This document summarizes bone formation and resorption. It classifies bones based on shape, development, and microscopic structure. It describes the composition of bone including bone cells like osteoblasts, osteoclasts, and osteocytes. Bone formation is influenced by growth factors while resorption involves acid secretion and enzyme activity by osteoclasts. Bone remodeling maintains bone mass through coupled formation and resorption, regulated by hormones and cytokines. Markers like TRAP indicate the rate of resorption.
Metabolic bone disease remodeling sequencesvinod naneria
1. The bone remodeling process involves over 25 steps across resorption and formation phases that can take up to 3 years to complete.
2. Osteoclasts resorb bone over 2-3 weeks under the direction of osteoblasts, precisely replacing the resorbed bone through new bone formation.
3. Microcracks detected by osteocytes trigger signaling that activates stem cells to mature into pre-osteoblasts and pre-osteoclasts, initiating the remodeling cycle through RANK-L secretion and osteoclast maturation.
Metabolic Bone Disease Molecular Biologyvinod naneria
The discovery of RANKL, RANK, and OPG led to a new understanding of bone and calcium metabolism and the pathogenesis of metabolic bone diseases. These molecules orchestrate physiological bone remodeling by regulating osteoclast differentiation and function. Specifically, the interaction between RANKL and its receptor RANK is required for osteoclastogenesis, while OPG acts as a soluble receptor to inhibit this interaction and prevent osteoclast activation. Osteocytes play a key role in bone remodeling by sensing mechanical loads and signaling other cells to initiate resorption or formation.
Bone turnover in a clinical perspective involves three key factors: 1) remodeling balance per bone multicellular unit (BMU), which determines if bone is lost or gained, 2) remodeling rate (turnover), which depends on the number of active BMUs, and 3) remodeling space, or non-permanent bone loss from remodeling. Hormones can affect remodeling balance, turnover, and bone compartments. Diseases often cause bone loss through high turnover and a negative remodeling balance, while successful osteoporosis treatments restore balance and decrease turnover.
The document discusses the alveolar bone, which forms, supports, and protects the teeth. It has three parts: the alveolar bone proper, compact bone, and cancellous bone. Its functions include supporting teeth, attaching muscles, housing bone marrow, and storing ions. The alveolar bone is made up of water, organic components like collagen and cells, and inorganic hydroxyapatite crystals and ions. Osteoblasts form bone by synthesizing an uncalcified bone matrix and depositing hydroxyapatite crystals, while osteoclasts resorb bone by secreting acids and enzymes to dissolve the mineral and collagen phases.
This document provides an overview of bone physiology, metabolism, and biomechanics. It discusses the historical perspectives on bone anatomy and physiology. It also summarizes calcium metabolism and homeostasis, how bone is remodeled through modeling and remodeling, and the roles of hormones like parathyroid hormone, calcitonin, vitamin D, and sex hormones. Biomechanical concepts like Frost's mechanostat theory are introduced. Assessment methods and the genetic regulation of bone remodeling are also briefly covered.
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.
This document summarizes research on communication between osteoblasts and osteoclasts, the two main cells involved in bone remodeling. It discusses how osteoblasts can affect osteoclast formation and differentiation through several pathways, such as OPG/RANKL/RANK, ephrin2/ephB4, and M-CSF. It also reviews how osteoclasts can influence osteoblast activity through factors like Atp6v0d2. Direct cell-cell contact and cytokines released from resorbed bone matrix also facilitate communication between osteoblasts and osteoclasts. Imbalances in this communication can lead to bone diseases like osteoporosis.
Metabolic bone disease remodeling sequencesvinod naneria
1. The bone remodeling process involves over 25 steps across resorption and formation phases that can take up to 3 years to complete.
2. Osteoclasts resorb bone over 2-3 weeks under the direction of osteoblasts, precisely replacing the resorbed bone through new bone formation.
3. Microcracks detected by osteocytes trigger signaling that activates stem cells to mature into pre-osteoblasts and pre-osteoclasts, initiating the remodeling cycle through RANK-L secretion and osteoclast maturation.
Metabolic Bone Disease Molecular Biologyvinod naneria
The discovery of RANKL, RANK, and OPG led to a new understanding of bone and calcium metabolism and the pathogenesis of metabolic bone diseases. These molecules orchestrate physiological bone remodeling by regulating osteoclast differentiation and function. Specifically, the interaction between RANKL and its receptor RANK is required for osteoclastogenesis, while OPG acts as a soluble receptor to inhibit this interaction and prevent osteoclast activation. Osteocytes play a key role in bone remodeling by sensing mechanical loads and signaling other cells to initiate resorption or formation.
Bone turnover in a clinical perspective involves three key factors: 1) remodeling balance per bone multicellular unit (BMU), which determines if bone is lost or gained, 2) remodeling rate (turnover), which depends on the number of active BMUs, and 3) remodeling space, or non-permanent bone loss from remodeling. Hormones can affect remodeling balance, turnover, and bone compartments. Diseases often cause bone loss through high turnover and a negative remodeling balance, while successful osteoporosis treatments restore balance and decrease turnover.
The document discusses the alveolar bone, which forms, supports, and protects the teeth. It has three parts: the alveolar bone proper, compact bone, and cancellous bone. Its functions include supporting teeth, attaching muscles, housing bone marrow, and storing ions. The alveolar bone is made up of water, organic components like collagen and cells, and inorganic hydroxyapatite crystals and ions. Osteoblasts form bone by synthesizing an uncalcified bone matrix and depositing hydroxyapatite crystals, while osteoclasts resorb bone by secreting acids and enzymes to dissolve the mineral and collagen phases.
This document provides an overview of bone physiology, metabolism, and biomechanics. It discusses the historical perspectives on bone anatomy and physiology. It also summarizes calcium metabolism and homeostasis, how bone is remodeled through modeling and remodeling, and the roles of hormones like parathyroid hormone, calcitonin, vitamin D, and sex hormones. Biomechanical concepts like Frost's mechanostat theory are introduced. Assessment methods and the genetic regulation of bone remodeling are also briefly covered.
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.
This document summarizes research on communication between osteoblasts and osteoclasts, the two main cells involved in bone remodeling. It discusses how osteoblasts can affect osteoclast formation and differentiation through several pathways, such as OPG/RANKL/RANK, ephrin2/ephB4, and M-CSF. It also reviews how osteoclasts can influence osteoblast activity through factors like Atp6v0d2. Direct cell-cell contact and cytokines released from resorbed bone matrix also facilitate communication between osteoblasts and osteoclasts. Imbalances in this communication can lead to bone diseases like osteoporosis.
This document discusses biochemical markers that can be used to monitor bone formation and resorption. It notes that these markers may provide preferable alternatives to densitometry in some clinical settings. The document reviews the history of using biochemical markers in orthopedics and describes markers of bone formation mediated by osteoblasts and bone resorption mediated by osteoclasts. It also discusses factors like hormones, local stresses, and the environment that can impact bone turnover.
The document discusses biochemical markers of bone turnover. It notes that in adults, bone undergoes constant remodeling through resorption by osteoclasts and formation by osteoblasts. Biochemical markers measure bone formation or resorption products in blood and urine, allowing serial assessment of bone turnover. Formation markers include osteocalcin and procollagen peptides, while resorption markers include collagen telopeptides and hydroxypyridinium cross-links. These markers can help evaluate treatment response, predict fracture risk and bone loss, and select patients who may benefit most from treatment. However, markers have limitations due to biological and analytical variability.
This document provides information on bone structure and cells. It discusses the composition of bone as mineralized connective tissue composed of organic matrix and inorganic salts. It classifies bones based on shape and development. It describes the microscopic structure of compact and spongy bone. It details the types of bone cells - osteoprogenitor cells, osteoblasts, osteocytes, and osteoclasts - and their roles and functions in bone formation and remodeling. It also addresses factors that regulate the activity of bone cells.
Bone is a specialized connective tissue composed of both organic and inorganic parts. The organic part includes collagen and other proteins, while the inorganic part contains calcium and phosphate minerals. Bone contains three main cell types - osteoprogenitor cells that develop into osteoblasts or osteoclasts. Osteoblasts form new bone by secreting proteins and minerals, osteoclasts break down bone, and osteocytes maintain bone structure. Together these cells regulate bone remodeling through signals that stimulate or inhibit each other's activity.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Bone physiology and calcium homeostasisAbdulla Kamal
Bone is a highly specialized supporting framework of the body, characterized by its rigidity, hardness, and power of regeneration and repair.
It protects the vital organs, provides an environment for marrow ,acts as a mineral reservoir for calcium homeostasis and a reservoir of growth factors and cytokines, and also takes part in acid–base balance.
Bone constantly undergoes modeling (reshaping) during life to help it adapt to changing biomechanical forces, as well as remodeling to remove old, micro-damaged bone and replace it with new, mechanically stronger bone to help preserve bone strength.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
1) Bone tissue is a specialized connective tissue composed of cells and an extracellular matrix that becomes calcified. There are two types of bone tissue: compact bone and spongy bone.
2) The alveolar bone is a specialized bone structure that contains the tooth sockets (alveoli) and supports the teeth. It develops from the dental follicle and is composed of alveolar bone proper and supporting bone.
3) The alveolar process contains the tooth sockets and develops during tooth eruption. It is resorbed if teeth are lost. Key features include the alveolar sockets, interdental septa, interradicular septa, and the cribriform plate containing
Bone undergoes changes during orthodontic tooth movement. Bone is made up of an organic collagen matrix embedded in an inorganic mineral substance. When teeth are moved with orthodontic forces, bone remodeling occurs as the piezoelectric effect generates electric currents that signal bone cells. Woven bone is initially formed, followed by remodeling into mature lamellar bone through the coordinated actions of osteoblasts and osteoclasts.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Bone is composed of organic and inorganic components and water. It undergoes constant metabolism regulated by hormones like parathyroid hormone and calcitonin. Fractures are breaks in bone continuity and are classified based on features like displacement and soft tissue involvement. Treatment involves reduction, immobilization with splints or internal fixation, and rehabilitation. Complications can include delayed healing, malunion, and secondary osteoarthritis if not managed properly.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Metabolic bone disorders can result from disruptions to the complex system regulating bone mineralization and turnover. Rickets and osteomalacia are conditions of poor bone mineralization that present with skeletal abnormalities and deformities. They are caused by vitamin D deficiency or disorders of vitamin D metabolism, resulting in failure of bone matrix to properly mineralize. Diagnosis involves x-rays showing characteristic changes and biochemical testing demonstrating abnormalities in markers of bone formation and mineralization. Treatment focuses on correcting the underlying metabolic disorder through vitamin D supplementation or other medical management.
The document summarizes a seminar presentation on the utility of bone markers in the diagnosis and management of osteoporosis. It defines bone and describes its structure, formation, and resorption processes. It then discusses osteoporosis, its risk factors and impact. The document outlines diagnostic tools for osteoporosis including bone mineral density scans and bone markers. It describes markers of bone formation like bone alkaline phosphatase and osteocalcin, and markers of bone resorption like CTX and NTX. It concludes that bone markers are helpful complementary tools to static bone scans in detecting treatment effects and monitoring patients.
This document discusses metabolic bone diseases and provides details on bone morphology and functions. It describes the two types of bone tissue in the mature skeleton, compact cortical bone and cancellous bone. It also outlines the different components that make up bone morphology, including the organic matrix, bone cells, bone mineral, blood vessels, and bone marrow. The various cell types involved in bone formation and resorption are identified as well. Metabolic bone diseases can be caused by defects in mineralization, the bone matrix, excessive bone resorption, or Paget's disease.
The document discusses bone mineral homeostasis and the roles of parathyroid hormone (PTH), vitamin D, and calcitonin in regulating calcium and phosphate levels. It notes that 99% of calcium and 85% of phosphate in the body are stored in bone. PTH increases blood calcium by stimulating bone resorption and renal reabsorption of calcium. Vitamin D increases intestinal absorption of calcium and phosphate. Calcitonin decreases blood calcium by inhibiting bone resorption and renal reabsorption. Together these hormones tightly control bone remodeling and mineral levels through effects on osteoclasts and osteoblasts.
6. alveolar bone in health part b dr-ibrahim_shaikhDrIbrahim Shaikh
This document discusses the cells and components that make up healthy alveolar bone. It describes the main cell types, including osteoprogenitor cells that develop into osteoblasts or osteoclasts. Osteoblasts secrete osteoid and regulate mineralization, while osteoclasts are responsible for bone resorption. The bone matrix contains collagen fibers and hydroxyapatite crystals, along with noncollagenous proteins. Alveolar bone undergoes physiological remodeling through the coordinated actions of osteoblasts and osteoclasts, allowing adaptation to tooth movement and replacement over time.
This document provides an overview of alveolar bone structure and function. It begins with introductions to bone composition, development, and cell types. Key bone cells include osteoblasts, which form bone, and osteoclasts, which resorb bone. The document then discusses alveolar bone morphology, blood supply, and functions. Importantly, alveolar bone is in a constant state of flux, undergoing remodeling as bone is broken down and rebuilt through the coupled actions of osteoblasts and osteoclasts. Healing of alveolar bone after tooth extraction and age-related changes are also covered.
This document discusses biochemical markers that can be used to monitor bone formation and resorption. It notes that these markers may provide preferable alternatives to densitometry in some clinical settings. The document reviews the history of using biochemical markers in orthopedics and describes markers of bone formation mediated by osteoblasts and bone resorption mediated by osteoclasts. It also discusses factors like hormones, local stresses, and the environment that can impact bone turnover.
The document discusses biochemical markers of bone turnover. It notes that in adults, bone undergoes constant remodeling through resorption by osteoclasts and formation by osteoblasts. Biochemical markers measure bone formation or resorption products in blood and urine, allowing serial assessment of bone turnover. Formation markers include osteocalcin and procollagen peptides, while resorption markers include collagen telopeptides and hydroxypyridinium cross-links. These markers can help evaluate treatment response, predict fracture risk and bone loss, and select patients who may benefit most from treatment. However, markers have limitations due to biological and analytical variability.
This document provides information on bone structure and cells. It discusses the composition of bone as mineralized connective tissue composed of organic matrix and inorganic salts. It classifies bones based on shape and development. It describes the microscopic structure of compact and spongy bone. It details the types of bone cells - osteoprogenitor cells, osteoblasts, osteocytes, and osteoclasts - and their roles and functions in bone formation and remodeling. It also addresses factors that regulate the activity of bone cells.
Bone is a specialized connective tissue composed of both organic and inorganic parts. The organic part includes collagen and other proteins, while the inorganic part contains calcium and phosphate minerals. Bone contains three main cell types - osteoprogenitor cells that develop into osteoblasts or osteoclasts. Osteoblasts form new bone by secreting proteins and minerals, osteoclasts break down bone, and osteocytes maintain bone structure. Together these cells regulate bone remodeling through signals that stimulate or inhibit each other's activity.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Bone physiology and calcium homeostasisAbdulla Kamal
Bone is a highly specialized supporting framework of the body, characterized by its rigidity, hardness, and power of regeneration and repair.
It protects the vital organs, provides an environment for marrow ,acts as a mineral reservoir for calcium homeostasis and a reservoir of growth factors and cytokines, and also takes part in acid–base balance.
Bone constantly undergoes modeling (reshaping) during life to help it adapt to changing biomechanical forces, as well as remodeling to remove old, micro-damaged bone and replace it with new, mechanically stronger bone to help preserve bone strength.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
1) Bone tissue is a specialized connective tissue composed of cells and an extracellular matrix that becomes calcified. There are two types of bone tissue: compact bone and spongy bone.
2) The alveolar bone is a specialized bone structure that contains the tooth sockets (alveoli) and supports the teeth. It develops from the dental follicle and is composed of alveolar bone proper and supporting bone.
3) The alveolar process contains the tooth sockets and develops during tooth eruption. It is resorbed if teeth are lost. Key features include the alveolar sockets, interdental septa, interradicular septa, and the cribriform plate containing
Bone undergoes changes during orthodontic tooth movement. Bone is made up of an organic collagen matrix embedded in an inorganic mineral substance. When teeth are moved with orthodontic forces, bone remodeling occurs as the piezoelectric effect generates electric currents that signal bone cells. Woven bone is initially formed, followed by remodeling into mature lamellar bone through the coordinated actions of osteoblasts and osteoclasts.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Bone is composed of organic and inorganic components and water. It undergoes constant metabolism regulated by hormones like parathyroid hormone and calcitonin. Fractures are breaks in bone continuity and are classified based on features like displacement and soft tissue involvement. Treatment involves reduction, immobilization with splints or internal fixation, and rehabilitation. Complications can include delayed healing, malunion, and secondary osteoarthritis if not managed properly.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
Metabolic bone disorders can result from disruptions to the complex system regulating bone mineralization and turnover. Rickets and osteomalacia are conditions of poor bone mineralization that present with skeletal abnormalities and deformities. They are caused by vitamin D deficiency or disorders of vitamin D metabolism, resulting in failure of bone matrix to properly mineralize. Diagnosis involves x-rays showing characteristic changes and biochemical testing demonstrating abnormalities in markers of bone formation and mineralization. Treatment focuses on correcting the underlying metabolic disorder through vitamin D supplementation or other medical management.
The document summarizes a seminar presentation on the utility of bone markers in the diagnosis and management of osteoporosis. It defines bone and describes its structure, formation, and resorption processes. It then discusses osteoporosis, its risk factors and impact. The document outlines diagnostic tools for osteoporosis including bone mineral density scans and bone markers. It describes markers of bone formation like bone alkaline phosphatase and osteocalcin, and markers of bone resorption like CTX and NTX. It concludes that bone markers are helpful complementary tools to static bone scans in detecting treatment effects and monitoring patients.
This document discusses metabolic bone diseases and provides details on bone morphology and functions. It describes the two types of bone tissue in the mature skeleton, compact cortical bone and cancellous bone. It also outlines the different components that make up bone morphology, including the organic matrix, bone cells, bone mineral, blood vessels, and bone marrow. The various cell types involved in bone formation and resorption are identified as well. Metabolic bone diseases can be caused by defects in mineralization, the bone matrix, excessive bone resorption, or Paget's disease.
The document discusses bone mineral homeostasis and the roles of parathyroid hormone (PTH), vitamin D, and calcitonin in regulating calcium and phosphate levels. It notes that 99% of calcium and 85% of phosphate in the body are stored in bone. PTH increases blood calcium by stimulating bone resorption and renal reabsorption of calcium. Vitamin D increases intestinal absorption of calcium and phosphate. Calcitonin decreases blood calcium by inhibiting bone resorption and renal reabsorption. Together these hormones tightly control bone remodeling and mineral levels through effects on osteoclasts and osteoblasts.
6. alveolar bone in health part b dr-ibrahim_shaikhDrIbrahim Shaikh
This document discusses the cells and components that make up healthy alveolar bone. It describes the main cell types, including osteoprogenitor cells that develop into osteoblasts or osteoclasts. Osteoblasts secrete osteoid and regulate mineralization, while osteoclasts are responsible for bone resorption. The bone matrix contains collagen fibers and hydroxyapatite crystals, along with noncollagenous proteins. Alveolar bone undergoes physiological remodeling through the coordinated actions of osteoblasts and osteoclasts, allowing adaptation to tooth movement and replacement over time.
This document provides an overview of alveolar bone structure and function. It begins with introductions to bone composition, development, and cell types. Key bone cells include osteoblasts, which form bone, and osteoclasts, which resorb bone. The document then discusses alveolar bone morphology, blood supply, and functions. Importantly, alveolar bone is in a constant state of flux, undergoing remodeling as bone is broken down and rebuilt through the coupled actions of osteoblasts and osteoclasts. Healing of alveolar bone after tooth extraction and age-related changes are also covered.
This document provides an overview of bone structure and function. It begins with an introduction to bone and classifications of bone. It then discusses the composition of bone, including its inorganic and organic components. Various bone cells are described, such as osteoblasts, osteocytes, and osteoclasts. The document reviews bone development processes including endochondral and intramembranous bone formation. Bone remodeling and regulation of bone cells are also summarized.
This document provides information on the anatomy, histology, development and clinical implications of alveolar bone. It describes the components and cellular makeup of bone, including osteoblasts, osteocytes and osteoclasts. It explains that the alveolar process develops with tooth eruption and is tooth-dependent. Factors that regulate bone formation and resorption are also discussed. The document outlines how alveolar bone is affected by tooth loss, orthodontic forces and non-functioning teeth.
This document provides an overview of the anatomy, histology, development and clinical implications of alveolar bone. It describes the components and cellular makeup of bone, including osteoblasts, osteocytes and osteoclasts. It explains that the alveolar process develops with tooth eruption and is resorbed after tooth loss. Factors that regulate bone formation and resorption are discussed. The document also outlines how alveolar bone is affected by tooth loss, orthodontic forces and non-functioning teeth.
This document provides an overview of bone anatomy, physiology, and pathology. It discusses the following key points in 3 sentences or less:
- Bone is composed of inorganic minerals (hydroxyapatite crystals) and organic collagen fibers, which provide strength and allow bone to withstand compression and tension. Bone develops through two processes: intramembranous and endochondral ossification. Bone remodeling is a continuous process where old bone is resorbed and new bone is formed, enabling calcium homeostasis and repair of microdamage.
Bone changes during ortho. tooth movement dr.anusha /certified fixed orthodon...Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
0091-9248678078
Osteoprogenitor cells: pre-osteoblast, are bone stem cells derived from mesenchymal cells that eventually differentiate into mature osteoblast and osteocyte.
Osteoblast: large metabolically active cell with increased endoplasmic reticulum(ER)
1- Produce high level of alkaline phosphatase.
2- Produce type I collagen which is necessary for calcification.
3- Produce osteocalcine, produce signal to activate osteoclast.
= osteoblast has receptors for hormones such as parathyroid hormone, Vit. D, osteogen, cytokines and growth factors
= after osteoblast have secrete un-mineralized bone they usually become inactive, a few osteoblasts remain in the mineralized osteoid and become osteocyte.
Osteocyte: are osteoblast that have become surrounded by the calcified matrix of bone, these cells acts as mechanoreceptor identifying the loads placed on the individual bones and establishing the nature of such loads.
Osteoclasts: are large multi-nucleated cells, found attached to the surface of active bone formation.
= Found in well-defined pits known as Howships Lacuna.
= Derived from mono-nuclear stem cells in bone marrow and travel through blood vessels to the site of activity. It is activated by: inter-luckin II,I, cytokines.
= decreased endoplasmic reticulum.
Bone lining cells: elongated cells covering bone surface, they are inactive and have a high nucleus to cytoplasmic ratio, these cells has a major impact on calcium metabolism within the body.
Bone development:
Cellular mechanisms:
= skeleton formation begins when mesenchymal cells migrate to the site of skeleton-genesis. The cells then interact with epithelial cells, which in then trigger the mesenchymal cells to cluster together and undergo condensation to form compact mass of cells.
= each step is regulated by special type of genes such as member of home box genes.
= condensed cell then undergo differentiation either chondrocyte or osteoblast.
Core bonding factor-1 (CBFA-1)— (now known as Runx2)
One of the most important bone specified genes in differentiation of mesenchymal cells into – osteoblast.
Core bonding factor -1: CBFA-1 now is known as Runx2.
One of the most important bone specific genes in differentiation of mesenchymal cells into------osteoblast.
Bone morphogenetic protein: BMP:
= Play important role in the developing skeleton.
= BMP has been used ti improving healing and bone defect.
= BMP’s are probably involved in intramembranous bone formation.
= BMP-7 is found in area of brain to induce formation of cranial bones
= BMP’S 2—4 and 5 are expressed in some regions where mesenchymal condensation later give rise to craniofacial bone.
Novel mechanisms of osteoblast and osteoclast interaction:
Osteoblast interact with osteoclast to regulate the osteoclastic action.
Receptor activator of nuclear factor ligand (RANKL) is produced by pre-osteoblast and osteoblast and cell membrane of osteoblastic precursors.
This factor is essential factor for differentiation, fusion into multinucleated
Bone is a living tissue composed of collagen, proteins, and hydroxyapatite crystals. Bone remodeling is carried out by osteoblasts, osteoclasts, and osteocytes through a basic multicellular unit process where bone is resorbed and formed at equal rates. During remodeling, osteoclasts resorb bone through the secretion of acids and proteases, while osteoblasts form new bone matrix through the deposition of collagen and minerals. The remodeling cycle maintains bone strength and mineral homeostasis.
This document provides an overview of ossification, the process of bone formation. It discusses the classification of ossification into primary and secondary ossification, with the latter including intramembranous and endochondral ossification. The stages and factors involved in intramembranous and endochondral ossification are described in detail. Bone resorption, remodeling and the factors that influence these processes are also summarized.
The periodontium connects teeth to the jaws and includes the periodontal ligament, lamina propria, cementum, and alveolar bone. Cementum covers tooth roots and provides attachment for collagen fibers binding the tooth. The periodontal ligament contains collagen fibers connecting cementum to bone, along with blood vessels and cells that form and resorb bone and cementum. Alveolar bone has outer cortical and inner cancellous bone. Bone is composed of mineralized hydroxyapatite and collagen matrix, along with osteoblasts, osteoclasts, and osteocytes that form and resorb bone. The document discusses bone cell types and functions, bone development, remodeling, and disorders relevant to orthodontics such
Alvelor bone has several important functions including supporting tissues, providing muscle attachments, and storing ions like calcium. It has the ability to remodel according to functional demands. Alveolar bone development depends on the presence of teeth. Bone is classified as either endochondral or intramembranous bone developmentally, and as compact or cancellous bone histologically. The main cell types in bone are osteoblasts, osteocytes, bone lining cells, osteoprogenitor cells, and osteoclasts. Bone undergoes remodeling through the stages of resorption, reversal, formation, and resting. Microdamage signals bone remodeling through resorption and calcified matrix filling cracks. Clinical considerations for bone include resorption
This document discusses the basic structure and function of bones, including their cellular components and processes of development, homeostasis, and remodeling. It covers various bone diseases including congenital disorders (such as osteogenesis imperfecta and osteopetrosis), metabolic bone diseases (like osteoporosis and rickets/osteomalacia), hyperparathyroidism, Paget's disease, fractures, osteonecrosis, and osteomyelitis. The roles of osteoblasts, osteoclasts, and osteocytes in bone formation, resorption, and mechanotransduction are also summarized.
This document provides an overview of alveolar bone, including its development, histology, cellular components, and remodeling. It begins with a brief introduction to bone classification and composition. Key points include that alveolar bone forms via intramembranous ossification, and is composed of inorganic minerals and organic collagen fibers. It contains two main cell types - osteoblasts, which build bone, and osteoclasts, which resorb bone. Alveolar bone is continually modeled and remodeled throughout life to adapt to forces.
This document discusses metabolic bone diseases. It begins by describing the basic structure and function of bone, including its cellular components like osteoblasts and osteoclasts. It then discusses the constituents of bone matrix, including collagen, proteoglycans, and minerals. Bone development and homeostasis are explained, involving processes like remodeling. Specific metabolic bone diseases are then outlined in more detail, including osteogenesis imperfecta (brittle bone disease), osteomalacia/rickets due to abnormal mineralization, and hypophosphatasia due to a genetic disturbance in alkaline phosphatase synthesis. Throughout, the document provides microscopic and radiographic characteristics of these conditions.
The periodontal ligament is a complex connective tissue that connects teeth to the alveolar bone. It contains fibroblasts, cementoblasts, osteoblasts, osteoclasts and epithelial rests of Malassez. The fibroblasts are the predominant cells and produce collagen fibers that develop into principal fiber bundles. The periodontal ligament allows for adaptation during function by remodeling its collagen fibers and allows movement within the periodontal space. It develops from the dental follicle prior to tooth eruption and contains stem cells that can differentiate into cementoblasts, osteoblasts or fibroblasts.
ALVEOLAR BONE IN HEALTH AND DISEASE [Autosaved].pptHelipatel56
This document provides an overview of alveolar bone, including its:
1) Development from the dental follicle during tooth eruption and dependence on tooth size.
2) Anatomy consisting of alveolar bone proper with bundle bone and supporting alveolar bone with cortical and spongy bone.
3) Composition of inorganic hydroxyapatite and organic collagen fibers, along with cellular components like osteoblasts and osteoclasts that form and resorb bone.
Osteoporosis is a progressive systemic skeletal disease characterized by low bone mass and microarchitecture deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk.
- This document discusses mediators of bone loss, focusing on alveolar bone destruction in periodontal disease. It outlines the cellular mechanisms and local mediators involved in bone remodeling and resorption, including pro-inflammatory cytokines, prostaglandins, and RANKL.
- Diagnostic tools for detecting periodontal bone resorption are discussed, including indirect clinical measures like probing depth and radiographs, which have limitations. Systemic biochemical markers of bone resorption are mentioned as another potential diagnostic method.
- The key cellular players in bone remodeling - osteoblasts, osteoclasts, and osteocytes - are described. Homeostatic balance between bone formation and resorption is maintained through
Walmart Business+ and Spark Good for Nonprofits.pdfTechSoup
"Learn about all the ways Walmart supports nonprofit organizations.
You will hear from Liz Willett, the Head of Nonprofits, and hear about what Walmart is doing to help nonprofits, including Walmart Business and Spark Good. Walmart Business+ is a new offer for nonprofits that offers discounts and also streamlines nonprofits order and expense tracking, saving time and money.
The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
Special TechSoup offer for a free 180 days membership, and up to $150 in discounts on eligible orders.
Spark Good (walmart.com/sparkgood) is a charitable platform that enables nonprofits to receive donations directly from customers and associates.
Answers about how you can do more with Walmart!"
Temple of Asclepius in Thrace. Excavation resultsKrassimira Luka
The temple and the sanctuary around were dedicated to Asklepios Zmidrenus. This name has been known since 1875 when an inscription dedicated to him was discovered in Rome. The inscription is dated in 227 AD and was left by soldiers originating from the city of Philippopolis (modern Plovdiv).
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
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In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
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Chapter wise All Notes of First year Basic Civil Engineering.pptxDenish Jangid
Chapter wise All Notes of First year Basic Civil Engineering
Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
Linear Measurements: Instruments used. Linear Measurement by Tape, Ranging out Survey Lines and overcoming Obstructions; Measurements on sloping ground; Tape corrections, conventional symbols. Angular Measurements: Instruments used; Introduction to Compass Surveying, Bearings and Longitude & Latitude of a Line, Introduction to total station.
Levelling: Instrument used Object of levelling, Methods of levelling in brief, and Contour maps.
Chapter 4
Buildings: Selection of site for Buildings, Layout of Building Plan, Types of buildings, Plinth area, carpet area, floor space index, Introduction to building byelaws, concept of sun light & ventilation. Components of Buildings & their functions, Basic concept of R.C.C., Introduction to types of foundation
Chapter 5
Transportation: Introduction to Transportation Engineering; Traffic and Road Safety: Types and Characteristics of Various Modes of Transportation; Various Road Traffic Signs, Causes of Accidents and Road Safety Measures.
Chapter 6
Environmental Engineering: Environmental Pollution, Environmental Acts and Regulations, Functional Concepts of Ecology, Basics of Species, Biodiversity, Ecosystem, Hydrological Cycle; Chemical Cycles: Carbon, Nitrogen & Phosphorus; Energy Flow in Ecosystems.
Water Pollution: Water Quality standards, Introduction to Treatment & Disposal of Waste Water. Reuse and Saving of Water, Rain Water Harvesting. Solid Waste Management: Classification of Solid Waste, Collection, Transportation and Disposal of Solid. Recycling of Solid Waste: Energy Recovery, Sanitary Landfill, On-Site Sanitation. Air & Noise Pollution: Primary and Secondary air pollutants, Harmful effects of Air Pollution, Control of Air Pollution. . Noise Pollution Harmful Effects of noise pollution, control of noise pollution, Global warming & Climate Change, Ozone depletion, Greenhouse effect
Text Books:
1. Palancharmy, Basic Civil Engineering, McGraw Hill publishers.
2. Satheesh Gopi, Basic Civil Engineering, Pearson Publishers.
3. Ketki Rangwala Dalal, Essentials of Civil Engineering, Charotar Publishing House.
4. BCP, Surveying volume 1
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In this webinar, participants learned how to utilize Generative AI to streamline operations and elevate member engagement. Amazon Web Service experts provided a customer specific use cases and dived into low/no-code tools that are quick and easy to deploy through Amazon Web Service (AWS.)
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
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How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
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Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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3. •Bone formation and factors affecting bone formation
•Bone resorption
Differences between resorbed and unresorbed
surfaces
Role of TRAP in bone resorption
Factors affecting bone resorption
•Bone remodelling
Sequence of events
Mediators
Markers of bone turn over
•Conclusion
• References
5. CLASSIFICATION OF BONES:
Shape development histology
Long flat irregular endochondral Intramembranous sutural mature immature
compact cancellous
short
12. Composition of Bone…
Inorganic component:
Hydroxyapatite crystals with carbonate content
Organic component:
- Osteoid
Type I collagen (95%)
type V collagen (<5%)
Non collagenous proteins
Osteocalcin,
Osteopontin,
Bone sialoprotein,
Osteonectin.(SPARC)- Cell adhesion ,proliferation,
modulation of cytokine activity.
13. Osteoblasts :
Derived from osteoprogenitor cells
Periosteum serves as important reservoir .
Morphology :
basophilic
cuboidal or slightly elongated cells
contain prominent bundles of actin, myosin
BONE CELLS:
16. FUNCTIONS
New bone formation
Controls bone mineralization at 3 levels-
i. In its initial phase, by production of matrix vesicle.
ii. At a later stage, by controlling the ongoing process of
mineralization.
iii. By regulating the number of ions available.
Regulation of bone remodeling and mineral metabolism.
17. FUNCTIONS
Osteoblasts secrete type I collagen, small amount of
type V collagen, osteonectin, osteopontin, RANKL,
osteoprotegerin, Proteoglycans, latent proteases and
growth factors including bone morphogenic proteins.
Osteoblasts exhibit high levels of alkaline phosphatase -
cytochemical marker.
18. Vitamin D3:
Stimulates bone resorption.
essential for normal bone growth and mineralization
Stimulates osteopontin and osteocalcin – suppresses collagen
production
Growth hormone:
required for attaining normal bone mass - mediated by local
production of IGF-1.
Insulin:
stimulates bone matrix formation and mineralization
19. Bone morphogenic proteins :
TGF-β family
migration, aggregation and proliferation of mesenchymal
type cells and their differentiation in to osteogenic cells
Insulin growth factor I and II (IGF):
Effects similar to TGF-β
They also stimulate proliferation of osteoblast precursors
Fibroblast growth factor (FGF) :
increases proliferation of osteoprogenitor cells.
promotes osteogenic differentiation
20. BONE LINING CELLS:
Osteoblasts flatten, when bone is not forming and extend
along the bone surface and hence the name.
They are present on periosteal as well as endosteal
surfaces.
21. OSTEOCYTES:
Nerve cells
Sense the change in environment and send signals that affect
response of other cells involved in bone remodelling
Maintains balance between
resorption and remodelling
Bone that forms more rapidly
shows more osteocytes.
22. Osteocytic lacunae
Canaliculi- narrow extension of lacunae, permits
diffusion of gases and nutrients
Maintains bone integrity and vitality
Failure of inter connecting system between osteocytes
and osteoblasts leads to sclerosis and death of bone
23. OSTEOCLAST:
In Greek it means “ bone and broken ’’
Morphology
Howship’s lacunae
Diameter – 50-100 um
15 to 20 nuclei ( more nuclei more
resorption)
TRAP – distinguishes from other
multinucleated giant cells
24. MORPHOLOGY
Extensive mitochondria except below the ruffled border
Ruffled border – deep folds
Cathepsin containing vesicles and vacuoles are present
close to ruffled border – resorptive capacity
Clear or sealing zone
27. Cells of monocyte macrophage lineage differentiate into
osteoclast by cell to cell interaction
RANKL and M-CSF are produced by osteoblasts. These are
required for formation of osteoclasts
M-CSF – proliferation and differentiation. It acts through c-fms
present on osteoclasts
RANKL- differentiation in to matured osteoclast and their activity.
RANKL/ ODF / TRANCE( TNF related induced cytokine) /
OPGL
Formation of osteoclast
29. BONE FORMATION AND FACTORS AFFECTING BONE
FORMATION
Two theories have been put forward for how the bone is formed
and calcified.
1st theory:
Matrix vacuoles, which are produced as an outgrowth of
osteoblasts or chondroblasts or odontoblasts are responsible for
calcification.
2nd theory
Macromolecular constituents of bone and cartilage matrix
directly implicates in calcification
30. Factors regulating bone formation:
Platelet derived growth factor
Cationic heparin binding polypeptide
Collagen synthesis and rate of bone apposition
Acidic fibroblast growth factors and basic fibroblast
growth factor
Increases collagen synthesis
31. Insulin like growth factor
Increase preosteoblasts replication and stimulates collagen
synthesis
Transforming growth factor
TGF-α – resorption
TGF-β – formation
Bone morphogenetic proteins (BMPs)
during repair they are released and are required for healing
32. BONE RESORPTION:
Sequence of events of bone resorption: Involves 3 phases
First phase -
formation of osteoclast
Second phase-
activation of osteoclast
Third phase -
resorption of bone
33. Alterations in the osteoclast
Removal of hydroxyapatite
acidic environment by proton pump
Degradation of organic matrix
acid phosphatase, cathepsin B
Removal of degradation products from lacunae
endocytosis
Translocation of degraded products and extracellular release
34. Alterations in the osteoclast:
The osteoclasts create - Howship’s lacunae.
assumes polarity of structure and function.
The two distinct alterations are the
development of a ruffled border
sealing zone at the plasma membrane.
The cytoplasm adjacent to ruffled border is devoid of cell
organelles, contains actin microfilaments surrounded by vinculin
rings- clear zone.
When osteoclasts arrive at resorption site, they use the sealing
zone to attach themselves to the bone surface.
35.
36. Removal of hydroxyapatite:
The initial phase involves the dissolution of the mineral phase –
HCl
The protons for the acid arise from the activity of cytoplasmic
carbonic anhydrase II, which is synthesized in osteoclast.
The protons are then released across the ruffled border into the
resorption zone by an ATP consuming proton pump.
This leads to a fall in pH to 2.5 to 3.0 in the osteoclast resorption
space.
37. Degradation of organic matrix:
Proteolytic enzymes are synthesized by osteoclasts- cathepsin
k and MMP-9.
cathepsin k is the most important enzyme in bone. It degrades
major amount of type I collagen and other non collagen proteins
MMP-9(collagenase B) - osteoclast migration.
MMP-13 -bone resorption and osteoclast differentiation.
38. Removal of degradation products from lacunae:
Once liberated from bone, the free organic and non organic
particles of bone matrix are taken in or endocytosed from
resorption lacunae, across the ruffled border, into the osteoclast.
These are then packed into membrane bound vesicles within
cytoplasm of osteoclast.
These vesicles and their contents pass across the cell and fuse
with functional secretory domain (FSD) a specialized region of
the basement membrane.
Then the vesicles are released by exocytosis.
39. Factors associated with mechanism of bone Resorption:
Interleukin 1 – IL-1α, IL-1β. It stimulates production and release of
prostaglandin PGE2
Interleukin-6 (IL-6)
Tumor necrosis factor
lymphotoxin
Gamma interferon – inhibits resorption
Colony stimulating factors
Prostaglandins and other arachidonic acid metabolites
40. Role of trap in bone resorption:
Synthesized as inactive pro enzyme
Bone resorption inside and outside the cell
Concentration of TRAP in serum can be assessed which
indicates resorption day by day basis
41. BONE REMODELLING
The process by which overall size and shape of bone is
established- bone modelling.
Embryo to pre-adult period.
Rapidly formed on periosteal surface simultaneous destruction
on endosteal surface at focal points and with in the osteon.
Bone formation greater than resorption.
Bone turnover or remodelling – replacement of old bone by new
bone.
42. As age increases resorption exceeds
Cortical bone turnover-5% per year
Trabecular and endosteal surface – 15% per year
Coupling
The processes of bone synthesis and bone breakdown go on
simultaneously and the status of the bone represents the net result
of a balance between the two processes. This phenomenon is
called coupling.
43. Hormones and coupling
With the exception of calcitonin, all the hormones, cytokines, and
growth factors that act on bone, as an organ, mediate their activity
through osteoblasts.
Resorbing hormones act directly on osteoblasts, which then
produce other factors that regulate osteoclast activity.
This results in both bone formation and bone resorption being
coupled.
44. The coupling theory is based on the observation that once
resorption occurs, osteoblasts respond by making bone matrix.
That is, any change in resorption or formation results in
change in the other.
A hypothetical mechanism for explaining the coupling
phenomenon is that resorbing bone produces a factor that
influence the rate or extent of osteoblastic activity.
45. Functions of remodelling
To prevent accumulation of damaged bone by regenerating
new bone.
Allowing to respond to the changes in mechanical forces.
Mineral homeostasis.
46. •First the osteoclasts tunnel into surface of bone, which lasts for 3
weeks- resorb the haversian lamellae, and form a resorption
tunnel or cutting cone.
•After sometime resorption ceases and osteoclasts are replaced by
osteoblasts. These osteoblasts lay down a new set of haversian
lamellae, encircling a vessel upon a reversal line.
•This cement line is a thin layer of glycoproteins comprising bone
sialoprotein and osteopontin that acts as a cohesive mineralized
layer between the old bone and new bone to be secreted.
47. •The entire area of osteon, where active formation occurs is
termed the filling cone.
•The osteoblasts get entrapped in new bone and are called
osteocytes. Fragments of lamellae from old bone haversian
systems are left behind as interstitial lamellae
49. MEDIATORS OF BONE REMODELLING:
Parathyroid hormone
Calcitonin
Vitamin D metabolites i.e., 1, 25-dihydroxycholecalciferol
Cytokines
Prostaglandins
Growth factors
Mechanical factors
Bacterial products.
50. MARKERS OF BONE TURNOVER:
The markers of bone formation are: (serum markers)
•Alkaline phosphatase (total)
•Alkaline phosphatase (skeletal isoenzymes)
•Osteocalcin
•Procollagen I extension peptide
51. The markers of bone resorption are: (urinary markers)
•Urine calcium
•Urine hydroxy proline
•Collagen cross linking fragments
•Urine N – telopeptide
•Urine C- telopeptide
•Urine total pyridinoline
•Urine free deoxypyridinoline
52. Serum markers of bone resorption:
•Serum TRAP
•Serum β2 macroglobulin
Pathologies caused due to improper control of remodelling are:
•Osteoporosis
•Osteopetrosis
•Malignant bone tumors
•Inflammatory joint diseases
53. CONCLUSION :
The response of bone to inflammation includes bone
formation as well as resorption. Thus bone loss in disease is not
simply a destructive process, but results from the predominance
of resorption over formation
Proper understanding of changes seen in the bone in
variety of diseases will help in finding new therapeutic
strategies
54. REFERENCES:
•Carranza’s clinical periodontology-10th edition
•Lindhe – Textbook of periodontology-5th edition
•Orban’s oral histology & embryology-13th edition
•Tencate oral histology-8th edition
•Fundamentals of Periodontics.- Thomas G. Wilson, Kenneth S. Kornman
-2nd Edition
•Biology of periodontal tissues. P. Mark Bartold and A.SampathNarayanan-1st
edition
•Periodontology 2000, Vol. 24, 2000, 99-126