This document discusses periodontal pockets, including their classification, clinical features, histopathology, and treatment. It begins by defining a periodontal pocket and classifying them as suprabony, infrabony, or intrabony based on the location of bone loss. The document then examines the clinical and histological characteristics of active versus inactive pockets. It discusses the contents of pockets and changes that occur to the root surface and cementum within pockets. The document concludes by outlining methods for detecting and probing pockets, as well as treatment approaches based on pocket depth and location in the mouth.
This document provides an overview of pulp capping agents and procedures. It begins with definitions of indirect and direct pulp capping. It then discusses various pulp capping agents that have been used historically and currently, including calcium hydroxide, zinc oxide-eugenol, glass ionomer cement, and mineral trioxide aggregate. For each agent, the document outlines their proposed mechanisms of action, advantages, and disadvantages based on literature. Overall, the document provides a comprehensive review of the key considerations and materials used for pulp capping procedures.
This document discusses various sequelae that can be caused by wearing complete dentures, including direct sequelae like denture stomatitis and residual ridge reduction, as well as indirect sequelae like burning mouth syndrome and reduction of masticatory muscles. It describes the clinical features and risk factors for different conditions and provides treatment recommendations, such as improving denture hygiene and fit to manage denture stomatitis. The document also discusses syndromes that can arise from the opposing relationship between a maxillary complete denture and natural mandibular teeth, like combination syndrome.
Periodontal pockets can form when the gingival sulcus deepens through movement of the gingival margin or displacement of the gingival attachment. Pockets are classified based on their morphology, relationship to crestal bone, number of tooth surfaces involved, and nature of the soft tissue wall. The pathogenesis of pockets involves inflammatory changes that lead to degradation of collagen fibers and destruction of connective tissue and bone. Clinically, pockets present with signs like bleeding and suppuration. Microscopic examination reveals areas of bacterial accumulation, leukocyte emergence and interaction, and epithelial desquamation. Pockets contain debris, microorganisms, and inflammatory products. Probing is used to detect and measure pocket depth.
This document discusses the classification, clinical features, and histopathology of periodontal pockets. It classifies pockets as gingival/pseudo pockets or true periodontal pockets. Periodontal pockets are further classified based on their location relative to the alveolar bone as supra bony or infra bony. The clinical features include signs like thickened gingiva and bleeding on probing. Histopathologically, the soft tissue wall shows increased blood vessels and plasma cells, while the root surface shows changes like pathologic granules and mineralization/demineralization. Treatment involves scaling and root planing, with surgery for persistent deep pockets.
The document defines and classifies periodontal pockets. Key points:
- Periodontal pockets are pathologically deepened gingival sulci with destruction of supporting tissues.
- They are classified as suprabony, infrabony, or furcation pockets based on their location relative to alveolar bone.
- Periodontal pockets contain plaque, microorganisms, inflammatory cells and products that drive the pathogenesis of periodontitis through host immune response and tissue destruction.
- Probing depth measures pocket depth while attachment loss measures loss of supporting tissues from their original position. Pocket depth does not always correlate with severity of bone loss.
The document discusses periodontal pockets, including their classification, clinical features, pathogenesis, and treatment. Periodontal pockets are classified based on their morphology, relationship to crestal bone, number of tooth surfaces involved, nature of the soft tissue wall, and disease activity. Pockets form due to apical migration of the junctional epithelium and contain debris, microorganisms, and inflammatory cells. Treatment involves removing the pocket through nonsurgical or surgical methods like scaling, root planing, gingivectomy, or bone grafting to allow for reattachment of tissues at a higher level on the tooth.
Understanding of etiology and pathogensis of periodontal pocket will help to treat periodontal pocket successfully. Here I have descried the entire process with diagrams.
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.
This document provides an overview of pulp capping agents and procedures. It begins with definitions of indirect and direct pulp capping. It then discusses various pulp capping agents that have been used historically and currently, including calcium hydroxide, zinc oxide-eugenol, glass ionomer cement, and mineral trioxide aggregate. For each agent, the document outlines their proposed mechanisms of action, advantages, and disadvantages based on literature. Overall, the document provides a comprehensive review of the key considerations and materials used for pulp capping procedures.
This document discusses various sequelae that can be caused by wearing complete dentures, including direct sequelae like denture stomatitis and residual ridge reduction, as well as indirect sequelae like burning mouth syndrome and reduction of masticatory muscles. It describes the clinical features and risk factors for different conditions and provides treatment recommendations, such as improving denture hygiene and fit to manage denture stomatitis. The document also discusses syndromes that can arise from the opposing relationship between a maxillary complete denture and natural mandibular teeth, like combination syndrome.
Periodontal pockets can form when the gingival sulcus deepens through movement of the gingival margin or displacement of the gingival attachment. Pockets are classified based on their morphology, relationship to crestal bone, number of tooth surfaces involved, and nature of the soft tissue wall. The pathogenesis of pockets involves inflammatory changes that lead to degradation of collagen fibers and destruction of connective tissue and bone. Clinically, pockets present with signs like bleeding and suppuration. Microscopic examination reveals areas of bacterial accumulation, leukocyte emergence and interaction, and epithelial desquamation. Pockets contain debris, microorganisms, and inflammatory products. Probing is used to detect and measure pocket depth.
This document discusses the classification, clinical features, and histopathology of periodontal pockets. It classifies pockets as gingival/pseudo pockets or true periodontal pockets. Periodontal pockets are further classified based on their location relative to the alveolar bone as supra bony or infra bony. The clinical features include signs like thickened gingiva and bleeding on probing. Histopathologically, the soft tissue wall shows increased blood vessels and plasma cells, while the root surface shows changes like pathologic granules and mineralization/demineralization. Treatment involves scaling and root planing, with surgery for persistent deep pockets.
The document defines and classifies periodontal pockets. Key points:
- Periodontal pockets are pathologically deepened gingival sulci with destruction of supporting tissues.
- They are classified as suprabony, infrabony, or furcation pockets based on their location relative to alveolar bone.
- Periodontal pockets contain plaque, microorganisms, inflammatory cells and products that drive the pathogenesis of periodontitis through host immune response and tissue destruction.
- Probing depth measures pocket depth while attachment loss measures loss of supporting tissues from their original position. Pocket depth does not always correlate with severity of bone loss.
The document discusses periodontal pockets, including their classification, clinical features, pathogenesis, and treatment. Periodontal pockets are classified based on their morphology, relationship to crestal bone, number of tooth surfaces involved, nature of the soft tissue wall, and disease activity. Pockets form due to apical migration of the junctional epithelium and contain debris, microorganisms, and inflammatory cells. Treatment involves removing the pocket through nonsurgical or surgical methods like scaling, root planing, gingivectomy, or bone grafting to allow for reattachment of tissues at a higher level on the tooth.
Understanding of etiology and pathogensis of periodontal pocket will help to treat periodontal pocket successfully. Here I have descried the entire process with diagrams.
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 defines a periodontal pocket as a pathological deepening of the gingival sulcus bounded by the tooth surface and soft tissue wall. Pockets are classified as supracrestal or infrabony and simple, compound, or complex. Supracrestal pockets have a coronal base while infrabony pockets have an apical base below the alveolar crest. Histopathology shows the soft tissue wall is edematous and infiltrated with plasma cells, lymphocytes, and PMNs. Bacteria can invade the epithelium and connective tissue. Clinical features include red, swollen gingiva while histology reveals increased vascularity and thinning/degeneration of the epithelium. Pocket depth does not
This document discusses periodontal pockets, including their classification, clinical features, pathogenesis, and histopathology. Periodontal pockets are pathologically deepened gingival sulci that can form through coronal movement of the gingival margin, apical displacement of the gingival attachment, or a combination. They are classified based on their morphology (gingival vs periodontal) and number of tooth surfaces involved (simple, compound, complex). Periodontal pockets develop due to bacterial plaque initiating an inflammatory response and host tissue destruction through the action of leukocytes and enzymes. Histologically, the soft tissue wall shows inflammation and the junctional epithelium is shortened.
This document discusses periodontal pockets, including their classification, clinical features, pathogenesis, and treatment. Periodontal pockets are classified based on their morphology, relationship to crestal bone, number of tooth surfaces involved, nature of the soft tissue wall, and disease activity. Clinical features include enlarged gingiva and signs of inflammation. Pathogenesis involves changes in the soft tissue wall and pocket contents. Treatment depends on the type of pocket, and may include techniques to promote new attachment like non-graft or graft procedures.
The periodontal pocket is a pathologically deepened gingival sulcus that is a key sign of periodontal disease. Pockets can be classified based on their morphology, relationship to crestal bone, number of tooth surfaces involved, soft tissue walls, and disease activity. The pathogenesis involves bacterial plaque that leads to inflammation, collagen loss, and detachment of the junctional epithelium from the tooth, forming a pocket. Pockets contain debris and can promote further attachment and bone loss if left untreated. Treatment involves non-surgical approaches like scaling and root planing or surgical procedures to reduce pocket depth.
This document discusses periodontal pockets, which are a characteristic feature of periodontitis. A periodontal pocket forms due to destruction of the supporting periodontal tissues and is classified as either true or false. True pockets involve bone loss while false pockets are due to gingival enlargement without bone loss. Pockets are also classified based on their location relative to the bone (supra/intra-bony) and the number of tooth surfaces involved (simple, compound, complex). The document outlines the clinical signs and symptoms of pockets, how they are detected via probing, and their histopathology. Bacteria can invade pockets and cause further inflammation and tissue destruction, leading to deeper pockets if not treated.
Gingivectomy is the surgical excision of gum tissue to eliminate periodontal pockets and create a favorable environment for gum healing. It involves marking pockets, making internal bevel incisions, removing gum tissue and granulation, and root planing. Healing occurs through clot formation, granulation tissue growth, and epithelialization over 2-7 weeks. While it effectively eliminates pockets, gingivectomy risks reducing attached gum and exposing root surfaces.
This document discusses peri-implantitis, a disease affecting the tissues surrounding dental implants. Peri-implant mucositis is a mild inflammatory condition confined to soft tissues, similar to gingivitis. Peri-implantitis is a more severe condition involving bone loss due to infection. Treatment involves initial therapy like antibiotics and implant surface decontamination, followed by surgical therapies like regenerative treatment or resective surgery depending on the severity of bone loss. Long-term supportive therapy and plaque control are important to prevent disease recurrence.
This document discusses peri-implant diseases, their management, and differences from periodontal diseases. It defines peri-implant mucositis as an inflammatory reaction restricted to soft tissues around implants that is reversible with treatment. Peri-implantitis is defined as inflammatory reaction of soft tissues plus clinically detectable bone loss around implants. Key differences between tooth and implant interfaces are described. Etiology of peri-implant diseases includes poor oral hygiene and microbial factors. Diagnosis involves probing depth, bleeding, bone loss on radiographs. Management involves non-surgical debridement followed by systemic antibiotics and surgical therapies like bone grafting for advanced cases.
This document discusses periodontal pockets, including their definition, classification, formation, clinical features, histopathology, pathogenesis, and healing process. It defines a periodontal pocket as a pathologically deepened gingival sulcus due to migration of the junctional epithelium. Periodontal pockets are classified based on their morphology, number of tooth surfaces involved, and relation to the alveolar bone crest. The formation of pockets depends on host response, anatomical factors, local irritants like plaque and calculus. Successful treatment and healing of pockets involves removing irritants and providing a compatible surface for regeneration of periodontal tissues.
The document discusses diagnosis and treatment of peri-implant disease. It begins by introducing the history of dental implants and defines peri-implant mucositis and peri-implantitis. The main causes are bacterial infection and biomechanical overload. Treatment involves non-surgical and surgical approaches to arrest disease progression and maintain the implant site. The document then examines the histology and microbiology of healthy and diseased peri-implant tissues.
This document discusses furcation involvement, which refers to periodontal disease affecting the bifurcation or trifurcation areas of multi-rooted teeth. It begins by defining key terminology related to furcation anatomy. It then describes several classifications of furcation involvement based on the degree and extent of horizontal bone and attachment loss. The main causes of furcation involvement are said to be microbial dental plaque and local anatomic factors that impede access for proper cleaning. Diagnosis involves careful examination using probes and radiographs to determine the classification. Treatment options range from non-surgical to surgical approaches depending on the classification and severity, with more advanced cases sometimes requiring extraction.
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.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Sinus lift procedures. final copy of presentation pptxNAMITHA ANAND
This document discusses maxillary sinus lift procedures. It begins with the anatomy of the maxillary sinus, including its bony walls, blood supply, and Schneiderian membrane. It then covers clinical assessment of the sinus and various factors that can affect sinus health. The document discusses contraindications for sinus lift procedures and techniques for reducing complications. It also covers classifications of sinus lifts, different surgical techniques, potential intraoperative and postoperative complications, and instrumentation used. In summary, the document provides an overview of maxillary sinus anatomy and considerations, techniques, and risks associated with sinus lift procedures.
Dental hard tissues are resorbed by multinucleate cells called odontoclasts or dentinoclasts. They are classified as physiological or pathological, with pathological further divided into external root resorption due to trauma, pulp/apical pathology, or pressure and internal root resorption. A new clinical classification is based on injury to protective tissues by chemical or mechanical means and stimulation by infection or pressure. Odontoclasts/dentinoclasts resorb dental tissues through a process that begins with injury exposing mineralized tissue, followed by colonization and resorption stimulated continuously by pressure or infection.
Osteoradionecrosis is a serious complication of radiotherapy to the jaws that results in chronic non-healing of irradiated bone. Radiotherapy damages the vasculature of bone tissue, impairing healing. Risk factors include higher radiation dose, larger irradiated mandibular volume, and dental extractions within the radiation field. Symptoms include pain, exposed bone, and pathologic fracture. Treatment involves controlling infection with antibiotics and debridement. Hyperbaric oxygen therapy increases healing by enhancing angiogenesis and is often used as an adjuvant. Reconstruction of large defects from osteoradionecrosis requires free tissue transfer due to poor healing in irradiated tissue.
Diagnosis & treatment plan for periimplant desease/ dental implant coursesIndian dental academy
This document discusses diagnosis and treatment of peri-implant disease. It begins by describing the history of dental implants and defines peri-implant mucositis and peri-implantitis. Peri-implant tissue breakdown can result from microbial and mechanical factors. Treatment aims to arrest disease progression and maintain implant sites. Bacterial infection and biomechanical overload are major causes of peri-implant bone loss. Implant shape, surface, and soft tissue attachment can also influence peri-implant health.
Aggressive periodontitis is a type of periodontal disease characterized by rapid destruction of periodontal ligament and alveolar bone, leading to early tooth loss. It occurs in otherwise healthy individuals younger than 30 years of age. There are two main types - localized aggressive periodontitis, which affects first molars and incisors, and generalized aggressive periodontitis, which has more widespread involvement. Key features include rapid rate of attachment and bone loss, minimal plaque and calculus deposits relative to the destruction, and possible familial aggregation.
Calculus consists of mineralized bacterial plaque that forms on tooth surfaces. It is classified as supragingival or subgingival based on its location relative to the gingival margin. Supragingival calculus forms above the gingiva while subgingival forms below. Both have inorganic crystals like hydroxyapatite and organic components from plaque and saliva. Calculus attaches tightly to teeth through various mechanisms, making it difficult to remove. Its formation involves the mineralization of plaque over time. Factors like restorative overhangs and material imperfections can contribute to its development by promoting plaque retention.
This document discusses HIV/AIDS and its effects on the periodontium. It begins with an overview of HIV, how it is transmitted, and its pathogenesis. It then describes various oral manifestations of HIV infection, including oral candidiasis, hairy leukoplakia, Kaposi's sarcoma, non-Hodgkin's lymphoma, and periodontal diseases. Diagnosis and treatment approaches for each condition are provided. The document emphasizes that proper oral hygiene and treatment can help support periodontal health in HIV-positive individuals.
The document defines a periodontal pocket as a pathological deepening of the gingival sulcus bounded by the tooth surface and soft tissue wall. Pockets are classified as supracrestal or infrabony and simple, compound, or complex. Supracrestal pockets have a coronal base while infrabony pockets have an apical base below the alveolar crest. Histopathology shows the soft tissue wall is edematous and infiltrated with plasma cells, lymphocytes, and PMNs. Bacteria can invade the epithelium and connective tissue. Clinical features include red, swollen gingiva while histology reveals increased vascularity and thinning/degeneration of the epithelium. Pocket depth does not
This document discusses periodontal pockets, including their classification, clinical features, pathogenesis, and histopathology. Periodontal pockets are pathologically deepened gingival sulci that can form through coronal movement of the gingival margin, apical displacement of the gingival attachment, or a combination. They are classified based on their morphology (gingival vs periodontal) and number of tooth surfaces involved (simple, compound, complex). Periodontal pockets develop due to bacterial plaque initiating an inflammatory response and host tissue destruction through the action of leukocytes and enzymes. Histologically, the soft tissue wall shows inflammation and the junctional epithelium is shortened.
This document discusses periodontal pockets, including their classification, clinical features, pathogenesis, and treatment. Periodontal pockets are classified based on their morphology, relationship to crestal bone, number of tooth surfaces involved, nature of the soft tissue wall, and disease activity. Clinical features include enlarged gingiva and signs of inflammation. Pathogenesis involves changes in the soft tissue wall and pocket contents. Treatment depends on the type of pocket, and may include techniques to promote new attachment like non-graft or graft procedures.
The periodontal pocket is a pathologically deepened gingival sulcus that is a key sign of periodontal disease. Pockets can be classified based on their morphology, relationship to crestal bone, number of tooth surfaces involved, soft tissue walls, and disease activity. The pathogenesis involves bacterial plaque that leads to inflammation, collagen loss, and detachment of the junctional epithelium from the tooth, forming a pocket. Pockets contain debris and can promote further attachment and bone loss if left untreated. Treatment involves non-surgical approaches like scaling and root planing or surgical procedures to reduce pocket depth.
This document discusses periodontal pockets, which are a characteristic feature of periodontitis. A periodontal pocket forms due to destruction of the supporting periodontal tissues and is classified as either true or false. True pockets involve bone loss while false pockets are due to gingival enlargement without bone loss. Pockets are also classified based on their location relative to the bone (supra/intra-bony) and the number of tooth surfaces involved (simple, compound, complex). The document outlines the clinical signs and symptoms of pockets, how they are detected via probing, and their histopathology. Bacteria can invade pockets and cause further inflammation and tissue destruction, leading to deeper pockets if not treated.
Gingivectomy is the surgical excision of gum tissue to eliminate periodontal pockets and create a favorable environment for gum healing. It involves marking pockets, making internal bevel incisions, removing gum tissue and granulation, and root planing. Healing occurs through clot formation, granulation tissue growth, and epithelialization over 2-7 weeks. While it effectively eliminates pockets, gingivectomy risks reducing attached gum and exposing root surfaces.
This document discusses peri-implantitis, a disease affecting the tissues surrounding dental implants. Peri-implant mucositis is a mild inflammatory condition confined to soft tissues, similar to gingivitis. Peri-implantitis is a more severe condition involving bone loss due to infection. Treatment involves initial therapy like antibiotics and implant surface decontamination, followed by surgical therapies like regenerative treatment or resective surgery depending on the severity of bone loss. Long-term supportive therapy and plaque control are important to prevent disease recurrence.
This document discusses peri-implant diseases, their management, and differences from periodontal diseases. It defines peri-implant mucositis as an inflammatory reaction restricted to soft tissues around implants that is reversible with treatment. Peri-implantitis is defined as inflammatory reaction of soft tissues plus clinically detectable bone loss around implants. Key differences between tooth and implant interfaces are described. Etiology of peri-implant diseases includes poor oral hygiene and microbial factors. Diagnosis involves probing depth, bleeding, bone loss on radiographs. Management involves non-surgical debridement followed by systemic antibiotics and surgical therapies like bone grafting for advanced cases.
This document discusses periodontal pockets, including their definition, classification, formation, clinical features, histopathology, pathogenesis, and healing process. It defines a periodontal pocket as a pathologically deepened gingival sulcus due to migration of the junctional epithelium. Periodontal pockets are classified based on their morphology, number of tooth surfaces involved, and relation to the alveolar bone crest. The formation of pockets depends on host response, anatomical factors, local irritants like plaque and calculus. Successful treatment and healing of pockets involves removing irritants and providing a compatible surface for regeneration of periodontal tissues.
The document discusses diagnosis and treatment of peri-implant disease. It begins by introducing the history of dental implants and defines peri-implant mucositis and peri-implantitis. The main causes are bacterial infection and biomechanical overload. Treatment involves non-surgical and surgical approaches to arrest disease progression and maintain the implant site. The document then examines the histology and microbiology of healthy and diseased peri-implant tissues.
This document discusses furcation involvement, which refers to periodontal disease affecting the bifurcation or trifurcation areas of multi-rooted teeth. It begins by defining key terminology related to furcation anatomy. It then describes several classifications of furcation involvement based on the degree and extent of horizontal bone and attachment loss. The main causes of furcation involvement are said to be microbial dental plaque and local anatomic factors that impede access for proper cleaning. Diagnosis involves careful examination using probes and radiographs to determine the classification. Treatment options range from non-surgical to surgical approaches depending on the classification and severity, with more advanced cases sometimes requiring extraction.
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.
Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Sinus lift procedures. final copy of presentation pptxNAMITHA ANAND
This document discusses maxillary sinus lift procedures. It begins with the anatomy of the maxillary sinus, including its bony walls, blood supply, and Schneiderian membrane. It then covers clinical assessment of the sinus and various factors that can affect sinus health. The document discusses contraindications for sinus lift procedures and techniques for reducing complications. It also covers classifications of sinus lifts, different surgical techniques, potential intraoperative and postoperative complications, and instrumentation used. In summary, the document provides an overview of maxillary sinus anatomy and considerations, techniques, and risks associated with sinus lift procedures.
Dental hard tissues are resorbed by multinucleate cells called odontoclasts or dentinoclasts. They are classified as physiological or pathological, with pathological further divided into external root resorption due to trauma, pulp/apical pathology, or pressure and internal root resorption. A new clinical classification is based on injury to protective tissues by chemical or mechanical means and stimulation by infection or pressure. Odontoclasts/dentinoclasts resorb dental tissues through a process that begins with injury exposing mineralized tissue, followed by colonization and resorption stimulated continuously by pressure or infection.
Osteoradionecrosis is a serious complication of radiotherapy to the jaws that results in chronic non-healing of irradiated bone. Radiotherapy damages the vasculature of bone tissue, impairing healing. Risk factors include higher radiation dose, larger irradiated mandibular volume, and dental extractions within the radiation field. Symptoms include pain, exposed bone, and pathologic fracture. Treatment involves controlling infection with antibiotics and debridement. Hyperbaric oxygen therapy increases healing by enhancing angiogenesis and is often used as an adjuvant. Reconstruction of large defects from osteoradionecrosis requires free tissue transfer due to poor healing in irradiated tissue.
Diagnosis & treatment plan for periimplant desease/ dental implant coursesIndian dental academy
This document discusses diagnosis and treatment of peri-implant disease. It begins by describing the history of dental implants and defines peri-implant mucositis and peri-implantitis. Peri-implant tissue breakdown can result from microbial and mechanical factors. Treatment aims to arrest disease progression and maintain implant sites. Bacterial infection and biomechanical overload are major causes of peri-implant bone loss. Implant shape, surface, and soft tissue attachment can also influence peri-implant health.
Aggressive periodontitis is a type of periodontal disease characterized by rapid destruction of periodontal ligament and alveolar bone, leading to early tooth loss. It occurs in otherwise healthy individuals younger than 30 years of age. There are two main types - localized aggressive periodontitis, which affects first molars and incisors, and generalized aggressive periodontitis, which has more widespread involvement. Key features include rapid rate of attachment and bone loss, minimal plaque and calculus deposits relative to the destruction, and possible familial aggregation.
Calculus consists of mineralized bacterial plaque that forms on tooth surfaces. It is classified as supragingival or subgingival based on its location relative to the gingival margin. Supragingival calculus forms above the gingiva while subgingival forms below. Both have inorganic crystals like hydroxyapatite and organic components from plaque and saliva. Calculus attaches tightly to teeth through various mechanisms, making it difficult to remove. Its formation involves the mineralization of plaque over time. Factors like restorative overhangs and material imperfections can contribute to its development by promoting plaque retention.
This document discusses HIV/AIDS and its effects on the periodontium. It begins with an overview of HIV, how it is transmitted, and its pathogenesis. It then describes various oral manifestations of HIV infection, including oral candidiasis, hairy leukoplakia, Kaposi's sarcoma, non-Hodgkin's lymphoma, and periodontal diseases. Diagnosis and treatment approaches for each condition are provided. The document emphasizes that proper oral hygiene and treatment can help support periodontal health in HIV-positive individuals.
This document discusses halitosis (bad breath) including its causes, diagnosis, and treatment. It covers intraoral causes like periodontal disease, dry mouth, and tongue coating, as well as extraoral causes like liver or kidney disease. Diagnosis involves patient history, organoleptic rating, and tests to detect volatile sulfur compounds. Treatment focuses on reducing oral bacteria and nutrients through methods like tongue scraping, toothbrushing, and mouthwashes containing chemicals like chlorhexidine that can reduce microbial load.
Smoking has significant negative effects on periodontal health in several ways:
1) Chemicals in tobacco smoke such as nicotine and tar impair wound healing and increase inflammatory responses in the gingiva.
2) Smokers have higher levels of dental plaque, calculus, and poorer oral hygiene than non-smokers.
3) Smoking is a major risk factor for periodontal disease, with heavy long-term smokers having up to a 20-fold increased risk of destructive periodontitis compared to non-smokers.
Pathological tooth migration occurs when the balance of factors maintaining normal tooth position is disturbed by periodontal disease. It is common and may be an early sign of disease or occur with pocket formation as disease progresses. Teeth can migrate in any direction and usually have increased mobility. Key factors are changes that weaken periodontal support or alter forces on teeth. Treatment involves periodontal and orthodontic therapy to correct severe migration. Mobility is an important indicator of periodontal disease with single-rooted teeth having more mobility.
This document discusses dental plaque and the role of bacteria in periodontal diseases. It begins by describing how the oral cavity is colonized by bacteria from birth and how plaque forms on teeth. Plaque is made up of over 500 types of bacteria embedded in an extracellular matrix. The document then discusses plaque structure and composition, the diversity of surfaces in the oral cavity that bacteria can adhere to, and factors that influence individual plaque formation. It describes the ultrastructure of plaque formation over time, as early colonizers attach followed by maturation into a biofilm. Physiological properties and growth dynamics of plaque are also summarized.
This document summarizes the stages of gingival inflammation. It begins with initial inflammation seen as vascular changes like dilated capillaries. Early inflammation occurs within 1 week, shown microscopically as PMN infiltration. Established inflammation happens after 2-3 weeks of plaque accumulation and is characterized by B and T lymphocyte accumulation and plasma cell domination. Advanced inflammation involves bone loss and widespread tissue damage. The document provides histological details of the progression from healthy gingiva to advanced periodontitis.
Chronic periodontitis is a slowly progressive infectious disease that results in inflammation of the supporting tissues of the teeth and bone loss. It is caused by an extension of gingival inflammation into deeper periodontal tissues due to plaque accumulation. Key characteristics include a localized or generalized onset at any age, usually in adults, with periods of rapid progression possible. Treatment involves non-surgical procedures like scaling, root planing, and curettage as well as surgical procedures like pocket reduction surgery to correct anatomical defects. Prognosis depends on factors like patient compliance, systemic involvement, disease severity, and status of remaining teeth.
Pathological tooth migration occurs when the balance of factors maintaining normal tooth position is disturbed by periodontal disease. It is common and may be an early sign of disease or occur with pocket formation as disease progresses. Teeth can migrate in any direction and usually have increased mobility. Key factors are changes that weaken periodontal support or alter forces on teeth. Treatment involves periodontal and orthodontic therapy to correct severe migration. Mobility is an important indicator of periodontal disease with single-rooted teeth having more mobility.
This document discusses trauma from occlusion (TFO), which is defined as injury to the periodontal attachment apparatus resulting from excessive occlusal forces. It explores the role of occlusion in periodontal health and disease, as well as the relationship between plaque, inflammation and TFO. The effects of TFO depend on factors like force magnitude, direction, duration and frequency. TFO can be acute or chronic, and primary (directly caused by occlusion) or secondary (exacerbated by pre-existing periodontal disease). The document also examines Glickman's and Waerhaug's concepts regarding TFO and periodontal breakdown, as well as the tissue response and changes that can result from increased or insufficient occlusal forces. It notes
This document provides information on desquamative gingivitis, including its classification, diagnosis, and associated diseases. It classifies desquamative gingivitis into 7 categories including dermatosis, endocrine imbalance, aging, metabolic disturbances, abnormal response to irritation, chronic infection, and drug reactions. Key aspects of diagnosis include clinical history, examination, biopsy, and microscopic/immunofluorescence examination. Associated diseases discussed in detail include lichen planus, pemphigoid, pemphigus vulgaris, chronic ulcerative stomatitis, and linear IgA disease. Treatment varies depending on the underlying cause and severity of symptoms.
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.
7.Bone loss n patterns of bone destruction.pptxDrNavyadidla
This document discusses periodontal bone loss and the various patterns that can occur. It begins by explaining that periodontal disease leads to the destruction of connective tissue and bone in the apical direction. It then describes the main patterns of bone loss as being horizontal, where bone level is reduced uniformly, and vertical/angular defects where bone is lost in an oblique direction. It discusses various classifications of bone defects and factors that can influence bone loss patterns such as trauma from occlusion, local anatomy, and systemic factors like osteoporosis. It emphasizes that bone loss occurs intermittently through periods of activity and remission and aims to provide an understanding of bone loss for effective diagnosis and treatment planning.
This document discusses aging changes in the oral cavity. It notes that aging results in thinning gingiva with increased permeability and reduced resistance. The connective tissue becomes more dense and fibrotic with fewer cells. Blood vessels in the gingiva decrease in number and blood flow. Tooth structure experiences attrition and the alveolar bone level decreases. Plaque composition and immune response also change with age. Treatment for the elderly requires considering medical status, expectations, and balancing extent of intervention versus quality of life.
This document summarizes and provides details on three acute gingival infections: necrotizing ulcerative gingivitis (NUG), primary herpetic gingivostomatitis, and pericoronitis. NUG is characterized by ulcerations of the gums that can progress to bone loss if left untreated. It is caused by bacterial infection and often occurs during times of stress or illness that weaken the immune system. Primary herpetic gingivostomatitis is a viral infection of the mouth caused by the herpes simplex virus, appearing as sores and blisters on the gums and mouth in children. Pericoronitis refers to inflammation under an impacted wisdom tooth, which can
This document summarizes the clinical features of gingivitis. It describes the different types of gingivitis including acute, chronic, and recurrent gingivitis. It discusses the distribution, clinical findings such as bleeding and color changes, and causes of gingivitis. Local factors like trauma from toothbrushing and systemic factors like vitamin deficiencies that can cause abnormal bleeding are explained. The document also covers changes in gingival consistency, position, contour and other signs of gingivitis.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
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
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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
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2. INTRODUCTION
Periodontal pocket is defined as
a pathologically deepened gingival
sulcus [Carranza,10th Edi]
A pathologic fissure between a tooth and the
crevicular epithelium, and limited at its apex by the
junctional epithelium. [GPT]
Clinically speaking, the lesion should be termed a
“diseased gingival attachment”
18-07-2023 2
SAUL SCHLUGER, RALPH YUODELIS, ROY C PAGE, ROBERT H. JOHNSON
Periodontal Diseases 2nd Edition
4. SUPRABONY
base of pocket is
coronal to the crest of
the bone.
Horizontal bone loss
Interproximally,
transseptal fibers are
arranged horizontally
Pdl fibers are
arranged in their
normal pattern
18-07-2023 4
•Apical
•Vertical / Angular bone
loss
•Interproximally,
transseptal fibers are
arranged obliquely
•Angular pattern
INFRABONY
6. ACTIVE & INACTIVE
POCKETS
Active pocket :-
underlying bone Is lost
diagnosed clinically by bleeding
Inactive pocket:
after phase I therapy the inflammatory changes in
pocket wall subside, rendering the pocket inactive
with decreased depth.
They may heal by long junctional epithelium
18-07-2023 7
7. CLINICAL FEATURES
a bluish – red vertical zone from the gingival
margin to the alveolar mucosa
gingival bleeding
suppuration
tooth mobility
diastema formation
localized pain or pain “deep in the bone”
18-07-2023 CARRANZA Clinical Periodontology 10th
Edition
8
8. Clinical
Features
Bluish red
discoloration
Flaccidity
Smooth & shiny
surface
Pitting on pressure
Gingival wall- pink &
firm
18-07-2023 CARRANZA Clinical Periodontology 10th
Edition
9
Histopathological
Features
Circulatory
stagnation
Destruction of
gingival fibers
Atrophy of
epithelium & edema
Edema &
degeneration
Predominant Fibrotic
changes
9. Clinical
Features
Bleeding on probing
Pain On Probing
Pus
18-07-2023 CARRANZA Clinical Periodontology 10th
Edition
10
Histopathological
Features
Increased
vasculature
Degeneration of
epithelium
Ulceration
Suppurative
inflammation
11. HISTOPATHOLOGY
SOFT TISSUE WALL
Connective tissue – edematous, with plasma
cells(80%),PMNs (scattered)
- shows proliferative and
degenerative changes
Blood Vessels – dilated, engorged, increase in
no.
JE – Shorter than normal sulcus
Severe degeneration occurs at lateral wall
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CARRANZA Clinical Periodontology 10th
Edition
12
12. MICROTOPOGRAPHY OF
GINGIVAL WALL
Pocket wall is constantly changing as a result of
interaction between host & bacteria
Gingival wall has Following Areas :-
1. Relative quiescence
2. Bacterial accumulation
3. Emergence of leukocytes
4. Leukocyte – bacteria interaction
5. Intense epithelial desquamation
6. Ulceration
7. Areas of hemorrhage
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CARRANZA Clinical Periodontology 10th
Edition
13
17. SIGNIFICANCE OF PUS
FORMATION
The presence of pus or the ease with which it can
be expressed from the pocket merely reflects the
nature of the inflammatory changes in the pocket
wall.
It is not an indication of the depth of the pocket or
the severity of the destruction of the supporting
tissues.
Extensive pus formation may occur in shallow
pockets, whereas deep pockets may exhibit little or
no pus.
18
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CARRANZA Clinical Periodontology 10th
18. Pus is a common feature of periodontal
disease, but it is only a secondary sign.
Localized accumulation of pus constitutes
an abscess.
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CARRANZA Clinical Periodontology 10th
19. ROOT SURFACE WALL
Pocket deepens
Collagen fibers in cementum – destroyed
Exposure of cementum to environment
Penetration of bacteria into cementum
Areas of necrotic cementum separated by
masses of bacteria
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CARRANZA Clinical Periodontology 10th
Edition
20
20. Pathologic granules - represent areas of
collagen degeneration or areas where collagen
fibrils have not been fully mineralized initially.
Clinically – softening of cementum surface which
is usually asymptomatic but painful on probing.
Treatment should be aimed at removal of
necrotic areas by root planing
18-07-2023
CARRANZA Clinical Periodontology 10th
Edition
21
21. MINERALIZATION OF
CEMENTUM
INCREASED MINERALIZATION:-
They are probably a result of an exchange of
minerals and organic compounds at cementum
at cementum saliva interface
Mineral content of exposed cementum increases
Ca,Mg,P,F - in diseased roots
This increases resistance to decay
Selvig et. al (1977) – these zones as a layer 10-
20µm thick with areas as thick as 50µm
18-07-2023 22
CARRANZA Clinical Periodontology 10th
Edition
22. AREAS OF DEMINERALIZATION:-
Exposure to oral fluid and bacterial plaque
causes proteolysis of embedded remnants of
sharpey’s fibers
The cementum undergoes fragmentation and
cavitations leading to root caries
Dominant microorganism – Actinomyces
viscosus
[ Syed et al(1975)]
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CARRANZA Clinical Periodontology 10th
23. Caries of cementum requires special attention
when pocket is treated
Necrotic cementum must be treated by scaling &
root planing until firm tooth surface is reached
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CARRANZA Clinical Periodontology 10th
25. PERIODONTAL DISEASE
ACTIVITY
Earlier – Loss of attachment is slow but
continuously progressive phenomenon
Now – Periodontal disease activity (specificity of
plaque bacteria)
Pockets undergo periods of exacerbation &
Quiescence
Results in episodic bursts of activity followed by
periods of remission
18-07-2023
CARRANZA Clinical Periodontology 10th
Edition
26
26. ACTIVITY Vs INACTIVITY
Period of
Quiescence
Inflammatory
response
Little /no bone & CT
loss
18-07-2023
CARRANZA Clinical Periodontology 10th
Edition
27
Built up of
unattached plaque
with Gm –ve, Motile
anaerobic bacteria
Bone & CT loss
Pocket deepens
Proliferation Of Grm
+ve bacteria
27. SITE SPECIFICTIY
Periodontal destruction doesn't occur in all parts
of the mouth at same time
But it occurs on few teeth at a time or even only
some aspects of some teeth at any given time
This is site specificity
Severity of periodontitis increases with
development of new disease sites & increased
breakdown of existing sites.
18-07-2023 28
CARRANZA Clinical Periodontology 10th
28. PULPAL CHANGES
Spread of infection from periodontal pocket to
pulp causes pathological changes in pulp
Involvement of pulp occurs through either apical
foramen or lateral canals via PDL
18-07-2023 29
CARRANZA Clinical Periodontology 10th
Edition
1.Periodontal pocket deepens
into apex and secondarily
involve pulp
2.Periodontal pocket can
infect pulp through lateral wall
29. POCKET DEPTH Vs CAL
18-07-2023 30
Pocket depth – distance between base of pocket &
gingival margin
Clinical Attachment Level [CAL] – distance
between base of pocket & fixed portion on the
crown like CEJ
CARRANZA Clinical Periodontology 10th
32. POCKET DEPTH & BONE
LOSS
Severity of bone loss is generally but not always
correlated to pocket depth.
Extensive attachment & bone loss may be
accompanied by recession of gingival margin
where pocket can be less
Slight bone loss can occur with deep pockets
18-07-2023 33
CARRANZA Clinical Periodontology 10th
33. PERIODONTAL ABSCESS
Localized purulent inflammation in periodontal
tissues
Also called lateral abscess/ parietal abscess
Classification
Abscess in supporting periodontal tissues along
lateral aspect of root
Abscess in soft tissue wall of deep pocket
Mainly Grm –ve anerobic rods
Others – grm –ve cocci,diplococci,fusiforms &
spirochetes
18-07-2023 34
34. Formation
Infection from pocket deeply into supporting
periodontal tissue
Lateral extension of inflammation from inner surface
of pocket into connective tissue
Formation in a pocket with tortuous course around
root
Incomplete removal of calculus
With perforation of lateral wall of root in endodontic
therapy
18-07-2023 35
35. DETECTION OF POCKET
Inserted parallel to vertical
axis of tooth
WALKED circumferentially
around each surface of
each tooth
Graduated periodontal probe with
a standardized tip diameter of
approximately 0.4–0.5 mm
Probing force should be 25g or 0.75N
[Van der Velden (1979), Chamberlain et
al(1985)]
18-07-2023
CARRANZA Clinical Periodontology 10th
Edition
36
36. WHEN TO PROBE ?
INTIAL PROBING
Usually masked by heavy inflammation &
abundant calculus. So cannot be done
accurately.
Purpose – determine whether tooth can be
saved or should be extracted.
SECOND PROBING
Establish accuracy of level of attachment &
degree of involvement of roots & furcation
Sulcus can be safely probed after periodontal
surgery – 3 months post op
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CARRANZA Clinical Periodontology 10th
Edition
37
37. TREATMENT
According to pocket depth, periodontitis can be
divided into
Purpose of surgical treatment
To eliminate the pathologic changes in pocket
wall.
To create a stable, easily maintainable state.
To promote periodontal regeneration if possible.
18-07-2023 38
38. THERAPY FOR GINGIVAL
POCKETS
Factors to be considered
Character of the pocket wall
Edematous Fibrotic
SRP SRP followed by gingivectomy
Modified Widman Flap Technique (in
marked enlargements)
Accessibility of the pocket
18-07-2023 39
39. THERAPY FOR SLIGHT
PERIODONTITIS
Pockets are shallow, small degree of bone loss
A thorough Scaling & root planing is sufficient
18-07-2023 40
40. THERAPY FOR MODERATE TO SEVERE
PERIODONTITIS IN ANTERIORS
Scaling & root planing
Papilla preservation flap- For esthetics in wide
embrasures
In narrow embrasures – sulcular incision
Modified widman flap – when esthetics are not
concerned
When bone contouring is needed – apically
displaced flap with bone contouring is technique
of choice
18-07-2023 41
41. THERAPY FOR MODERATE TO SEVERE
PERIODONTITIS IN POSTERIORS
Offers no esthetic problem but difficult
accessibility
18-07-2023 42
44. A through and sound knowledge of nature of
pocket along with its lining, contents and the
tooth wall surface is necessary for appropriate
planning of its treatment
However, the benefit to the patient should
always be minded in long run.
18-07-2023 45