The document discusses periodontal pockets, which are a characteristic feature of periodontitis. It defines a periodontal pocket as a pathologically deepened gingival sulcus and classifies pockets as either gingival, suprabonny, or intrabony based on their location relative to the alveolar bone. The document outlines several theories on the pathogenesis of periodontal pockets, including the destruction of gingival fibers, changes in the cementum, stimulation of the junctional epithelium by inflammation, destruction of the junctional epithelium by infection or trauma, and bacterial invasion at the base of the sulcus.
A periodontal pocket is a pathologically deepened gingival sulcus caused by an inflammatory response to oral infection. It is characterized by the apical migration of junctional epithelium along the root surface. Periodontal pockets can be classified based on their morphology, the surfaces and structures involved, and the nature of the soft tissue wall. The pathogenesis of pocket formation involves the destruction of collagen fibers by collagenases and other enzymes released during the host inflammatory response to bacterial plaque accumulation. This results in the apical migration and proliferation of junctional epithelium along the root, forming a periodontal pocket. Histopathologically, the soft tissue wall shows edema, inflammation and ulceration while the root surface undergoes structural and chemical changes with
The document discusses various periodontal regenerative procedures. It describes techniques such as bone grafting using autogenous bone or other bone substitutes to regenerate alveolar bone defects. Bone grafts can aid regeneration through osteogenesis, osteoinduction and osteoconduction. Autogenous bone is often considered the best option but alternatives include allografts and synthetic grafts when autogenous bone is not feasible. The ideal properties and use of various graft materials are also discussed.
The future of dentistry and periodontics lies in regeneration. The goals of periodontal therapy lies in not only the arrest of periodontal disease progression but also regeneration of the lost periodontal structures. This presentation provides a review of the current understanding of the regeneration of the periodontium and the procedures involved to restore the periodontal tissues around the teeth.
This document discusses the process and techniques for coronoplasty, which is a selective reduction of occlusal areas to influence mechanical contact situations and neural sensory input patterns. It describes the 10 basic steps for performing coronoplasty, which include adjusting the intercuspal position and retruded contact position, removing prematurities, establishing stable simultaneous contacts, testing and adjusting incisal contacts and excursions, and finishing with polishing rough surfaces. The goal is to establish an optimal occlusion with stable contacts, smooth excursions, and decreased tooth mobility and stress on the teeth and temporomandibular joints.
Dental implants are placed into the jawbone to support crowns, bridges, dentures or facial prosthetics. There are several types but they generally involve a titanium implant being surgically placed into the jawbone in either a one-stage or two-stage procedure. In a two-stage procedure, the top of the implant is submerged under gingiva and uncovered in a second surgery once integrated. Proper placement, biocompatible materials, and avoiding overheating the bone are important for integration. Implants can replace single or multiple teeth and have advantages over other options but also have higher costs and longer treatment times.
Scaling and root planing (SRP) is a non-surgical treatment for periodontitis that aims to remove dental plaque and calculus from tooth surfaces. It involves scaling to remove deposits and root planing to smooth root surfaces. The goals are to eliminate periodontitis by removing irritants and restoring a healthy environment for tissue healing. The long-term effectiveness depends on factors like patient compliance, disease severity, and anatomical challenges. Overhanging restorations can interfere with cleaning and disturb the ecological balance, allowing disease-causing bacteria to proliferate.
This document discusses various surgical techniques for preserving the interdental papilla during periodontal regeneration procedures. It describes the conventional papilla preservation flap technique introduced by Takei in 1985, as well as several modifications including the modified papilla preservation flap, simplified papilla preservation flap, interproximal tissue maintenance technique, and whale's tail technique. The advantages and disadvantages of each technique are summarized. A novel entire papilla preservation technique introduced in 2015 is also outlined, which aims to completely preserve the interdental papilla.
This document discusses risk assessment in periodontics. It defines key terminology like risk factors, risk determinants, risk indicators, and risk markers. It then describes the process of risk assessment, including assessing risk at the subject, tooth, and site levels. Several risk assessment tools and models are presented, including the Periodontal Risk Calculator, Periodontal Risk Assessment hexagonal diagram, and functional Periodontal Pentagon diagram. Risk factors for dental implants are also discussed. Overall the document aims to explain the importance of risk assessment for targeting periodontal treatment and providing proactive care for at-risk patients.
A periodontal pocket is a pathologically deepened gingival sulcus caused by an inflammatory response to oral infection. It is characterized by the apical migration of junctional epithelium along the root surface. Periodontal pockets can be classified based on their morphology, the surfaces and structures involved, and the nature of the soft tissue wall. The pathogenesis of pocket formation involves the destruction of collagen fibers by collagenases and other enzymes released during the host inflammatory response to bacterial plaque accumulation. This results in the apical migration and proliferation of junctional epithelium along the root, forming a periodontal pocket. Histopathologically, the soft tissue wall shows edema, inflammation and ulceration while the root surface undergoes structural and chemical changes with
The document discusses various periodontal regenerative procedures. It describes techniques such as bone grafting using autogenous bone or other bone substitutes to regenerate alveolar bone defects. Bone grafts can aid regeneration through osteogenesis, osteoinduction and osteoconduction. Autogenous bone is often considered the best option but alternatives include allografts and synthetic grafts when autogenous bone is not feasible. The ideal properties and use of various graft materials are also discussed.
The future of dentistry and periodontics lies in regeneration. The goals of periodontal therapy lies in not only the arrest of periodontal disease progression but also regeneration of the lost periodontal structures. This presentation provides a review of the current understanding of the regeneration of the periodontium and the procedures involved to restore the periodontal tissues around the teeth.
This document discusses the process and techniques for coronoplasty, which is a selective reduction of occlusal areas to influence mechanical contact situations and neural sensory input patterns. It describes the 10 basic steps for performing coronoplasty, which include adjusting the intercuspal position and retruded contact position, removing prematurities, establishing stable simultaneous contacts, testing and adjusting incisal contacts and excursions, and finishing with polishing rough surfaces. The goal is to establish an optimal occlusion with stable contacts, smooth excursions, and decreased tooth mobility and stress on the teeth and temporomandibular joints.
Dental implants are placed into the jawbone to support crowns, bridges, dentures or facial prosthetics. There are several types but they generally involve a titanium implant being surgically placed into the jawbone in either a one-stage or two-stage procedure. In a two-stage procedure, the top of the implant is submerged under gingiva and uncovered in a second surgery once integrated. Proper placement, biocompatible materials, and avoiding overheating the bone are important for integration. Implants can replace single or multiple teeth and have advantages over other options but also have higher costs and longer treatment times.
Scaling and root planing (SRP) is a non-surgical treatment for periodontitis that aims to remove dental plaque and calculus from tooth surfaces. It involves scaling to remove deposits and root planing to smooth root surfaces. The goals are to eliminate periodontitis by removing irritants and restoring a healthy environment for tissue healing. The long-term effectiveness depends on factors like patient compliance, disease severity, and anatomical challenges. Overhanging restorations can interfere with cleaning and disturb the ecological balance, allowing disease-causing bacteria to proliferate.
This document discusses various surgical techniques for preserving the interdental papilla during periodontal regeneration procedures. It describes the conventional papilla preservation flap technique introduced by Takei in 1985, as well as several modifications including the modified papilla preservation flap, simplified papilla preservation flap, interproximal tissue maintenance technique, and whale's tail technique. The advantages and disadvantages of each technique are summarized. A novel entire papilla preservation technique introduced in 2015 is also outlined, which aims to completely preserve the interdental papilla.
This document discusses risk assessment in periodontics. It defines key terminology like risk factors, risk determinants, risk indicators, and risk markers. It then describes the process of risk assessment, including assessing risk at the subject, tooth, and site levels. Several risk assessment tools and models are presented, including the Periodontal Risk Calculator, Periodontal Risk Assessment hexagonal diagram, and functional Periodontal Pentagon diagram. Risk factors for dental implants are also discussed. Overall the document aims to explain the importance of risk assessment for targeting periodontal treatment and providing proactive care for at-risk patients.
Periodontal medicine is the study of the relationship between periodontal health and systemic health. Periodontal disease can influence systemic health through direct effects of bacteria or indirect host-mediated inflammatory responses. Periodontitis has been linked to increased risk of cardiovascular disease, diabetes, and preterm low birth weight. Treatment of periodontal infection may help improve glycemic control in diabetic patients and reduce systemic inflammation.
This document provides an overview of periodontal wound healing and regeneration following periodontal surgery. It defines regeneration as the reproduction of lost or injured periodontal tissues, including cementum, periodontal ligament, and alveolar bone. Successful regeneration is assessed through probing, radiographs, direct measurements, and histology. The document discusses factors that influence regeneration outcomes, such as the surgical technique and local wound environment. Regenerative therapies aim to fully restore the lost periodontal structure and function.
This document discusses the classification, pathogenesis, histopathology, and progression of periodontal pockets. Periodontal pockets are classified as suprabony or intrabony based on their location relative to the alveolar bone. Theories on the pathogenesis suggest pockets form due to bacterial invasion, inflammation, or proliferation of the junctional epithelium leading to destruction of connective tissue and loss of attachment. Histopathology shows the soft tissue wall undergoes degenerative changes while the root surface develops structural and chemical alterations. Pockets progress in an episodic manner with periods of exacerbation and quiescence. Understanding the etiology and progression of pockets is important for providing successful treatment and monitoring response to therapy.
This document provides an overview of guided tissue regeneration (GTR). It begins with definitions of periodontal regeneration and GTR. It then discusses the history and development of GTR from the 1970s onwards. The core concept of GTR is explained, which is based on Melcher's hypothesis that only periodontal ligament cells can regenerate the periodontal attachment apparatus. Indications, contraindications, design criteria and objectives of GTR barriers are covered. The document classifies and compares advantages and disadvantages of absorbable versus non-absorbable membranes. Key factors affecting GTR outcomes are discussed. Surgical techniques and the healing of GTR-treated defects are described. The document concludes with additional considerations like complications and the
This document discusses HIV and periodontium. It begins with an introduction and overview of the history and epidemiology of AIDS. It then discusses the CDC definition and classification of AIDS, the virus structure, modes of transmission, and life cycle of HIV. It covers the clinical features and WHO classification of HIV-associated diseases. It also discusses the classification of oral lesions associated with HIV, periodontal manifestations, diagnostic tests, and occupational exposure and post-exposure prophylaxis. Management of HIV-infected patients and precautions are outlined.
The periodontal dressing is a physical barrier that is placed in the surgical site to protect the healing tissues from the forces produced during mastication, for comfort and close adaptation.
This document provides an overview of periimplantitis, including its definition, classification systems, epidemiology, etiology, pathogenesis, diagnosis, and treatment. Periimplantitis is defined as an inflammatory process involving both soft and hard tissues around a dental implant, resulting in loss of supporting bone. It is distinguished from peri-implant mucositis, which only involves inflammation of soft tissues. The document discusses various classification systems for periimplantitis and reviews potential etiologic factors such as plaque, biomechanical overload, genetic factors, and iatrogenic causes. Diagnosis involves clinical parameters like bleeding, probing depth, and radiographic bone loss. Treatment aims to eliminate infection and may include nonsurgical and surgical
This document discusses periodontal regeneration and the various factors involved. It begins by defining key terminology related to grafting and regeneration. It then discusses the biology and objectives of periodontal regeneration, including the ideal outcome of new attachment formation and factors that can influence outcomes. The document outlines various techniques for periodontal regeneration including non-graft associated approaches involving removal of epithelium and surgical techniques, as well as graft-associated approaches using various graft materials. Requirements for predictable regeneration and assessment methods are also summarized.
Minimally invasive surgical techniques in periodonticsDrGulafshaM
This document provides an overview of minimally invasive surgical techniques (MIST) in periodontology. It discusses the history and rationale for MIST, which aims to reduce trauma through smaller incisions and flap elevations. Features of minimally invasive periodontal surgery (MIPS) include precise incisions, sharp dissection for minimal flap elevation, use of an operating microscope, and careful suturing. Clinical trials show MIPS provides benefits like greater clinical attachment level gain compared to traditional techniques. The document reviews various MIPS approaches like tunneling, papilla preservation, and simplified papilla preservation flaps.
Bone loss occurs when resorption exceeds formation due to an imbalance between inflammatory and anti-inflammatory signals. Bacterial products stimulate immune cells like macrophages and T cells to release cytokines that promote osteoclast formation through the RANKL pathway. Mature osteoclasts attach to bone and secrete acids and enzymes to degrade the mineralized matrix and organic components. While inflammatory mediators increase resorption, anti-inflammatory cytokines from T cells and other cells inhibit osteoclasts and support new bone formation to maintain equilibrium. Periodontitis results from this inflammatory process overwhelming the protective mechanisms and leading to net bone destruction.
Wound healing is a complex process involving regeneration and repair. It consists of three overlapping phases - inflammatory, proliferative, and remodeling. In the inflammatory phase, coagulation and platelet aggregation form a fibrin clot and recruit inflammatory cells. The proliferative phase involves re-epithelialization through keratinocyte migration and proliferation. Fibroblasts are activated and form granulation tissue through angiogenesis and collagen deposition. Myofibroblasts aid wound contraction in the final remodeling phase. Growth factors influence each phase of wound healing after periodontal and oral procedures.
Periodontal wound healing involves four overlapping phases - exudative, resorptive, proliferative, and regenerative. The proliferative phase includes re-epithelialization, fibroplasia, granulation tissue formation, collagen deposition, angiogenesis, and wound contraction. Growth factors play an important role in regulating periodontal wound healing. Healing after periodontal procedures like scaling and root planing, curettage, ultrasonic curettage, and gingivectomy depends on the extent of tissue disruption and follows a timeline of inflammatory response, epithelial migration, granulation tissue formation, collagen deposition and remodeling.
This document provides an overview of the gingiva. It begins with definitions of gingiva from various sources and discusses the development, macroscopic features, microscopic features, fibers, cells, vascular supply, nerve supply, and matrix of the gingiva. Specifically, it describes the development of gingiva from mesoderm, its division into marginal, attached, and interdental papilla. It also discusses the layers of the gingival epithelium, the keratinization process, and cell types present like keratinocytes and non-keratinocytes.
The document discusses gingival curettage, which involves using instruments to remove diseased soft tissue from periodontal pockets. It defines curettage and provides the history of the procedure. The basic technique is described as using curettes to scrape the inner lining of the pocket to remove ulcerated epithelium and damaged connective tissue. Indications include edematous pockets aiming to reduce inflammation and shrink tissue. Healing after curettage is examined through a study showing revascularization of the wound site over time.
Periodontal pockets form when the gingival sulcus deepens due to the accumulation of bacteria and subsequent destruction of the supporting periodontal tissues. Pockets are classified as gingival, suprabonny, or intrabony based on the location of the base of the pocket relative to the underlying bone. Bacteria in the pocket cause inflammation and tissue destruction through the release of toxins and enzymes. Left untreated, pockets can deepen and cause increased bone and tissue loss. Probing is used to measure pocket depths and monitor periodontal disease progression and response to treatment.
This document discusses risk assessment in periodontal disease. It defines key terms like risk, risk factors, risk determinants, and risk markers. It categorizes different types of risk elements and describes several risk assessment tools that use various clinical and historical parameters to provide a risk score. The document concludes that while identification of risk factors has furthered understanding of periodontitis, predicting individual risk remains limited.
The document discusses the gingiva, which is the gum tissue surrounding the teeth. It defines gingiva and describes its functions of protecting the underlying tissues and maintaining periodontal health. The gingiva develops with tooth formation and eruption. Microscopically, it consists of stratified squamous epithelium and connective tissue. The epithelium can be oral, sulcular, or junctional depending on its location. The document also describes the anatomical structures of the gingiva including the marginal, attached, and interdental gingiva as well as the gingival sulcus.
This document discusses the rationale for periodontal treatment and the healing process after treatment. Local periodontal therapy aims to remove bacterial plaque and calculus that cause gum disease. Systemic therapy may also be used as an adjunct to treat infections or diseases that affect the periodontal condition. Healing after treatment involves regeneration of gingival epithelium, connective tissue, bone, and cementum. The key to new attachment is regeneration of the periodontal ligament, which provides continuity between the bone and cementum. The sequence in which different cell types repopulate the treated area determines the healing outcome and possibility of new attachment.
The document provides information on periodontal pockets, including their definition, classification, clinical features, pathogenesis, histopathology, and microtopography. Key points include:
- Periodontal pockets are pathologically deepened gingival sulci that form due to apical migration of the junctional epithelium and/or coronal movement of the gingival margin.
- Pockets can be classified based on their morphology, relationship to bone, number of tooth surfaces involved, and nature of the soft tissue wall.
- Pocket formation involves destruction of gingival fibers and collagen by host inflammatory responses to bacterial plaque, leading to apical migration of junctional epithelium.
- Histologically, pocket walls
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.
Periodontal medicine is the study of the relationship between periodontal health and systemic health. Periodontal disease can influence systemic health through direct effects of bacteria or indirect host-mediated inflammatory responses. Periodontitis has been linked to increased risk of cardiovascular disease, diabetes, and preterm low birth weight. Treatment of periodontal infection may help improve glycemic control in diabetic patients and reduce systemic inflammation.
This document provides an overview of periodontal wound healing and regeneration following periodontal surgery. It defines regeneration as the reproduction of lost or injured periodontal tissues, including cementum, periodontal ligament, and alveolar bone. Successful regeneration is assessed through probing, radiographs, direct measurements, and histology. The document discusses factors that influence regeneration outcomes, such as the surgical technique and local wound environment. Regenerative therapies aim to fully restore the lost periodontal structure and function.
This document discusses the classification, pathogenesis, histopathology, and progression of periodontal pockets. Periodontal pockets are classified as suprabony or intrabony based on their location relative to the alveolar bone. Theories on the pathogenesis suggest pockets form due to bacterial invasion, inflammation, or proliferation of the junctional epithelium leading to destruction of connective tissue and loss of attachment. Histopathology shows the soft tissue wall undergoes degenerative changes while the root surface develops structural and chemical alterations. Pockets progress in an episodic manner with periods of exacerbation and quiescence. Understanding the etiology and progression of pockets is important for providing successful treatment and monitoring response to therapy.
This document provides an overview of guided tissue regeneration (GTR). It begins with definitions of periodontal regeneration and GTR. It then discusses the history and development of GTR from the 1970s onwards. The core concept of GTR is explained, which is based on Melcher's hypothesis that only periodontal ligament cells can regenerate the periodontal attachment apparatus. Indications, contraindications, design criteria and objectives of GTR barriers are covered. The document classifies and compares advantages and disadvantages of absorbable versus non-absorbable membranes. Key factors affecting GTR outcomes are discussed. Surgical techniques and the healing of GTR-treated defects are described. The document concludes with additional considerations like complications and the
This document discusses HIV and periodontium. It begins with an introduction and overview of the history and epidemiology of AIDS. It then discusses the CDC definition and classification of AIDS, the virus structure, modes of transmission, and life cycle of HIV. It covers the clinical features and WHO classification of HIV-associated diseases. It also discusses the classification of oral lesions associated with HIV, periodontal manifestations, diagnostic tests, and occupational exposure and post-exposure prophylaxis. Management of HIV-infected patients and precautions are outlined.
The periodontal dressing is a physical barrier that is placed in the surgical site to protect the healing tissues from the forces produced during mastication, for comfort and close adaptation.
This document provides an overview of periimplantitis, including its definition, classification systems, epidemiology, etiology, pathogenesis, diagnosis, and treatment. Periimplantitis is defined as an inflammatory process involving both soft and hard tissues around a dental implant, resulting in loss of supporting bone. It is distinguished from peri-implant mucositis, which only involves inflammation of soft tissues. The document discusses various classification systems for periimplantitis and reviews potential etiologic factors such as plaque, biomechanical overload, genetic factors, and iatrogenic causes. Diagnosis involves clinical parameters like bleeding, probing depth, and radiographic bone loss. Treatment aims to eliminate infection and may include nonsurgical and surgical
This document discusses periodontal regeneration and the various factors involved. It begins by defining key terminology related to grafting and regeneration. It then discusses the biology and objectives of periodontal regeneration, including the ideal outcome of new attachment formation and factors that can influence outcomes. The document outlines various techniques for periodontal regeneration including non-graft associated approaches involving removal of epithelium and surgical techniques, as well as graft-associated approaches using various graft materials. Requirements for predictable regeneration and assessment methods are also summarized.
Minimally invasive surgical techniques in periodonticsDrGulafshaM
This document provides an overview of minimally invasive surgical techniques (MIST) in periodontology. It discusses the history and rationale for MIST, which aims to reduce trauma through smaller incisions and flap elevations. Features of minimally invasive periodontal surgery (MIPS) include precise incisions, sharp dissection for minimal flap elevation, use of an operating microscope, and careful suturing. Clinical trials show MIPS provides benefits like greater clinical attachment level gain compared to traditional techniques. The document reviews various MIPS approaches like tunneling, papilla preservation, and simplified papilla preservation flaps.
Bone loss occurs when resorption exceeds formation due to an imbalance between inflammatory and anti-inflammatory signals. Bacterial products stimulate immune cells like macrophages and T cells to release cytokines that promote osteoclast formation through the RANKL pathway. Mature osteoclasts attach to bone and secrete acids and enzymes to degrade the mineralized matrix and organic components. While inflammatory mediators increase resorption, anti-inflammatory cytokines from T cells and other cells inhibit osteoclasts and support new bone formation to maintain equilibrium. Periodontitis results from this inflammatory process overwhelming the protective mechanisms and leading to net bone destruction.
Wound healing is a complex process involving regeneration and repair. It consists of three overlapping phases - inflammatory, proliferative, and remodeling. In the inflammatory phase, coagulation and platelet aggregation form a fibrin clot and recruit inflammatory cells. The proliferative phase involves re-epithelialization through keratinocyte migration and proliferation. Fibroblasts are activated and form granulation tissue through angiogenesis and collagen deposition. Myofibroblasts aid wound contraction in the final remodeling phase. Growth factors influence each phase of wound healing after periodontal and oral procedures.
Periodontal wound healing involves four overlapping phases - exudative, resorptive, proliferative, and regenerative. The proliferative phase includes re-epithelialization, fibroplasia, granulation tissue formation, collagen deposition, angiogenesis, and wound contraction. Growth factors play an important role in regulating periodontal wound healing. Healing after periodontal procedures like scaling and root planing, curettage, ultrasonic curettage, and gingivectomy depends on the extent of tissue disruption and follows a timeline of inflammatory response, epithelial migration, granulation tissue formation, collagen deposition and remodeling.
This document provides an overview of the gingiva. It begins with definitions of gingiva from various sources and discusses the development, macroscopic features, microscopic features, fibers, cells, vascular supply, nerve supply, and matrix of the gingiva. Specifically, it describes the development of gingiva from mesoderm, its division into marginal, attached, and interdental papilla. It also discusses the layers of the gingival epithelium, the keratinization process, and cell types present like keratinocytes and non-keratinocytes.
The document discusses gingival curettage, which involves using instruments to remove diseased soft tissue from periodontal pockets. It defines curettage and provides the history of the procedure. The basic technique is described as using curettes to scrape the inner lining of the pocket to remove ulcerated epithelium and damaged connective tissue. Indications include edematous pockets aiming to reduce inflammation and shrink tissue. Healing after curettage is examined through a study showing revascularization of the wound site over time.
Periodontal pockets form when the gingival sulcus deepens due to the accumulation of bacteria and subsequent destruction of the supporting periodontal tissues. Pockets are classified as gingival, suprabonny, or intrabony based on the location of the base of the pocket relative to the underlying bone. Bacteria in the pocket cause inflammation and tissue destruction through the release of toxins and enzymes. Left untreated, pockets can deepen and cause increased bone and tissue loss. Probing is used to measure pocket depths and monitor periodontal disease progression and response to treatment.
This document discusses risk assessment in periodontal disease. It defines key terms like risk, risk factors, risk determinants, and risk markers. It categorizes different types of risk elements and describes several risk assessment tools that use various clinical and historical parameters to provide a risk score. The document concludes that while identification of risk factors has furthered understanding of periodontitis, predicting individual risk remains limited.
The document discusses the gingiva, which is the gum tissue surrounding the teeth. It defines gingiva and describes its functions of protecting the underlying tissues and maintaining periodontal health. The gingiva develops with tooth formation and eruption. Microscopically, it consists of stratified squamous epithelium and connective tissue. The epithelium can be oral, sulcular, or junctional depending on its location. The document also describes the anatomical structures of the gingiva including the marginal, attached, and interdental gingiva as well as the gingival sulcus.
This document discusses the rationale for periodontal treatment and the healing process after treatment. Local periodontal therapy aims to remove bacterial plaque and calculus that cause gum disease. Systemic therapy may also be used as an adjunct to treat infections or diseases that affect the periodontal condition. Healing after treatment involves regeneration of gingival epithelium, connective tissue, bone, and cementum. The key to new attachment is regeneration of the periodontal ligament, which provides continuity between the bone and cementum. The sequence in which different cell types repopulate the treated area determines the healing outcome and possibility of new attachment.
The document provides information on periodontal pockets, including their definition, classification, clinical features, pathogenesis, histopathology, and microtopography. Key points include:
- Periodontal pockets are pathologically deepened gingival sulci that form due to apical migration of the junctional epithelium and/or coronal movement of the gingival margin.
- Pockets can be classified based on their morphology, relationship to bone, number of tooth surfaces involved, and nature of the soft tissue wall.
- Pocket formation involves destruction of gingival fibers and collagen by host inflammatory responses to bacterial plaque, leading to apical migration of junctional epithelium.
- Histologically, pocket walls
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.
The document discusses periodontal pockets, which are deepening of the gingival sulcus caused by movement of the gingival margin or displacement of the gingival attachment. Pockets can be classified as gingival, suprabony, or intrabony depending on the level of underlying bone loss. Pockets contain debris, fluids, and microorganisms. Clinical features of pockets include discolored, flaccid gingiva and bleeding when probed. The root surface within pockets can undergo changes like cementum fragmentation. Periodontal abscesses are localized infections that can form through extension of infection from pockets or incomplete treatment leaving debris behind.
This document provides an overview of periodontal pockets, including their definition, classification, clinical features, pathogenesis, histopathology, and relationship to other periodontal diseases and conditions. Some key points:
- Periodontal pockets are pathologically deepened gingival sulci caused by apical migration of the junctional epithelium and loss of attachment.
- They are classified based on their morphology (gingival vs. periodontal), nature of the soft tissue wall (edematous vs. fibrotic), number of tooth surfaces involved (simple, compound, complex), and disease activity (active vs. inactive).
- Histopathologically, the soft tissue wall shows inflammatory cell infiltration and degeneration, while the root surface
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, 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 defines and describes periodontal pockets. It notes that periodontal pockets can be classified based on their location relative to the alveolar bone as either suprabony or infrabony. Suprabony pockets have bone loss horizontally while infrabony pockets have bone loss vertically. The document also discusses the pathogenesis of pocket formation, clinical features, histopathology, and diagnosis and probing of periodontal pockets.
Definition of periodontal pocket, classification, Histopathology of periodontal pocket, microflora involved, pathogenesis, periodontal pocket as a healing lesion, microtopography of root surface, treatment of periodontal pocket
The document discusses pulp pathology and its sequelae. It covers the response of the pulp to dental caries, including immune response, hard tissue response to irritation, and histologic changes in acute and chronic inflammation. It also discusses neural changes during pulpal inflammation, antiinflammatory mechanisms, less common responses, iatrogenic effects, systemic factors, and pulpal sequelae to trauma. Causes of pulp inflammation, necrosis, and dystrophy include bacterial, traumatic, iatrogenic, chemical, and idiopathic factors.
This document discusses periodontal disease and its effects. It describes the principal fiber groups in the periodontal ligament that help retain teeth. It then discusses signs of periodontal disease like pocket formation, gingival recession, and tooth mobility. Pocket types like gingival and periodontal pockets are defined. Diagnosis involves using a periodontal probe to measure pocket depth and check for furcation involvement. Treatment aims to reduce inflammation and regenerate lost bone and tissues.
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 defines and classifies periodontal pockets, describing their pathogenesis and histopathological features. It discusses gingival pockets, periodontal pockets (which can be suprabonny or infrabonny), and pseudo pockets. The key stages in pocket formation are outlined, from bacterial plaque initiation to colonization by anaerobic bacteria and collagen destruction. Clinical and histological characteristics of pocket walls and contents are also summarized.
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.
The document discusses cysts of the jaws and oral region. It defines a cyst as a fluid or semi-fluid filled cavity lined by epithelium. Cysts are classified as true cysts, which are epithelial lined, or false/pseudocysts without an epithelial lining. Odontogenic cysts are associated with teeth and develop from epithelial cell rests involved in tooth development. Non-odontogenic cysts occur in areas unrelated to teeth. Theories of cyst pathogenesis include proliferation of dormant epithelial cells due to growth factors, central cell death creating a cavity, and growth through osmotic pressure differences.
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.
This document provides an overview of the management of periodontal pockets. It defines periodontal pockets as the deepening of the gingival sulcus and classifies pockets based on their morphology, relationship to crestal bone, number of tooth surfaces involved, and soft tissue wall nature. The document discusses the normal anatomy of the periodontium, differences between suprabonny and infrabony pockets, pathogenesis of pockets, pocket contents, clinical signs and symptoms, treatment modalities including non-surgical and surgical approaches, and concludes with the importance of understanding pocket classifications for providing treatment.
This document discusses dentigerous cysts. It defines a dentigerous cyst as a cyst that forms around the crown of an unerupted tooth due to fluid accumulation between the reduced enamel epithelium and enamel surface. Dentigerous cysts most commonly occur in males in the first three decades of life in the mandibular third molar and maxillary canine regions. Clinical features include swelling and expansion of bone that may cause facial asymmetry. Treatment options include enucleation, marsupialization, or a combination of the two to remove the cyst lining while preserving adjacent structures.
This document discusses dental plaque, including its definition, classification, composition, and development. It defines dental plaque as a soft deposit that adheres to teeth and consists of bacteria embedded in an extracellular matrix. Plaque is classified based on location, such as supragingival vs subgingival. It has both bacterial and non-bacterial components, with bacteria making up 70-80% of the solid content. Plaque develops first through the formation of a salivary pellicle on the tooth surface, followed by initial bacterial attachment and colonization by primary colonizers like streptococci. Over time, secondary colonizers adhere and plaque matures into a biofilm.
Dental plaque is a biofilm that forms on teeth and consists of bacteria embedded in an extracellular matrix. It develops in stages, beginning with the formation of a protein pellicle layer on the tooth surface within seconds of cleaning. Initial colonizers like streptococci then adhere to the pellicle. Secondary colonization involves more species adhering directly or co-aggregating with initial colonizers. Co-aggregation involves specific adhesins on bacteria binding together different species in complex biofilms. The plaque matures into distinct supragingival and subgingival biofilms as the environment changes below the gumline.
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3. INTRODUCTIONINTRODUCTION
Periodontitis is defined as “an inflammatory disease
of the supporting tissues of the teeth caused by
specific organisms or groups of specific organisms,
resulting in progressive destruction of the
periodontal ligament and alveolar bone with pocket
formation, recession or both.”
Pocket formation is one of the characteristic feature
of periodontitis.
4. DEFINITIONDEFINITION
• The periodontal pocket, defined as “a pathologically
deepened gingival sulcus.”
Deepening of the gingival sulcus
by coronal movement apical displacement combination
of the gingival margin of the gingival attachment
5. CLASSIFICATION OF POCKETS:CLASSIFICATION OF POCKETS:
1. Gingival pocket
(pseudo pocket)
2. Periodontal
pocket:
a. Suprabony pocket:
bottom of the pocket is coronal
to the underlying alveolar bone
b. Intrabony pocket:
bottom of the pocket is apical
to the level of the adjacent
alveolar bone.
6. Differences between Intrabony and
Suprabony Pockets
Suprabony Pockets Infrabony Pockets
Base of pocket is coronal to
alveolar bone
Base of pocket is apical to the crest
of alveolar bone
Bone destructive pattern is horizontal Pattern of bone destruction is vertical
Interproximally, transseptal fibers
restored during progressive
periodontal disease are arranged
horizontally.
Transseptal fibers are oblique
On facial and lingual surfaces, PDL
fibers beneath the pocket follow
normal horizontal-oblique course
between tooth and bone.
PDL fibers follow angular pattern of
adjacent bone
7. According to involved tooth surfaces
1. Simple: Involves one tooth
surface.
2. Compound: Involves 2 or
more tooth surfaces.
3. Complex: Spiral type of
pocket -most common in
furcation areas.
8. CLINICAL FEATURESCLINICAL FEATURES
SIGNS OF PERIODONTAL POCKET:
1. Enlarged bluish-red marginal gingiva with rolled edge
separated from the tooth surface.
2. A reddish blue vertical zone extending from the gingival
margin to the attached gingiva and sometimes into alveolar
mucosa.
3. A break in the faciolingual continuity of interdental gingiva.
4. Shiny, discolored and puffy gingiva associated with exposed
root surface.
5. Gingival bleeding.
6. Purulent exudate or its appearance in response to digital
pressure on lateral aspect of gingival margin.
7. Looseness, extrusion and migration of teeth.
8. Diastema formation.
9. CLINICAL FEATURESCLINICAL FEATURES
SYMPTOMS OF PERIODONTAL POCKET:
1. Localized pain or sensation of pressure after eating.
2. Foul taste in localized area.
3. Tendency to suck material from interproximal space.
4. Radiating pain deep in bone.
5. A gnawing feeling or feeling of itchiness into the gums.
6. Urge to dig a pointed instrument into the gums with relief
obtained from the resultant bleeding.
7. Complain that food sticks between the teeth.
8. Teeth feel loose, preference to eat on the other side.
9. Sensitivity to heat and cold and toothache in absence of
caries.
10. The only reliable method of locating periodontal pockets
and determining their extent is careful probing of the
gingival margin along each tooth surface.
On the basis of depth alone, however, it is sometimes
difficult to differentiate between a deep normal sulcus
and a shallow periodontal pocket.
In such borderline cases, pathologic changes in the
gingiva distinguish the two conditions.
11. CORRELATION OF CLINICAL ANDCORRELATION OF CLINICAL AND
HISTOPATHOLOGIC FEATURES OF POCKETHISTOPATHOLOGIC FEATURES OF POCKET
CLINICAL FEATURES HISTOPATHOLOGY
Bluish red discoloration circulatory stagnation.
Flaccidity destruction of gingival fibres & CT.
Smooth, shiny surface atrophy of epithelium & edema.
Pitting on pressure edema & degeneration.
Firm & pink fibrotic changes.
Bleeding on probing ↑ed vascularity, thinning &
degeneration of epithelium, proximity
of engorged vessels.
Inner aspect of pocket painful ulceration of inner aspect of pocket.
Expression of pus from pocket suppurative inflammation of inner wall.
12. PATHOGENESISPATHOGENESIS
• There are many hypotheses on pocket formation.
– Some imply that the subgingival bacterial growth is
secondary to the opening of the pocket, others suggest that
the pocket formation is a result of bacteria spreading
subgingivally.
• Schroeder and Attstrom proposed a hypothesis of the
development of the gingival pocket using experimentally
produced neutropenic dogs.
• They suggested that pathological pockets are formed by
microbial invasion of the subgingival dentogingival junction, thus
destroying the coronal epithelial attachment.
13. • In addition to the bacterial factors, the mechanism of
deepening of the sulcus, along with its pathological
counterparts, is also the subject of long standing interest.
• The deepening has been considered to be initiated at the
interface between
– (1) the junctional epithelium and tooth, and
– (2) at the line of fusion between the junctional
epithelium and the reduced enamel epithelium within the
junctional epithelium.
14. THEORIES ON THE PATHOGENESIS OFTHEORIES ON THE PATHOGENESIS OF
PERIODONTAL POCKETSPERIODONTAL POCKETS
15. I. Destruction of the Gingival Fibers is a PrerequisiteI. Destruction of the Gingival Fibers is a Prerequisite
for the Initiation of Pocket Formation.for the Initiation of Pocket Formation.
• This concept focuses attention upon the migration of gingival fibers.
• The contention is that proliferation of the junctional epithelium along
the root can take place only if the underlying gingival fibers are
destroyed.
• These fibers are considered a barrier to the normal migratory
tendency of the epithelium at the base of the sulcus, and it is believed
that their degeneration and necrosis occur secondary to gingival
inflammation or the action of bacterial enzymes such as hyaluronidase.
• As soon as the topmost fiber is digested and absorbed, the epithelium
proliferates along the root until a healthy fiber is reached.
16. • Gottlieb and Orban have questioned this concept.
• They pointed to areas of repaired idiopathic tooth resorption
immediately beneath the junctional epithelium, and noted that since the
resorption of the tooth entailed detachment of the gingival fibers,
repair would not have been possible had the epithelium proliferated
simply because the fibers had been destroyed.
• They also point out that when the junctional epithelium is attached to
the enamel and is separated from the cementum by unattached
connective tissue rather than fibers embedded in the tooth, so
pathologic migration of the epithelium does not occur.
17. II. The Initial Change in Pocket FormationII. The Initial Change in Pocket Formation
Occurs in the CementumOccurs in the Cementum
• In seeking an explanation for pocket formation, Gottlieb stresses the
changes in tooth surface rather than in the gingiva.
• He envisions downgrowth of the junctional epithelium as a physiologic
phenomenon that is part of the process of continuous eruption of teeth
throughout life.
• Under physiologic conditions, the continuous deposition of new
cementum acts as a barrier that prevents accelerated migration of the
junctional epithelium.
• So long as continuous cementum deposition is not disturbed, migration
of the junctional epithelium at a pathologic rate cannot occur.
18. • However, if the tooth surface is of low resistance, or if the normal
deposition of cementum is impaired, inflammation or trauma can do
additional harm by destroying either the cementum or the gingiva,
or both.
• This dissolves the organic connection between the two, and the
epithelium proliferates along the root until it meets undisturbed
connective tissue fibers and cementum.
• Death of the cementum does not necessarily occur under such
circumstances, as evidenced by the fact that epithelium attaches
itself to cementum after its organic connection with the periodontal
ligament fibers is destroyed.
19. III. Stimulation of the Junctional Epithelium by Inflammation Rather
than Destruction of Gingival Fibers is the Prerequisite for the
Initiation of the Periodontal Pocket.
• Destruction of the underlying gingival fibers is not a prerequisite for
epithelial migration.
• Stimulated by inflammation, the epithelium migrates along the root
without preceding destruction of the gingival fibers.
• In such instances the epithelial cells burrow between the intact
gingival fibers and attach themselves farther apically on the cementum
in bundle free areas.
• The junctional epithelium may move between healthy connective tissue
fibers, enmesh them in an epithelial network, and produce secondary
fiber degeneration.
20. IV. Pathologic Destruction of the junctionalIV. Pathologic Destruction of the junctional
Epithelium due to Infection or Trauma is the InitialEpithelium due to Infection or Trauma is the Initial
Histologic Change in Pocket FormationHistologic Change in Pocket Formation
• According to Skilien, the junctional epithelium has few protective qualities for
safeguarding the underlying connective tissue against spread of infection.
• It is the normal down growth of the oral epithelium behind the junctional
epithelium that protects the underlying connective tissue.
• The junctional epithelium is an area of low-resistance subject to infection.
– In experimental animals, pocket formation occurs because of pathologic
dissolution of the junctional epithelium due to infection or trauma, or both.
Accumulation of debris in the pocket may be secondary after the pocket is
formed by dissolution of the junctional epithelium.
21. V. The Periodontal Pocket is Initiated by Invasion of BacteriaV. The Periodontal Pocket is Initiated by Invasion of Bacteria
at the Base of the Sulcus or the Absorption of Bacterialat the Base of the Sulcus or the Absorption of Bacterial
Toxins Through the Epithelial Lining of the Sulcus.Toxins Through the Epithelial Lining of the Sulcus.
• According to Box, either because of imperfect junction of the
epithelial cells and the cementum or extreme thinness of the
epithelium, the base of the sulcus offers a poor defense against
bacteria.
• In the evolution of a pocket, initial invasion of bacteria at the base of
the sulcus leads to the following changes: inflammation in the
underlying connective tissue, ulceration at the base of the crevices,
sloughing of the epithelium and loss of attachment to the cementum,
progressive loss of connective tissue, and penetration of the pocket
into the deeper tissues.
• Specific infective agents possibly related to Leptothrix falciformis
are capable of deepening the periodontal pocket.
• Also Holt considers the epithelial lining of the sulcus a poor barrier
against bacterial toxins, which initiate inflammatory changes leading
to pocket formation.
22. VI. Pocket Formation is initiated in a Defect in theVI. Pocket Formation is initiated in a Defect in the
Sulcus Wall.Sulcus Wall.
• According to Becks," the formation and maintenance of the
normal 1 mm deep sulcus results from the coordination of
degeneration of the enamel epithelium, proliferation of the oral
epithelium, and atrophy of the gingival papilla.
• Disturbance of this correlation, whether by inflammation or
injury, leads to pathologic pocket formation.
• Pocket formation occurs between the oral epithelium and the
enamel epithelium, rather than by separation of enamel
epithelium from the cuticle.
• If degeneration of the enamel epithelium takes place rapidly
without being covered by the oral epithelium, a defect occurs in
the lateral sulcus wall.
23. • This defect constitutes a "locus minoris resistentiae" which is a
portal of entry for bacteria with resultant inflammation.
• This induces proliferation of the basal cells of the enamel
epithelium and the oral epithelium, a protective mechanism for
the connective tissue.
• Inflammation is a stimulant to oral epithelium proliferation,
which shuts off nutrition from enamel epithelium, hastens its
degeneration, and increases the pocket
• In some cases, pathologic pocket formation may be initiated
without inflammation appearing to play a role.
• In such instances there is an accelerated degeneration of the
enamel epithelium, possibly of systemic origin. This is followed
by proliferation of the oral epithelium to cover the defect.
24. Vll. Proliferation of the Epithelium of the lateral Wall, ratherVll. Proliferation of the Epithelium of the lateral Wall, rather
than the Epithelium at the Base of the Sulcus, is the Initialthan the Epithelium at the Base of the Sulcus, is the Initial
change in the Formation of the Periodontal pocket.change in the Formation of the Periodontal pocket.
• Wilkinson regards epithelial proliferation as the primary change in
pocket formation.
• He describes the following sequence of changes:
– Proliferation and down growth of the oral epithelium or
proliferation of the junctional epithelium result in a thickening of
the epithelial lining of the sulcus.
– The cause of this proliferation is not known. Because of the
increased thickness, the cells along the inner aspect of the sulcus
are deprived of nutrition and undergo degeneration and necrosis.
– The degenerated and necrotic epithelial cells become calcified
(serumal calculus). Separation of the calcified masses from the
adjacent normal epithelium produces a pocket or trough.
25. • These changes are followed by proliferation of the epithelium along the
cementum, and detachment of its coronal portion from the root
surface.
• The epithelial changes that initiate pocket formation are not caused by
infection. Inflammatory changes in pocket formation are secondary to
the epithelial changes.
– Wilkinson suggests that vitamin A deficiency may be an important
factor in initiating pocket formation.
26. VIII. Two-stage Pocket Formation.VIII. Two-stage Pocket Formation.
• James and Counsel disagree with the concept that proliferation of
junctional epithelium followed by separation from cementum forms a
pocket.
• Instead, they feel pocket formation occurs in two stages:
– The first stage is proliferation of the sub-gingival epithelium
(junctional epithelium).
– The second stage is loss of the superficial layers of the
proliferated epithelium, which produces a space or pocket.
• The rate of proliferation of the epithelium at the base is such that it
precedes the destruction of the superficial epithelium, and the pocket
is therefore always lined with epithelium
27. IX. Inflammation is the Initial Change in theIX. Inflammation is the Initial Change in the
Formation of the Periodontal Pocket.Formation of the Periodontal Pocket.
• According to this concept periodontal pockets start as inflammatory
lesions. The first reaction is a vascular change in the underlying
connective tissue.
• Inflammation in the connective tissue stimulates the following changes
in the epithelial lining of the sulcus and in the junctional epithelium:
increased mitotic activity in the basal epithelial layer, and sometimes in
the prickle cell layer; increased production of keratin with
desquamation.’
• The cellular desquamation adjacent to the tooth surface tends to
deepen the pocket.
28. • The epithelial cells of the basal layer at the bottom of the sulcus and in
the area of attachment proliferate into the underlying connective
tissue and break up the gingival fibers.
• It is the repair of the lesion in the absence of treatment that
establishes the periodontal pocket. Granulation tissue fills in the
defect created by the open lesion, and the epithelium proliferates
inward.
• In pocket formation, the epithelium does not proliferate along the root;
instead it proliferates from the gingival surface to cover the
connective tissue lesion created by inflammation, and thereby forms
the lining of the pocket.
29. X. Pathologic Epithelial Proliferation Occurs Secondary to Non-X. Pathologic Epithelial Proliferation Occurs Secondary to Non-
inflammatory Degenerative Changes in the Periodontal Ligament.inflammatory Degenerative Changes in the Periodontal Ligament.
• Under the term "periodontosis" a condition has been described which is
characterized by generalized non-inflammatory degeneration of the
collagen fibers embedded in the cementum.
• Under such conditions, the normal barrier afforded by the gingival
fibers is diminished.
• This facilitates the migration of the junctional epithelium along the
root and pocket formation in the presence of local irritation.
30. EARLY LESIONEARLY LESION
• the degenerative changes occur first in the second or third
cell layer from the innermost cell layer of the most coronal
part of the junctional epithelium, which faces the microbial
plaque.
• an intraepithelial cleavage is formed followed by the
degeneration of the cells lining the cleavage, resulting in a
deep crevice formation.
• Schroeder and Attstrom pointed out that almost none of the
earlier studies related pocket formation to the presence of
bacterial deposits.
– They hypothesized that pocket formation is the result of a
split in the junctional epithelium from its attachment to
the tooth surface through the action of cocci.
31. THE ESTABLISHED LESIONTHE ESTABLISHED LESION
• As bacterial plaque spreads apically into the
deepened crevice,
– the preceding cellular degeneration of the
junctional epithelium,
– the intraepithelial cleavage formation, and
– the subsequent cell desquamation in the gingival
pocket occur at the bottom of the deepened
crevice in the same manner as described in the
early lesion.
32. THE ADVANCED LESIONTHE ADVANCED LESION
• The pocket becomes so deep with the pocket epithelium being
exposed for such a long periods to the subcrevicular plaque
and calculus, that the epithelium is easily and directly
affected by toxic bacterial products and mechanical irritation
by the calculus.
• While the pocket epithelium proliferates reactively in some
areas, it also become very thin and often ulcerates.
• Concomitant destruction of the periodontium and alveolar bone
provides access for the apical migration of the junctional
epithelium.
33. • Pocket formation starts as an inflammatory change in the
connective tissue wall of the gingival sulcus.
• The cellular and fluid inflammatory exudate causes degeneration
of the surrounding connective tissue, including the gingival
fibers.
• Just apical to the junctional epithelium, collagen fibers are
destroyed and the area becomes occupied by inflammatory cells
and edema.
34. Two mechanisms are considered to beTwo mechanisms are considered to be
associated with collagen loss:associated with collagen loss:
• (1) Collagenases and other enzymes secreted by various cells in
healthy and inflamed tissue such as fibroblasts,
polymorphonuclear leukocytes, and macrophages become
extracellular and destroy collagen (matrix metalloprpteinases)
• (2) Fibroblasts phagocytize collagen fibers by extending
cytoplasmic processes to the ligament-cementum interface and
degrade the inserted collagen fibrils and the fibrils of the
cementum matrix.
– As a consequence of the loss of collagen, the apical cells of
the junctional epithelium proliferate along the root,
extending fingerlike projections two or three cells in
thickness.
35. • The coronal portion of the junctional epithelium detaches from
the root as the apical portion migrates.
• As a result of inflammation, polymorphonuclear neutrophils
(PMNs) invade the coronal end of the junctional epithelium in
increasing numbers.
• The PMNs are not joined to one another or to the remaining
epithelial cells by desmosomes. When the relative volume of
PMNs reaches approximately 60% or more of the junctional
epithelium, the tissue loses cohesiveness and detaches from the
tooth surface.
• Thus the sulcus bottom shifts apically, and the oral sulcular
epithelium occupies a gradually increasing portion of the sulcular
(pocket) lining.
36. • Extension of the junctional epithelium along the root requires
the presence of healthy epithelial cells.
• Degenerative changes seen in the junctional epithelium at the
base of periodontal pockets are usually less severe than those
in the epithelium of the lateral pocket wall.
• Because migration of the junctional epithelium requires
healthy, viable cells, it is reasonable to assume that the
degenerative changes seen in this area occur after the
junctional epithelium reaches on to the cementum.
37. • The transformation of a gingival sulcus into a periodontal pocket
creates an area where plaque removal becomes impossible, and
the following feedback mechanism is established:
– Plaque Gingival inflammation Pocket formation
More plaque formation
• The rationale for pocket reduction is based on the need to
eliminate areas of plaque accumulation.
38. HISTOPATHOLOGICAL FEATURESHISTOPATHOLOGICAL FEATURES
• The connective tissue is edematous and densely infiltrated
with plasma cells (approximately 80%), lymphocytes, and a
scattering of PMNs.
• The blood vessels are increased in number, dilated, and
engorged, particularly in the subepithelial connective tissue
layer.
• The connective tissue exhibits varying degrees of
degeneration and shows proliferation of the endothelial cells,
with newly formed capillaries, fibroblasts, and collagen fibers.
Soft Tissue Wall
39. • The junctional epithelium at the base of the pocket is usually
much shorter than that of a normal sulcus.
• Although marked variations are found as to length, width, and
condition of the epithelial cells, usually the coronoapical length
of the junctional epithelium is reduced to only 50 to 100 μm.
• The cells may be well formed and in good condition or may
exhibit slight to marked degeneration.
40. • The most severe degenerative changes in the periodontal pocket
occur along the lateral wall.
• The epithelium of the lateral wall of the pocket presents
striking proliferative and degenerative changes.
• Epithelial buds or interlacing cords of epithelial cells project
from the lateral wall into the adjacent inflamed connective
tissue and may extend farther apically than the junctional
epithelium.
41. • The severity of the degenerative changes is not necessarily
related to pocket depth.
– Ulceration of the lateral wall may occur in shallow pockets,
and deep pockets are occasionally observed in which the
lateral epithelium is relatively intact or shows only slight
degeneration.
• The epithelium at the gingival crest of a periodontal pocket is
generally intact and thickened, with prominent rete pegs.
42. The SEM studies have shown the following
features in the lower part of pocket epithelium.
– Widening of intercellular spaces.
– Epithelial cell degeneration which mainly occurred in the
supra basal and superficial layers of the epithelium and in
nuclei and RER.
– Reduction in cell contacts was clear and enzymatic digestion
of desmosomes by trypsin in vitro proved this point.
– increased pocket wall permeability due to disruption of
intercellular spaces and basal lamina.
43. Bacterial Invasion
• Bacterial invasion of the apical and lateral areas of the pocket
wall has been described in human chronic periodontitis.
• Filaments, rods, and coccoid organisms with predominant gram-
negative cell walls have been found in intercellular spaces of
the epithelium.
• Bacteria may invade the intercellular space under exfoliating
epithelial cells, but they are also found between deeper
epithelial cells and accumulating on the basement lamina.
– Some bacteria traverse the basement lamina and invade
the subepithelial connective tissue.
• direct bacterial invasion or as passive translocation of
plaque bacteria.
44. Microtopography of the Gingival
Wall of the Pocket
• SEM has shown various areas of activity:
– 1. Areas of relative quiescence, showing a relatively flat
surface with minor depressions and mounds and occasional
shedding of cells.
– 2. Areas of bacterial accumulation, which appear as
depressions on the epithelial surface, with abundant debris
and bacterial clumps penetrating into the enlarged
intercellular spaces. These bacteria are mainly cocci, rods,
and filaments, with a few spirochetes.
– 3.Areas of emergence of leukocytes, where leukocytes
appear in the pocket wall through holes located in the
intercellular spaces.
– 4. Areas of leukocyte-bacteria interaction, where
numerous leukocytes are present and covered with bacteria
in an apparent process of phagocytosis.
45. • 5. Areas of intense epithelial desquamation, which consist of
semiattached and folded epithelial squames, some times partially
covered with bacteria.
• 6. Areas of ulceration, with exposed connective tissue.
• 7. Areas of hemorrhage, with numerous erythrocytes.
46. CONTENTS OF THE PERIODONTAL
POCKET
• Periodontal pockets contain debris consisting principally of:
• Microorganisms and their products (enzymes, endotoxins,
and other metabolic products),
• Food remnants,
• Salivary mucin,
• Gingival fluid,
• Desquamated epithelial cells, and
• Leukocytes
– Plaque covered calculus usually projects from the tooth
surface.
– Purulent exudate, if present, consists of living, degenerated,
and necrotic leukocytes; living and dead bacteria; serum; and
a scant amount of fibrin.
47. Importance of Pus Formation
• There is a tendency to overemphasize the importance of the
purulent exudate and to equate it with severity of periodontal
disease.
• Pus is a common feature of periodontal disease, but it is only a
secondary sign.
• The presence of pus expressed from the pocket is not an
indication of the depth of the pocket or the severity of the
destruction of the supporting tissues.
– It merely reflects the nature of the inflammatory changes in
the pocket wall. Extensive pus formation may occur in shallow
pockets, whereas deep pockets may exhibit little or no pus
48. Healing of Periodontal Pockets
• Periodontal pockets are chronic inflammatory lesions where
complete healing does not occur because of the persistence of
the bacterial attack, which continues to stimulate an
inflammatory response, causing degeneration of elements
formed at the time of repair.
• The status of the lateral wall of the periodontal pocket depends
upon the interplay between destructive and constructive tissue
changes which determines clinical features such as
– color,
– consistency, and
– surface texture of the pocket wall.
49. • If the inflammatory fluid and cellular exudate predominate, the
pocket wall is bluish-red, soft, spongy, and friable, with a
smooth, shiny surface (Edematous Pocket wall).
• If there is a relative predominance of newly formed connective
tissue cells and fibers, the pocket wall is more firm and pink
(Fibrotic pocket wall).
• Fibrotic pocket walls may be misleading because they
do not necessarily reflect what is taking place
throughout the pocket wall.
50. Root Surface Wall
• The root surface wall of periodontal pockets often undergoes
changes that are significant because they may perpetuate the
periodontal infection, cause pain, and complicate periodontal
treatment.
Exposure of the cementum to oral environment
proteolysis of Sharpeys fibres
fragmentation & cavitation.
51. • Bacterial products such as endotoxins have been
detected in the cementum wall of periodontal
pockets.
• Cementum is very thin in the cervical areas and
scaling and root planing often removes it entirely,
exposing the underlying dentin.
– Sensitivity to cold may result until secondary
dentin is formed by the pulp tissue
52. Areas of increased mineralization
• an exchange of minerals and organic components.
• The following minerals are increased in diseased root
surfaces: calcium, magnesium, phosphorus, and fluoride.
– Micro hardness, however, remains unchanged.
– The development of a highly mineralized superficial layer
may increase the tooth resistance to decay.
• The hypermineralized zones are associated with
increased perfection of the crystal structure and
organic changes suggestive of a subsurface cuticle.
• No decrease in mineralization was found in deeper areas,
thereby indicating that increased mineralization does not
come from adjacent areas.
53. Areas of demineralization
• These are commonly related to root caries. Exposure to oral fluid and
bacterial plaque results in proteolysis of the embedded remnants of
Sharpey's fibers;
• The cementum may be softened and may undergo fragmentation and
cavitation.
• Active root caries lesions appear as well defined yellowish or light-
brown areas, are frequently covered by plaque, and have a softened or
leathery consistency on probing.
• Inactive lesions are well-defined darker lesions with a smooth surface
and a harder consistency on probing.
54. • The dominant microorganism in root surface caries is Actinomyces
viscosus, although its specific responsibility in the development of
the lesion has not been established.
• Other associated bacteria are:
– Actinomyces naeslundii,
– Streptococcus mutans,
– Streptococcus salivarius,
– Streptococcus sanguis, and
– Bacillus cereus
• The tooth may not be painful, but exploration of the root surface
reveals the presence of a defect, and penetration of the involved
area with a probe causes pain.
• Caries of the root, however, may lead to pulpitis, sensitivity to
sweets and thermal changes, or severe pain. Pathologic exposure of
the pulp occurs in severe cases.
55. Areas of cellular resorption of cementum and
dentin
• These are common in roots unexposed by periodontal disease. These
areas are symptom free, and as long as the root is covered by the
periodontal ligament, they are apt to undergo repair.
• However, if the root is exposed by progressive pocket formation
before repair of such areas occurs, these appear as isolated cavitations
that penetrate into the dentin.
56. Surface Morphology of the Tooth
Wall of Periodontal Pockets
• The following zones can found in the
bottom of a periodontal pocket:
1. Cementum covered by calculus
2. Attached plaque, which covers calculus
and extends apically from it to a
variable degree, probably 100 to
500µm.
3. The zone of unattached plaque that
surrounds attached plaque and extends
apically to it.
4. The zone where the junctional
epithelium is attached to the tooth.
The extension of this zone, which in
normal sulci is more than 500 µm, is
usually reduced in periodontal pockets
to less than 100 µm.
5. Apical to the junctional epithelium,
there may be a zone of semidestroyed
connective tissue fibers.
57. PERIODONTAL DISEASE
ACTIVITY
• For many years the loss of attachment produced by periodontal disease
was thought to be a slow but continuously progressive phenomenon.
• More recently, as a result of studies on the specificity of plaque
bacteria, the concept of periodontal disease activity has evolved.
• According to this concept, periodontal pockets go through periods of
exacerbation and quiescence, resulting from episodic bursts of activity
followed by periods of remission.
58. • Periods of quiescence are characterized by a reduced inflammatory
response and little or no loss of bone and connective tissue attachment.
• Period of exacerbation starts with a buildup of unattached plaque, with
its gram-negative, motile, and anaerobic bacteria in which bone and
connective tissue attachment are lost and the pocket deepens.
• These periods of quiescence and exacerbation are also known as periods
of activity and inactivity.
– Clinically, active periods show bleeding, either spontaneously or
with probing, and greater amounts of gingival exudate.
– Histologically, the pocket epithelium appears thin and ulcerated,
and an infiltrate composed predominantly of plasma cells,
polymorphonuclear leukocytes, or both are seen.
59. Site Specificity
• Periodontal destruction does not occur in all parts of the mouth
at the same time but rather on a few teeth at a time or even
only some aspects of some teeth at any given time.
• This is referred to as the site specificity of periodontal
disease.
• Therefore the severity of periodontitis increases by the
development of new disease sites, the increased breakdown of
existing sites, or both.
60. RELATION OF ATTACHMENT LOSS
AND BONE LOSS TO POCKET DEPTH
• Pocket formation causes loss of attachment of the gingiva and denudation
of the root surface.
• The severity of the attachment loss is generally, but not always, correlated
with the depth of the pocket.
• This is because the degree of attachment loss depends on the location of
the base of the pocket on the root surface, whereas the pocket depth is the
distance between the base of the pocket and the crest of the gingival
margin.
• Pockets of the same depth may be associated with different degrees of
attachment loss, and pockets of different depths may be associated with the
same amount of attachment loss.
62. AREA BETWEEN THE BASE OF THE
POCKET AND THE ALVEOLAR BONE
• Normally, the distance between the apical end of the junctional
epithelium and the alveolar bone is relatively constant.
• The distance between the apical extent of calculus and the alveolar
crest in human periodontal pockets is most constant, having a mean
length of 1.97 mm ± 33.16%.
• The distance from attached plaque to bone is never less than 0.5 mm
and never more than 2.7 mm.
– These findings suggest that the bone resorbing activity induced by
the bacteria is exerted within these distances.
63. Differences between Intrabony and
Suprabony Pockets
Suprabony Pockets Infrabony Pockets
Base of pocket is coronal to
alveolar bone
Base of pocket is apical to the crest
of alveolar bone
Bone destructive pattern is horizontal Pattern of bone destruction is vertical
Interproximally, transseptal fibers
restored during progressive
periodontal disease are arranged
horizontally.
Transseptal fibers are oblique
On facial and lingual surfaces, PDL
fibers beneath the pocket follow
normal horizontal-oblique course
between tooth and bone.
PDL fibers follow angular pattern of
adjacent bone
64. Comment regarding pocket formationComment regarding pocket formation
• The following salient facts regard pocket formation are worthy of
special note:
• Local irritation is required for the initiation and progress of
pocket formation.
• Proliferation of the junctional epithelium along the root
and degeneration of underlying gingival fibers are
prim changes in pocket formation.
• Proliferation of the junctional epithelium is
stimulated by local irritation, inflammation caused by local
irritation produces degeneration of the gingival fibres.
65.
66. References:
• Clinical Periodontology, 10th Ed. Carranza.
• Clinical Periodontology, 9th Ed. Carranza.
• Clinical Periodontology, 8th Ed. Carranza.
• Clinical Periodontology and implant dentistry; 4th Ed. Jan Lindhe.
• Takashi Takata, Karl Donath. “The mechanism of pocket formation” J
Periodontol 1988; 59:215-221.
• Listgarten MA “Pathogenesis of Periodontitis” J Clin Periodontol 1986;
13: 418-425.
• Muller GW, Schroeder HE, “The Pocket Epithelium: A light and
electron microscopy study” J Periodontol 1982; 53: 133-144.
• Hiroshi Takarada et al. “Ultrastructural studies of human gingiva part
I & II.” J Periodontol 1974; 45: 155-169.