as a result of root resorption followed by fusion to the bone. This prevents normal exfoliation of deciduous teeth and impaction of the permanent successor. Ankylosis can be caused by local metabolic changes, trauma, infection or abnormal tongue pressure. Clinically, ankylosed teeth appear sunken, lack mobility, and percussion elicits a solid sound. Radiographically, there is partial or complete absence of the periodontal ligament space and lamina dura. Treatment depends on
This document discusses various classifications and types of periapical diseases including symptomatic and asymptomatic apical periodontitis, acute alveolar abscess, phoenix abscess, persistent apical periodontitis, chronic alveolar abscess, radicular cyst, condensing osteitis, and different types of external and internal root resorption. It provides definitions, causes, symptoms, diagnostic features and treatment options for each condition.
This document discusses various classifications of pulpal diseases. It describes classifications proposed by Grossman, Baume, Seltzer & Bender, Johnson, American Board of Endodontics, Reit et al., Walton & Torabinejad, Torabinejad & Shabahang, Tronstad, Ingle & Beveridge, Castelucci, Beer & Baumann, Abbott, and the World Health Organization. Many classifications divide pulpal diseases into categories such as normal pulp, reversible pulpitis, irreversible pulpitis, necrosis, hyperplastic pulpitis, and previously treated pulp. The classifications aim to help with treatment planning, prognosis determination, and assessing restorative needs based on the signs and symptoms of
Teeth don’t possess regenerative ability found in most other tissues. Therefore, once enamel & dentin are lost as a result of caries, trauma or wear, restorative material must be used, to reestablish form & function.
Teeth require preparation to receive restoration & these preparations must be based on fundamental principles, which are discussed in this presentation, from which basic criteria can be developed to help predict the success of prosthodontic treatment.
This document discusses Necrotizing Ulcerative Gingivitis (NUG), also known as trench mouth. It defines NUG as a microbial disease of the gingiva caused by an impaired host response. Key clinical features include necrosis of gingival tissue and pain. Diagnosis is based on these clinical findings and microscopic examination. Management involves reducing the microbial load, removing necrotic tissue, treating any systemic conditions, and supportive periodontal therapy. Prognosis is generally good with treatment but recurrence is possible without ongoing maintenance of oral hygiene.
This document describes the clinical features of the gingiva. It discusses the four main anatomical portions of the gingiva: the gingival sulcus, free gingiva, interdental gingiva, and attached gingiva. It provides details on the texture, color, contour, and size of healthy gingiva. Key anatomical landmarks are then described in more depth, including the gingival sulcus, marginal gingiva, attached gingiva, and interdental gingiva. Probings depths and widths of different regions are provided. Diagrams are included to illustrate features like the interdental col in different situations.
Dental caries leads to changes in the enamel and dentin, including tubular sclerosis, reactionary dentine, and dead tracts formation. Left untreated, dental caries can cause pulpitis, which involves inflammation of the pulp and can be reversible, acute, or chronic. Pulpitis and pulp necrosis can further lead to apical periodontitis, periapical abscess, osteomyelitis, or cellulitis as the infection spreads. Advanced stages include formation of a periapical cyst, bone destruction, and soft tissue infection.
Dental attrition is a type of tooth wear caused by tooth-to-tooth contact, resulting in loss of tooth tissue, usually starting at the incisal or occlusal surfaces. Tooth wear is a physiological process and is commonly seen as a normal part of aging.
This document discusses gingival diseases that can affect children. It begins by describing normal pediatric periodontium and then classifies and describes various gingival diseases including eruption gingivitis, dental plaque-induced gingivitis, acute conditions like herpes gingivostomatitis and recurrent aphthous ulcers, and gingival diseases modified by systemic factors. Treatment options are provided for each condition with an emphasis on prevention, improved oral hygiene and dental care, and management of predisposing factors.
This document discusses the anatomy and common conditions of the periodontium in children. It describes the features of the gingiva, periodontal ligament, cementum, and alveolar bone in children. Common gingival conditions in children mentioned include gingivitis, drug-induced gingival overgrowth, periodontal complications of orthodontic treatment, and early-onset aggressive periodontal disease. Specific conditions discussed in more detail include primary herpetic gingivostomatitis, acute necrotizing ulcerative gingivitis, chronic gingivitis, and Papillon-Lefevre Syndrome. The document emphasizes the importance of oral hygiene and prevention in children's oral health.
1. Periodontal disease is caused by bacterial plaque accumulation on the teeth and gums, leading to inflammation and potential bone and tissue destruction if left untreated.
2. Proper oral hygiene through regular brushing and flossing is important to mechanically remove plaque and prevent periodontal disease. Effective brushing techniques like the roll method and Charter's method can help clean between teeth and massage gums.
3. In addition to home care, regular dental cleanings every 3-4 months may be needed to remove tartar buildup which can lead to periodontal disease. Maintaining good oral hygiene from a young age helps prevent periodontal problems.
Gingival and Periodontal Diseases in children is a presentation that covers various gingival and periodontal diseases that can affect children. It begins with an introduction to how periodontal diseases often begin in childhood and the importance of early detection and treatment. It then discusses various gingival diseases including eruption gingivitis, dental plaque induced gingivitis, allergies and gingival inflammation. It also covers acute gingival diseases such as herpetic gingivostomatitis, recurrent aphthous ulcers, acute necrotizing ulcerative gingivitis, and acute candidiasis. Treatment options are provided for each condition.
The document discusses gingival and periodontal diseases in children. It notes key differences in the child periodontium compared to adults, such as a thicker and rounder free gingiva. Gingivitis is more common than periodontitis in children and tends to be more transient and acute. Common gingival diseases in children include pericoronitis, eruptive gingivitis, and acute necrotizing ulcerative gingivitis. Common periodontal diseases are prepubertal and early onset periodontitis. Localized and generalized early onset periodontitis are classifications. Gingivitis is characterized by inflammation, bleeding, and color/texture changes of the gingiva. Local irrit
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.
This document discusses gingival enlargement, including its classification, causes, clinical features, histopathology, and assessment methods. It covers inflammatory enlargement from chronic and acute causes. It also covers drug-induced enlargement, particularly from anticonvulsants like phenytoin. Assessment methods are described that measure the degree, location, and distribution of gingival enlargement. The document provides detailed information on the pathogenesis, clinical presentation, and microscopic features of different types of gingival enlargement.
This document provides information on gingival and periodontal diseases. It discusses various types of gingival diseases like gingivitis, acute gingival diseases, gingival enlargement. It also covers different types of periodontal diseases like chronic periodontitis, aggressive periodontitis. Periodontal diseases are infectious diseases that cause destruction of tissues supporting the teeth. Nearly 75% of adults suffer from some form of periodontal disease. Early detection and treatment can help most people keep their teeth for life.
This document discusses different types of gingival enlargement, including inflammatory, drug-induced, conditioned by systemic factors, idiopathic, neoplastic, and false enlargement. Inflammatory enlargement is usually caused by chronic inflammation from poor oral hygiene. Drug-induced enlargement can be caused by anticonvulsants, immunosuppressants, and calcium channel blockers. Conditioned enlargement is exacerbated by hormonal, allergic or nutritional factors. Neoplastic enlargement involves benign or malignant tumors of the gingiva. False enlargement is due to underlying dental or bone anomalies rather than issues with the gingiva.
This document discusses gingival diseases in children. It notes that the gingiva of deciduous dentition is normally pale and thin, with stippling appearing around age 3 in some children. The attached gingiva widens with age but is narrower mesiodistally. Chronic marginal gingivitis is the most common gingival disease in childhood, presenting as red linear inflammation, though bleeding and increased pocket depth are less common than in adults. Puberty gingivitis may also occur, with prevalence peaking from ages 11-13. Dental plaque and pathogens like P. gingivalis contribute to gingivitis in children.
This document discusses gingival enlargement from multiple perspectives. It begins by defining key terms like hyperplasia and hypertrophy. It then categorizes enlargement based on location, etiology, degree, and associated conditions. Chronic inflammatory enlargement and acute conditions like gingival abscesses are explained. Drug-induced, hereditary, and condition-associated enlargements are explored. Systemic diseases that can cause enlargement like leukemia and Wegener's granulomatosis are summarized. The document concludes with an overview of neoplastic enlargements.
This document provides an overview of gingival enlargement (gingival overgrowth). It discusses the classification of gingival enlargement, including inflammatory, drug-induced, idiopathic, and enlargement associated with systemic diseases. Drug-induced gingival enlargement is a common side effect of certain anticonvulsants, immunosuppressants, calcium channel blockers, and other drugs. The enlargement caused by drugs may be complicated by secondary inflammation from plaque and bacteria. Proper oral hygiene and discontinuing the causative drug can help resolve drug-induced gingival enlargement over time.
Dr. Hazem El Ajrami discusses the prevention of periodontal disease. He outlines several key points:
- Periodontal disease is caused by bacterial plaque accumulation along the gums and teeth. Regular removal of plaque through brushing and other methods can prevent periodontal disease.
- Both local factors like untreated cavities, occlusal abnormalities, and systemic factors like diabetes or medications can increase risk of periodontal disease by affecting the body's response to plaque.
- Preventive measures include regular dental cleanings to remove built-up calculus, maintaining good oral hygiene through proper brushing techniques, and eating a balanced diet to stimulate gum health. Periodic checkups are important to monitor for bone
This document discusses gingival and periodontal diseases. It describes gingivitis as inflammation of the gingiva that is limited to the gingival tissue and does not involve bone loss. Periodontal disease is an infectious disease that destroys the tissues supporting the teeth, including the gingiva, periodontal ligament, and alveolar bone, potentially leading to tooth loss. It affects 75% of American adults and is classified based on severity and location of tissue destruction. Treatment involves removing dental plaque and calculus through scaling and root planing along with antibiotics in some cases.
Chronic periodontitis is the most common form of periodontitis, characterized by a slowly progressive inflammation and destruction of the tissues surrounding the teeth. It is caused by an excessive host response to bacterial plaque accumulated at and below the gumline. Symptoms include bleeding gums, deepening pockets between teeth, and loose or mobile teeth. The disease progresses gradually over time as plaque accumulates. Risk factors include a prior history of periodontitis, poor plaque control, diabetes, smoking, stress, and certain genetic factors.
This document summarizes the clinical features and progression of gingivitis and chronic periodontitis. It begins by describing gingivitis, including its acute, chronic, and localized vs generalized forms. It then discusses how inflammation can extend from the gingiva into the supporting periodontal tissues, characterizing chronic periodontitis by microbial plaque, inflammation, attachment and bone loss over time. Key signs include pocket formation and bleeding on probing.
THE PRESENTATION INCLUDES VARIOUS ASPECTS IN PEDODONTIC AND PREVENTIVE DENTISTRY THAT PROVIDES both primary and comprehensive, preventive and therapeutic oral health care for infants and children through adolescence, including those with special health care needs.
Gingivitis is a non-destructive periodontal disease caused by bacterial biofilms (plaque) on tooth surfaces. It is characterized by swollen, red or purple gums that bleed easily. While gingivitis is reversible with improved oral hygiene, it can progress to periodontitis if left untreated. Risk factors include poor oral hygiene, smoking, stress, certain medical conditions and medications. Gingivitis is treated by removing the bacterial plaque through regular brushing, flossing and professional cleanings.
Similar to GINGIVAL and PERIODONTAL DISEASE.ppt (20)
1. Oral habits such as thumb sucking, lip biting, and tongue thrusting are common in children and can persist beyond normal development stages, potentially affecting dental development.
2. Thumb sucking is classified based on factors like intensity, duration, and psychological components, and can cause malocclusion if not addressed.
3. Management of oral habits involves psychological therapy, reminder therapy using bitter tastes, and mechanotherapy with intraoral appliances to discourage the habit.
This document discusses the management of children with disabilities in dentistry. It begins by defining various disabilities like physical, mental, medical, and social disabilities that may interfere with normal functioning. It emphasizes that children with disabilities should be managed by a multidisciplinary team. The dentist's role is to evaluate oral findings, establish a diagnosis, and identify the child's strengths and weaknesses for future care. Special preparation may be needed to provide acceptable dental care for these children. The document then discusses various disabilities like cerebral palsy and autism in more detail and provides guidance on managing these pediatric patients in a dental setting.
The document discusses the progression of early childhood caries (ECC) leading to poor quality of life. It then summarizes the use of stainless steel crowns in pediatric dentistry, including their introduction, classification based on morphology and composition, indications, advantages, disadvantages, modifications, and complications. Prefabricated stainless steel crowns provide a superior restoration to multi-surface fillings and can help prevent further dental problems if used for extensive decay, following pulp therapy, or as a preventive restoration in primary teeth.
This ppt describes about how teeth erupts into oral cavity from within jaws and various theories to explain the mechanism followed by various factors affecting eruption
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...Donc Test
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Study Guide Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Course Hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Answers Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Course hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Study Guide Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Ebook Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Questions Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Stuvia
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
4. • In maintenance of the tooth in the oral cavity, the health
of the periodontium is very important.
• Prevalence of gingivitis in children has been reported to
be as high as 99%.
• Gingivitis when occurs…..it is limited to marginal gingiva.
• Destructive forms of periodontal disease is lower in
young individuals than in adults.
5. Gingival Characteristics
• Colour: Pink (parfitt 1973) or
Red (magnusson 1981)
Colour varies according to
Degree of vascularity
Epithelial keratinisation
Pigmentation
Thickness of epithelium
7. Size: the size of gingiva corresponds with sum of cellular & intercellular elements and their vascular
supply
Alteration is a common feature of gingival disease
The contour or shape varies considerably & depends on the shape of the teeth & alignment in the
arch, the location, & size of the area of interproximal contact, the dimension of lingual & facial gingival
embrasure
Labial version- more apical- accentuated
Lingual- thicker n rounder
8. Stippling is a form of adaptive specialization or reinforcement for function
Feature of healthy gingiva
Seen on attached gingiva n center of interdental gingiva
Prominent on facial surface
Varies with age: appears about 5 yrs, increases untill adulthood, disappears in old age
Shape: shape is governed by- contour of proximal tooth surfaces & location, shape of gingival embrasure
interdental bone- thin MD, the gingival embrasures & interdental gingiva are narrow MD
the height of interdental gingiva varies acc to location of proximal contact
So anterior – pyramidal shape
Posterior more flattened
9. CHILDREN ADULT
MARGINAL
GINGIVA
Thicker and rounder due to cervical
bulge and underlying constriction
Flaccid, retractable due to
immature connective tissue and
gingival fiber system and also due
to increased vascularisation
Thin & Knife edge
ATTACHED
GINGIVA
Flaccid, Less dense, red
and less stippled, greater width
Firm & Resilient
More stippled
INTERDENTAL
GINGIVA
saddle areas Pyramidal or “col” shape
GINGIVAL
SULCUS
1-2mm 2-3mm
ALVEOLAR
MUCOSA
Thin epithelium & absence of
keratin
Thick epithelium and more keratinized
Difference between Children and adult periodontium
10. • Interdental clefts
• Retrocuspid papilla
• Periodontal space is wider with few fibers
• Alveolar bone:
less calcified, more vascular
Few but thicker trabeculae
Larger marrow space
Prominent lamina dura
Flattened interdental crests
11. • Gingivitis is common than periodontitis
• Gingivitis is transient and acute compared to progressive
and chronic in adults
• more anabolic activity
• due to increased metabolism absence of bacteria
responsible for periodontal disease such as spirochetes
and b.melaninogenicus, altered composition ofplaque
and decreased leukocytic migratory rate due to low
levels of immunoglobluins specific for plaque bacteria
and decreased vascular inflammatory response
13. Stages of gingivitis
Stage 1: INITIAL STAGE (subclinical gingivitis)
Stage 2: EARLY STAGE
Stage 3: ESTABLISHED STAGE
Stage 4: ADVANCED STAGE (phase of periodontol breakdown)
14. 1st manifestation: vascular changes- dilated capillaries, increased blood flow
Initial response of the gingiva is not apparent clinically
2nd stage develop after 1 week of plaque accumulation
Appears as early gingivitis
Signs of erythema
Bleeding on probing
2-3 weeks after plaque accumulation
Blood vessels-engorged and congested, venous return impaired-blood flow
sluggish- resulting in localized gingival anoxemia ( bluish hue on reddened
gingiva
This stage: moderately to severely inflamed gingiva
4th:: Extension of the lesion into alveolar bone
15. Simple gingivitis
Earliest sign
“Increased gingival crevicular fluid production rate
Bleeding from gingival sulcus on gentle probing”
• Color changes
• Surface texture
• Change in position- not seen
Management: oral prophylaxis, oral hygiene measures
“Gingivitis in children largely reversible”
16. Eruption gingivitis
• Temporary form of gingivitis
• Often associated with difficulty in eruption subsides after
emergence of tooth
• Commonly seen- 1st & 2nd permanent molar
• Treatment: proper oral hygiene measures
17. Pubertal gingivitis
Features: Enlarged interdental areas
Spontaneous bleeding from the gingiva
Management: oral prophylaxis
proper oral hygiene maintenance
Scorbutic gingivitis
Features: Limited to marginal tissue, papilla
Severe pain & spontaneous hemorrhage
Management: complete dental care, improved oral hygiene,
supplementation of vit c, water soluble vitamin
19. Necrotizing ulcerative gingivitis
Also called as Ulcerative gingivitis
Acute necrotizing gingivitis
Vincent’s infection(stomatitis)
Fuso spirochetal disease
Trench mouth
Peak incidence- late teens, 20’s
Occasionally 6-12 years
20. Causative organism : spirochetes, fusiform bacteria
Local predisposing factors: erupting teeth, inadequate restorations,
calculus accumulations, occlusal trauma,
poor oral hygiene, preexisting gingivitis
Systemic predisposing factors: Nutritional deficiency
Debilitating disease
Primary diagnostic features Secondary diagnostic features
Interdental ulceration & necrosis
Pain
Bleeding
Elevated temperature with resultant
blunting & cratering of gingiva
Pseudomembrane
Fetid mouth odor
Bad taste
21. Treatment:
Local debridement
Subgingival curettage, use of mild oxygenating solutions
Antibiotic of choice- penicillin or erythromycin, metronidazole
Analgesics
Mild & moderate
stage
In severe cases
In very severe cases
Local lymphadenopathy , Slight elevation in
temperature
Gingival soreness, metallic taste, excessive
salivation, halitosis
high fever, increased pulse rate, leucocytosis,
loss of appetite, General lassitude
noma, fusospirocheatal meningitis&
peritonitis, pulmonary infections, toxemia,
fatal brain abscess
Symptoms:
22. Primary Herpetic Gingivostomatitis
• Caused by the herpes Simplex Virus (type 1)
• Mostly occurs in a child under 6years of age
• Course of the disease: 7-10 days
23. • Symptoms: Generalized Soreness of the oral cavity, Pain,
Cervical adenitis, high Fever, Generalized malaise
• Management: Bed rest
Antipyretics, analgesics
Application of mild topical anesthetic
Drink lot of oral fluid, soft diet
In severe case: antiviral medications
Isolation from siblings, peers- to prevent spread of infection
24. Necrotising ulcerative gingivities Primary herpetic gingivostomatitis
Interaction between host and bacteria
Necrotizing condition
Punched out gingival margin,
pseudomembrane
Interdental gingiva affected
Uncommon in children
no definite duration
Specific viral etiology
Diffuse erythema & vesicular eruption
Oval or Spherical ulcer
Diffuse involvement
Common in children
7-10 days
25. Gingival enlargements
I
II
III
IV
V
Inflammatory enlargements
Chronic , Acute
Drug induced enlargements
Enlargements associated with systemic diseases or condition
- Conditioned enlargements
(Pregnancy, Puberty, Vitamin c def, Plasma cell gingivitis,
Nonspecific conditioned)
- Systemic diseases
(Leukemia, Granulomatosis diseases)
Neoplastic enlargements
Benign, Malignent
False enlargements
26. Degree of gingival enlargements can be scored as
Grade 0: No signs
Grade I: Confined to interdental papilla
Grade II: Involves papillary and marginal gingiva
Grade III: Covers 3 quarters or more of the crown
27. Chronic inflammatory enlargements
• Most prevalent type
• Etiology: prolonged exposure to the dental plaque
• Clinical features:
limited to marginal & papillary gingiva
Gingiva- red or bluish red, soft , friable,
smooth shiny, surface, bleed easily
• Treatment: rigorous plaque control
oral prophylaxis
28. Acute inflammatory enlargements
Gingival abscess
• Localised, painful, rapidly expanding lesion that is usually of
sudden onset
• Etiology: bacteria carried deep into tissues
• c/f: Generally limited to the marginal gingiva or interdental
papilla
• Treatment: incision
29. Drug induced gingival enlargements
Anticonvulscents,
Immunosuppresents
Calcium channel blockers
30. Phenytoin induced gingival hyperplasia
It appears as early as 2-3 weeks after
initiation of phenytoin therapy & peaks at
18-24 months
Initial clinical appearance: painless
enlargement of interdental gingiva
Buccal, anterior more than lingual &
posteriors
Unless a secondary infection or
inflammation is present, the gingiva appears
pink & firm, doesn't bleed on probing
As there is continuous growth of interdental
gingiva, clefting become prominent in
midline of the tooth, clefting coalesce-
forming pseudopockets, covering the crown
structure
31. Enlargements occurs in 50% of the patients receiving the drug
Prevalence
- Younger age group
- Increasing dose
- Increasing serum phenytoin levels
- Decreasing degree of oral hygiene
Treatment: replacement of the drug
Oral prophylaxis
Use of chlorhexidine
specific surgical approach
32. Enlargement associated with
systemic disease
• Is a disease characterized by progressive overproduction of WBC,
which usually appear in circulating blood in immature form
• Occurs in acute leukemia
• Diffused or marginal,
• Localized or generalized
• Appear as diffused enlargement of the gingival mucosa Or discrete
tumor like interproximal masses
• Bluish red, shiny cyanotic surface
• Rounding & tenseness of the gingival margin covers crown
• gingival hemorrhage- common- due to ulceration of sulcus
epithelium, necrosis of underlying tissue
33. • Gingivitis, Gingival hyperplasia, Petechia, hemorrhage, Ulceration of the
mucosa
Management: BT ,CT & platelet count should be checked , hematologist
should be consulted before periodontal treatment
Scaling & curettage
Plaque control
Administer antibiotics
35. Chronic Periodontitis
(Old Term-adult Onset Periodontitis)
• Defined as an infectious disease resulting in
inflammation within the supporting tissues of the
teeth, progressive attachment loss and bone loss
36. • Can occur in children & Adolescent
• Primary & permanent dentition –affected
• Symptoms: bleeding of gums, spacing, loose tooth, sensitivity,
food impaction
• Clinical features: plaque accumulation, gingival inflammation,
pocket formation, gingival bleeding
• Can be localized: <30%
Or generalized : >30%
Treatment: Oral hygiene instructions
Scaling root planing,
Correction of local contributory factors
Maintenance of oral hygiene
37. Aggressive Periodontitis
(Old Term: Early Onset Periodontitis)
• Localized aggressive periodontitis
(replaces localized juvenile periodontitis,
localized early onset periodontitis)
• Generalized aggressive periodontitis
(replaces generalized juvenile periodontitis,
generalized early onset periodontitis)
• Localized or generalized aggressive periodontitis occurring
prepubertally
(replaces prepubertal periodontitis)
Generally affect systemically healthy individuals less than 30yr old
Distinguished from chronic by age of onset
38. Localized Aggressive Periodontitis
• Etiology: hereditary
• Characterised by- localised 1st molar or incisor presentation
with interproximal attachment loss on atleast 2 teeth
• striking feature:
“Lack of clinical inflammation despite the presence of deep pd
pocket & advanced bone loss”
• Distolabial migration of maxillary incisors
• Mobility
• Deep, dull, radiating pain during mastication
• Root sensitivity
39. • Radiographic finding: vertical loss of alveolar bone around 1st
molars & incisors
“Arc shaped bone loss”
Loss of bone 3-4 times faster than chronic periodontitis
• Treatment: Subgingival irrigation
Scaling and root planing &
Systemic tetracycline therapy
40. Generalized aggressive
periodontitis
• Generalized interproximal attachment loss affecting atleast 3
teeth other than 1st molar & incisor
• Gingival condition: can be severely inflamed, or can be normal
• Treatment: Subgingival irrigation
Scaling and root planing &
Systemic tetracycline therapy
41. Prepubertal periodontitis
• Tends to occur in families
• Females> males
• It may began around 4years or before, may not be diagnosed
until 7-9 years
• Prevalence –less than 1%
• Clinical features: attachment loss, bone loss around primary
teeth
Defective peripheral blood leukocyte function, defects in
neutrophil or monocyte function
42. Treatment:
Curettage, antibiotic therapy, improved oral hygiene
Generalized Localized:
All primary teeth –affected, permanent
may or may not
Extremely acute gingival inflammation
Rapid destruction of the alveolar bone
Functional defect of peripheral blood
neutrophils & monocytes
Otitis media, upper respiratory infections
Refractory to antibiotics
Only few affected
Less inflammation
Destruction is not rapid
Same
Not frequent
Amenable to curettage, antibiotic
44. Etiology: unknown
- Endocrinopathy
- Vit A deficiency
- Bacteriodes gingivalis & capnocytophaga
Papillon-lefevre syndrome
Treatment: Vitamin A metabolites
45. Hyperkeratosis- starts 1st & 4 yr
after birth
It is progressive becomes dry&
scaly, deep n painful fissures in
winter
Primary dent- normal in development &
age of eruption
As soon as last decidous tooth erupts:
swollen gingiva, migration, mobility of
teeth pockets, exfoliation
By 3-4 yrs. all teeth are lost.
after loss-inflammation regresses
Eruption of permanent- enhanced,
completed by 5 yrs.
The disease recycles13-14yr-exfoliated
Ectopic intracranial calcifications
46. Hypophospatasia
(rathbun syndrome)
• Rare genetic disorder manifested by bone pain with spontaneous
fractures, rickets like bone lesions during childhood which are
resistant to treatment with vitamin D, premature loss of the
deciduous tooth
• Etiology:
familial disorder- recessive autosomal
deficiency of the enzyme alkaline phosphatese in serum or tissues
excretion of phospho-ethanelomine in urine
47. Divided in 3 forms
1) infantile type (Birth & 6month of age)
2) Childhood type (6-14 month)
3) Adult type (During childhood)
Treatment:
Oral phosphate supplements
DISEASE IS
CHARACTERISED BY
abnormal mineralization of
bone & dental tissues
Manifested by premature
exfoliation of the primary
teeth(75% of pt) 1st clinical
sign
Only deciduous incisors, are
affected, sometime canine ,
permanent- normal
48. Cyclic neutropenia
Def: “It is a unusual form of agranulocytosis characterized
by periodic or cyclic diminution in circulating
polymorphonuclear neutrophilic leukocytes as a results of
bone marrow maturation arrest, accompanied by mild
clinical manifestations, which spontaneously regresses
only to recur subsequently in a rhythmic pattern.”
49. Disappearance occurs approx every 3 weeks, after 5-10 days
neutrophil begin to reappear
During neutropenic stage: periodontal destruction
Non neutropenic stage: oral health returns
Prognosis: are at risk
for fatal bacterial
infection during this
stage
53. Insulin dependent diabetes(type I)
- Increased incidence of gingivitis
- Earlier onset of periodontitis
- Alv bone resorption
- Xerostomia
- Recurrent gingival abscesses
- Increased susceptibility to infections, reduced wound healing
- Both premature & delayed eruption of permanent teeth is observed
Management:
- Normal diet before dental appointment
- If the dental procedure is anticipated to be stressful- consult the physician for
adjustment in the insulin dosage
- Prophylactic antibiotic- recommended before procedure
54. Necrotizing ulcerative periodontitis
“ Cases of NUP are being described in immunocompromised patients(HIV)”
Diagnosis of NUP to be a marker for diagnosis of AIDS
Distinctive feature: periodontal attachment & bone loss
Other features: Deep interdental osseous craters
Advanced lesion: severe bone loss, tooth mobility,
ultimately tooth loss
Oral malodour, fever, malaise or lymphadenopathy
Etiology: fusiform-spirochete bacterial flora,
Various predisposing factors,
immunocompromised state
Stress, malnutrition
Editor's Notes
The gingiva forms an important part of the periodontium
In maintenance of the tooth in the oral cavity, the health of the periodontium is very important.
Prevalence of gingivitis in children has been reported to be as high as 99%.
Gingivitis when occurs…..it is limited to marginal gingiva.
Destructive forms of periodontal disease is lower in young individuals than in adults.
damle
Add pic
carrenza
damle
It is hereditary disease first recognized by Rathbun in 1948,
transmitted as a recessive autosomal characteristic.
Def: “The basic disorder is a deficiency of the enzyme alkaline
phosphatese in serum or tissues and excretion of phospho-
ethanelomine in urine.”