This document discusses several types of primary bone tumors. It begins with an introduction to the classification of bone tumors based on histologic criteria. It then discusses several benign bone tumors in more detail, including chondroma, osteoma, osteoid osteoma, benign osteoblastoma, and osteochondroma. For malignant tumors, it focuses on explaining osteosarcoma, including its etiology, classification, and characteristics. It provides histologic images and descriptions of the key features of many of these tumors. In summary, the document provides an overview of the classification and characteristics of both benign and malignant primary bone tumors.
Identified in 1921 by James Ewing
2nd most common bone tumor in children
Ewing’s Sarcoma Family of tumors:
Ewing’s sarcoma (Bone –87%)
Extraosseous Ewing’s sarcoma (8%)
Peripheral PNET(5%)
Askin’s tumor
Identified in 1921 by James Ewing
2nd most common bone tumor in children
Ewing’s Sarcoma Family of tumors:
Ewing’s sarcoma (Bone –87%)
Extraosseous Ewing’s sarcoma (8%)
Peripheral PNET(5%)
Askin’s tumor
Feature Extraction Techniques and Classification Algorithms for EEG Signals t...Editor IJCATR
EEG (Electroencephalogram) signal is a neuro signal which is generated due the different electrical activities in the brain.
Different types of electrical activities correspond to different states of the brain. Every physical activity of a person is due to some
activity in the brain which in turn generates an electrical signal. These signals can be captured and processed to get the useful information
that can be used in early detection of some mental diseases. This paper focus on the usefulness of EGG signal in detecting the human
stress levels. It also includes the comparison of various preprocessing algorithms ( DCT and DWT.) and various classification algorithms
(LDA, Naive Bayes and ANN.). The paper proposes a system which will process the EEG signal and by applying the combination of
classifiers, will detect the human stress levels.
Presentation on bone tumors for undergraduate 2nd year MBBS medical students. The information for this presentation has been taken from texbook of Robbins & Cotran Pathologic Basis of Disease 8th ed.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
3. Introduction
• Primary bone tumors are rare;
• Non-neoplastic conditions, metastatic disease, and
lymphohematologic malignancies, which may simulate
primary bone tumors, by far outnumber genuine bone tumors.
4. • The classification of bone tumor is based on histologic criteria,
particularly on the type of differentiation shown by tumor cells
and the type of intercellular material they produce, as seen by
conventional light microscopy.
• However, it is recognized that electron microscopy and especially
immunohistochemical techniques may be relevant for precise
classification and diagnosis in specific instances.
5. • The final diagnosis of bone tumors should be based on a
synthesis of histopathologic findings, clinical presentation,
and imaging characteristics.
6. Predominant tissue Benign Malignant
Bone forming Osteoma
Osteoid osteoma and
osteoblastoma
Osteosarcoma
-central
-peripheral
-parosteal
Cartilage forming Chondroma
Osteochondroma
Chondroblastoma
Chondromyxoid
fibroma
Chondrosarcoma
-Juxtacortical chondrosarcoma
-Mesenchymal chondrosarcoma
-Dedifferentiated chondrosarcoma
-Clear cell chondrosarcoma
-Malignant chondroblastoma
Marrow tumors -Ewing sarcoma
-Primitive neuroectodermal tumor of
bone (PNET)
-Malignant lymphoma of bone
-Myeloma
WHO Histologic Classification of Bone Tumors 1993
7. Chondroma
• A benign central tumor composed of mature cartilage, is a well-
recognized entity in certain areas of the bony skeleton
• Considerable clinical importance because of the propensity of the
tumor to undergo malignant degeneration in some instances, even
after remaining quiescent for long periods of time.
• Types: A) Central chondroma / Enchondroma- develop within
medullary cavity
• B) Periosteal chondroma / Ecchondroma - develops on the surface
• C) Soft tissue chondroma.
8. Clinical feature
• Develop at any age and
• Shows no apparent gender predilection
• Site: maxilla: anterior portion of the maxilla
mandible: posterior to the cuspid tooth, involving the
body of the mandible, the coronoid or condylar processes.
• c/p: arises as a painless, slowly progressive swelling of the
jaw, may cause loosening of the teeth
10. Histological Features
• Chondroma is made up of a mass of hyaline cartilage which
may exhibit areas of calcification or of necrosis.
• The cartilage cells appear small, contain only single nuclei and
do not exhibit great variation in size, shape or staining reaction.
• vary considerably in appearance from area to area.
11. A, Chondroma. Strands of epithelium-like cells with abundant eosinophilic cytoplasm
reside in a blue-gray mucinous stroma. B, Area of chondroma with tumor cells showing
cytoplasmic vacuolation with the formation of multivacuolated physaliferous cells.
12. A, Enchondroma shows small, uniform chondrocytes whose nuclei are densely
hyperchromatic (ink dot) without a visible chromatin pattern. Cells are well separated from
each other. B, An island of hyaline cartilage in an enchondroma is separated from the
adjacent bone trabeculae by a zone of normal marrow tissue
13. Osteoma
• Osteoma is a benign neoplasm characterized by a
proliferation of either compact or cancellous bone,
usually in an endosteal or periosteal location.
• Described as a specific entity by Jaffe in 1935
• Occurs almost exclusively in the head and neck region
• Not a common oral lesion.
14. Types:
Compact osteoma: consists of compact bone, which has a dense
lamellae of bone
Cancellous osteoma: consisting of trabeculae of bone
Periosteal, peripheral or exophytic osteoma: arise on the
surface of bone as sessile mass
Endosteal or central osteoma: located in the medullary bone
Osteoma cutis: extraskeletal lesion of soft tissue seen in the
dermis of the skin
15. Clinical features
• Age: second to fourth decades of life,
• males> female
• c/p: slow growing tumor.
• Periosteal origin → circumscribed swelling → obvious asymmetry.
• Endosteal origin → expansion of the cortical plates.
• Multiple osteomas of the jaws, as well as of long bones and skull,
are a characteristic manifestation of Gardner syndrome.
16. GARDNER SYNDROME
• It is an autosomal dominant disorder.
• Mutation in APC gene
• characterized by the triad of colonic polyposis, multiple
osteomas and mesenchymal tumors of the skin and soft tissues
including epidermal inclusion cyst, lipoma, fibroma, and
fibromatosis
17. Oral manifestations
• Multiple odontomas, Compound odontomas
• Supernumerary teeth
• Impacted permanent teeth
• One or more osteomas of the jaws
• Occult radiopaque lesions of the jaws are common
• Various incidental findings include hypercementosis, root
resorption, ankylosis and persistent primary teeth.
18.
19. Histologic Features.
• Composed either of extremely dense, compact bone or of
coarse cancellous bone.
• Bone formed appears normal
• Well circumscribed.
• In some tumors foci of cartilage may be found, in which
case the term ‘osteochondroma’ is often used.
• Myxomatous tissue also may be intermingled on rare
occasions.
20. Compact and trabecular bone is present beneath intact mucosa at the left of the field.
B, Compact cortical-type bone of the osteoma shown in A contains haversian systems
21. Treatment and Prognosis
• Symptomatic lesions→ local excision.
• No recurrence after surgical removal.
22. Osteoid osteoma
• Benign tumor of bone, seldom been described in the jaws.
Etiology:
• True nature → unknown.
• Jaffe and Lichtenstein have suggested “A true neoplasm of
osteoblastic derivation”.
• Trauma
• Inflammation
24. Clinical Features.
• Age: young persons, under the age of 10 years
• Sex: males:female - 2:1.
• Site: Frequently in the femur or in the tibia.
• In head and neck→ Cervical spine > mandible and maxilla.
• Chief symptoms → severe pain → unrelenting and sharp, worse at
night.
• Classically, the pain is relieved by aspirin.
25.
26. Pathologic Features
• In its active growth phase
considerable vascularity.
• Grossly appears as a discrete, round to oval lesion marked by a
cherry-red or reddish-brown color. Quite granular and friable and
easily displaced from the adjacent bone.
• In its mature phase → more calcification and bone production, the
lesion is hard and gritty and blends with the bone around it.
27. Histologic Features
• Characteristic and consists of a central nidus composed of compact
osteoid tissue, varying in degree of calcification, interspersed by a
vascular connective tissue.
• Formation of definite trabeculae occurs, particularly in older
lesions, outlined by active osteoblasts.
• Osteoclasts and foci of bone resorption are also usually evident.
• Overlying periosteum exhibits new bone formation, and in this
interstitial tissue collections of lymphocytes seen.
28. A, Nidus of osteoid osteoma abuts thickened mature bone. B, Osteoid trabeculae, some
partially calcified, within the nidus of an osteoid osteoma. The trabeculae are rimmed with
plump osteoblasts with occasional osteoclasts. The stroma is hemorrhagic.
29. Ultrastructural investigation by Steiner,
• The morphology of the osteoblasts to be similar to that of
normal osteoblasts.
• Although atypical mitochondria could be seen.
• Neural staining → many axons throughout an osteoid osteoma,
which probably accounts for the pain (the nidus).
• ↑Levels of prostaglandin E2 in the nidus; this is presumably
the cause of pain and vasodilatation.
32. Benign Osteoblastoma
(Giant osteoid osteoma)
• Osteoblastoma accounts →1% of primary bone tumors.
• It is typically a slow-growing, benign bone tumor.
• Incidence in the head and neck → 13% to 26%.
• Osteoblastoma frequently lacks the characteristic pain and the
halo of sclerotic bone associated with osteoid osteoma.
• Benign osteoblastoma → Jaffe and by Lichtenstein in 1956.
33. Etiopathogenesis
• Jaffe and Lichtenstein stated this lesion to be “a true neoplasm
of osteoblastic derivation”.
• Trauma,
• Inflammation,
• Abnormal local response of the tissues to injury, and
• Local alteration in bone physiology
34. Clinical Features
• Age: in young persons, 20-30 years.
• Sex: Males>Females.
• C/P: characterized clinically by pain and swelling.
pain → more generalized and less likely relieved by salicylates.
• Most common site → vertebral column.
• Mandible > Maxilla
• Occurs in Periosteal, cortical, or medullary location
35.
36. Pathologic Features.
On gross examination,
• Well delimited within either the cortex
or cancellous bone.
• Hemorrhagic
• Gritty or granular consistency with
cystic regions.
37. Histologic Features
The hallmark of the benign osteoblastoma consists of:
The vascularity of the lesion with many dilated capillaries
scattered throughout the tissue
The moderate numbers of multinucleated giant cells scattered
throughout the tissue, and
The actively proliferating osteoblasts which pave the
irregular trabeculae of new bone
It may or may not have a central sclerotic nidus
38. • In the less mature lesion → abundance of connective tissue
stroma in which osteoclast-type giant cells and small foci of
osteoid are present, some in a lacelike pattern.
• With maturation → progressive mineralization of the osteoid
with conversion to trabeculae of coarse woven bone, rimmed by
plump osteoblasts. The trabeculae may fuse to form an
anastomosing, netlike pattern.
• The osteoblasts usually lack any significant atypia, having
round to oval regular nuclei, often with prominent nucleoli.
Mitotic activity is infrequent.
• The combination of bone production and resorption → pagetoid
- appearing bone with prominent cement lines
39. A, Nidus of osteoblastoma shows active production of osteoid trabeculae, some in the early stage
of bone formation. The trabeculae are lined with enlarged osteoblasts with occasional osteoclasts.
Numerous dilated capillaries are present in the stroma. B, Large epithelioid osteoblasts, in
osteoblastoma, have abundant cytoplasm and large nuclei containing prominent nucleoli.
Formation of lacelike osteoid is seen.
41. irregular or mosaic-like reversal lines
indicative of active remodeling similar to
that seen in Paget disease
Tumor trabeculae frequently
connect with the surrounding bone
44. Aggressive Osteoblastoma
It is primarily defined by epithelioid osteoblasts,
cells with abundant eosinophilic cytoplasm twice
the size of conventional osteoblasts. These cells
are frequently arranged in sheets with little or no
intervening osteoid
Cytologically, the neoplastic osteoblasts have
abundant basophilic, finely granular cytoplasm
with a perinuclear holo of less dense cytoplasm
and an eccentric vesicular nucleus with a solitary
prominent nucleolus
47. OSTEOCHONDROMA
• Osteochondroma or solitary osteo-cartilaginous exostosis is an
exophytic lesion that arises from the cortex of bone and is capped
with cartilage.
• 35%-50% of all benign bone tumors
• 8%-15% of all primary bone tumors
• Occurs frequently in the metaphyseal region of the long bones
• Osteochondroma can eventually transform into a secondary peripheral
chondrosarcoma in 1–3% of patients with multiple osteochondromas.
48. Etiology:
• Different theories of etiopathogenesis proposed:
Developmental,
Reparative, and
Traumatic
Radiation-induced osteochondroma
Stress
49. Clinical features
• Age- 13-78 years, mean age- 38.4 years
• Sex: females> males
• Site: coronoid process and the mandibular condyle are the affected.
Especially the medial aspect of the mandibular condyle.
• slow growing.
Clinical presentation:
• facial asymmetry, malocclusion, cross-bite on contra-lateral side
and lateral open-bite on the affected side, deviation on opening,
hypomobility, pain and clicking
50.
51. A, Peripheral portion of osteochondroma shows a cartilage cap covered by a layer of
periosteum (perichondrium). Active enchondral ossification is present, with widely dilated
capillaries present at the base of the cartilage. The marrow is filled with fat. B, Bone within
osteochondroma shows persistence of partially ossified hyaline cartilage within the centers of
the trabeculae.
53. OSTEOSARCOMA / OSTEOGENIC SARCOMA
• Osteosarcoma is the third most common cancer in
adolescence, occurring less frequently than only
lymphomas and brain tumors.
• It is thought to arise from a primitive mesenchymal bone-
forming cell and is characterized by production of osteoid
54. Etiology
• Irradiation : 2% of osteosarcomas.
• pre-existing benign bone disorders –
bone dysplasia, fibrous dysplasia, Pagets disease
• Trauma
• Disturbance of bone growth and maturation -
corresponds with growth spurt
55. • Environmental factors:
Ultraviolet and ionising radiation
Viral origin: simian virus 40 (SV40)
• Transcription Factors
Excess production of transcription factors, or the production of a
new overactive transcription factor, may result from gene
rearrangement.
Overexpression of Myc
• Growth Factor
Dysregulated expression of growth factors such as TGF, IGF, and
CTGF leads to the accelerated proliferation of cells.
56. • Genetic predisposition
Alterations in genetic pathways including Rb, p53, SAS (sarcoma
amplified sequence)
Protein expression of the defective/amplified genes results in loss of
control of cell proliferation and differentiation
• Syndromes – Li-Fraumeni syndrome
- Rothmund-Thompson syndrome
57. Classification of osteosarcoma
Primary osteosarcomas
• Conventional-sub-typed as:
Osteoblastic (50%)
Chondroblastic (25%)
Fibroblastic (25%)
• Small cell
• Telangiectatic
• Intraosseous well differentiated and Intracortical
• Surface osteosarcomas:-Parosteal, Periosteal, High grade surface
58. • Secondary osteosarcomas
Paget’s disease and after radiation exposure.
• Unusual forms of osteosarcoma subtypes of conventional
osteosarcoma because their biological behavior is similar.
Osteoblastic osteosarcoma-sclerosing type
Osteosarcoma resembling osteoblastoma
Chondromyxoid fibroma-like osteosarcoma
Chondroblastoma-like osteosarcoma
Clear-cell osteosarcoma
Malignant fibrous histiocytoma-like osteosarcoma
Giant cell rich osteosarcoma
59. Clinical features
• Sex- M>F
• Age – 3rd and 4th decade
• Site - metaphysial growth plates of extremities of long bones
• femur>tibia>humerus>skull or jaw>pelvis
• Mandible : Maxilla = 1.5:1
• Mandible: body of the mandible > symphysis > angle of the
mandible > ascending ramus >TMJ.
61. • By their site of origin:
the conventional type - arising within the medullary cavity
juxtacortical tumors - arising from the periosteal surface
extraskeletal osteosarcomas - rare.
64. Gross pathology
• Osteoblastic - white-tan, yellow in color, firm in consistency
• Chondroblastic - translucent lobules
• Fibroblastic - tan colored with soft or firm in consistency
65. Histological features
• Presence of osteoid formation by malignant osteoblasts
• Stromal cells are spindle shaped and atypical with
irregularly shaped nuclei
• The amount of matrix material produced in the tumor
varies considerably.
• Mitotic activity with frequent abnormal forms
66. • Depending on the relative amounts of osteoid, cartilage.
or collagen fibers produced by the tumor.
Osteoblastic
Chondroblastic
Fibroblastic
67. Osteoblastic type
• Atypical neoplastic osteoblasts that exhibit variation in size and shape
• large deeply staining nuclei arranged in disordered fashion about
trabaculae of bone .
• Irregular pattern or solid sheets of new tumor osteoid and bone
formation.
68. • Fibroblastic type- varying degrees of proliferation of anaplastic
fibroblasts, absence of tumor osteoid.
• Occasional areas of neoplastic myxomatous tissue and cartilage.
• Comprised about 34%
69. • Chondroblastic- currently believe that even though a lesion is
composed chiefly of malignant cartilage, it should be diagnosed
as osteosarcoma, if significant malignant osteoblasts and tumor
osteoid or bone can be identified since the course of the lesion
will probably be that of an osteosarcoma rather than of a
chondrosarcoma
70. Lacelike streamers of pink osteoid
produced by malignant stromal cells
(osteoblasts).
Area in a conventional
osteosarcoma shows a combination
of osteoid, malignant cartilage, and
spindle cell fibrous zones
71. Telangiectatic osteosarcoma resemble an
aneurysmal bone cyst. Blood filled cystic
spaces are separated by delicate septa.
Benign giant cells resembling osteoclasts
are seen in about 25% of osteosarcomas.
77. Treatment
• Long bone involvement→ amputation is a prime requisite.
• Radical resection
• Primary X-ray radiation is of no avail.
• Preoperative chemotherapy →facilitate subsequent surgical removal
by shrinking the tumor.
• Adjuvant chemotherapy in combination with surgery, including
resection of pulmonary metastases, has appeared to offer promise of
increased survival from this disease
• Overall 5 years survival – 63%
78. CHONDROSARCOMA
• Chondrosarcoma is a malignant tumor characterized by the
formation of cartilage.
• Comprise about 10% of all primary tumors
• 1 % to 3% arise in the head and neck area.
Types:
• Primary: arise directly from the cartilage
• Secondary: develop in a pre-existing benign cartilaginous tumor.
79. Clinical features
• Age: 6th- 7th decade
• No significant sex predilection
• Site: In head and neck→ maxilla, mandible, base of the skull,
cervical vertebrae, nasal cavity and nasal septum.
• c/p: painless mass or swelling, loosening of teeth.
• Maxillary tumors may cause nasal obstruction, congestion ,
epistaxis, photophobia, or visual loss.
80.
81. Gross examination
• On sectioning→ lobular, blue-gray to gray-white, translucent,
glistening surface, although firm, they are usually easily cut with a
scalpel, except for areas with dense calcification or ossification.
• Necrosis within the center of the lobules is common.
82. Histopathologic Features
• Chondrosarcomas are composed of cartilage showing varying degrees
of maturation and cellularitywith typical lacunar formation.
• Lobular growth pattern, with tumor lobules separated by thin fibrous
connective tissue septa.
• Central areas of the lobules →greatest degree of maturation.
• Peripheral areas → immature cartilage & round or spindle shaped cells.
• Neoplastic cartilage may be replaced by bone in a manner similar to
normal endochondral ossification.
83. • Grade I chondrosarcomas closely mimic the appearance of a
chondroma, composed of chondroid matrix and chondroblasts
• Large, plump chondroblasts and binucleated chondrocytes seen.
• Calcification or ossification prominent, and mitoses are rare.
• Grade II chondrosarcomas show a greater proportion of
moderately sized nuclei and increased cellularity. More myxoid
with a less prominent hyaline matrix.
• Grade III chondrosarcomas are highly cellular and may show a
prominent spindle cell proliferation. Mitoses may be prominent .
84. Low-grade chondrosarcoma. The tumor cells
are larger than normal chondrocytes, with
larger, open-faced nuclei that have a uniform,
fine chromatin pattern. Several mitotic figures
are present, an uncommon finding in most
chondrosarcomas
High-grade chondrosarcoma. Hypercellular
tumor contains pleomorphic cells, some with
large, bizarre nuclei. A few cells are spindle
shaped
86. infiltration between existing normal bone,
resulting in trabeculae that are closely
abutted and surrounded by tumor.
Mesenchymal chondrosarcoma. showing
sheets of small basophilic cells with
focal areas of cartilaginous
differentiation (right).
87. A, myxoid chondrosarcoma. Tumor cells are more closely arranged at the periphery of
the lobules. B, Radial, cordlike arrangement of tumor cells in myxoid chondrosarcoma.
Cells are embedded in grayish myxoid stroma
90. Treatment and Prognosis
• Prognosis in chondrosarcoma depends primarily on the
ability to adequately excise the tumor
• Radical surgical excision.
• Radiation and chemotherapy are less effective
• 5-year survival rate →43% to 95%
91. Primitive neuroectodermal tumor (PNET)
• Term used to describe a category of neoplasm of neuroectodermal origin
with variable cell differentiation.
• “small round cell tumors of childhood”
Divided into two categories
• Group (I) tumors→ pituitary adenomas and carcinoid tumors, represent
tumors that show predominantly epithelial differentiation.
• Group (II) tumors→ Olfactory neuroblastoma, Malignant melanoma,
Ewing’s sarcoma (EWS) display features that are predominantly
neural and non-epithelial in origin
92. EWINGS SARCOMA
• Ewing’s sarcoma is a sarcoma of the bone, classically
described under small round cell tumors.
• uncommonly involve the head and neck
• Incidence →1-3 cases per million of population per year.
• Skull tumors constitute about 2% of tumors.
• James Ewing (1866–1943) first described the tumor
94. Pathogenesis
• Trauma
• Balanced t(11:22) (q24;q12) chromosomal translocation- 85%
• EWS-FLI1 → central player in the pathogenesis of ES
• Overexpression of CD99
• Dysregulated signaling of receptor tyrosine kinase.
• Altered pathways of RB and p53
95. Some of the potential molecular targets of Ewing’s sarcoma described in this review
include: (a) EWS-FLI1 fusion protein, (b) its target genes, (c) growth factor receptor, cell-
surface receptors and (d) molecules involved in cell survival, proliferation and anti-
apoptotic pathways
96. Clinical Features
• Age: children and young adults, 5-25 years,
• Male: female= 2:1
• uncommon in blacks.
• Site: long bones of the extremities,
In head and neck region,
It involves skull, clavicle, maxilla and mandible.
Mandible ˃ maxilla.
97. • Earliest sign: Pain, usually of an intermittent nature, and
Swelling of the involved bone
• Facial neuralgia and lip paresthesia
• Jaw swelling
• Ulcerated intraoral mass
• Low -grade fever
• Elevated white blood cell count
• Extraskeletal form- Ewing’s Sarcoma of soft tissue.
99. Histologic Features
• Extremely cellular neoplasm composed of solid sheets or masses
of small round cells with very little stroma.
• Cells are small and round, with scanty cytoplasm and relatively
large round or ovoid nuclei with dispersed chromatin and
hyperchromasia.
• Cell borders are indistinct.
100. • Mitotic figures are common.
• Cells are positive for glycogen and are diastase resistant
• Geographic necrosis with perivascular sparing
• Hemorrhage
many mitotic figures in the field
101. A, A lobular arrangement of primitive round cells with cytoplasmic clearing in
Ewing’s sarcoma/primitive neuroectodermal tumor. B, The cells of Ewing’s
sarcoma/primitive neuroectodermal tumor are usually uniform and small with
finely dispersed chromatin and small nucleoli.
104. Treatment and Prognosis
• Chemotherapy
• Radiation therapy
• Surgery
• Five-year survival with a combination of surgery and
chemotherapy is 74%.
105. Multiple Myeloma
• Most common primary neoplasm of the skeletal system.
• Malignancy of plasma cells.
• Plasma cells are a subset of B-cells, which are the producers
of humoral immunity factors termed antibodies.
• Underlying pathology → Expansion of a single line of plasma
cells that replace normal bone marrow and produce
monoclonal immunoglobulins.
• Diffuse disease of the bone marrow.
108. • Frequent aberrations of chromosomes 1 and 14
• Other chromosomal abnormalities include 6q-, 7q-, 5q-
• Abnormal expression of the bcl-2 protein
• Mutations of the ras oncogene and p53 gene mutations
• Interleukin-6 (IL-6), considered the most important
myeloma growth factor
109. Clinical features
• Age: 60-65 years
• Sex: males> females
• More common among black people
• Site: mandible> maxilla
• Number of lytic foci or diffuse demineralization.
• Anemia, azotemia, hypercalcemia, recurrent infection.
• Extramedullary plasmacytoma- tonsils, nasopharynx, or
paranasal sinuses
110.
111. Macroglobulinemia.
• Macroglobulinemia is a proliferation of plasmacytoid
lymphocytes secreting an IgM-protein.
• Patients often have lymphadenopathy and hepatosplenomegaly,
• Bony lesions are uncommon.
112.
113. Histologic Features
• Composed of sheets of closely packed cells resembling
plasma cells → round or ovoid cells with eccentrically
placed nuclei exhibiting chromatin clumping in a
‘cartwheel’ or ‘checkerboard’ pattern
• Two nuclei within a single cell membrane are seen
• Perinuclear halo may be present.
• Russell bodies are common
114. Ultrastructurally,
• Numerous mitochondria in a perinuclear distribution as
well as prominent Golgi complexes.
• Golgi complexes are most likely responsible for the
perinuclear halo which is observed by light microscopy.
(Chen)
115.
116. Laboratory Features
• Hyperglobulinemia (monoclonal gammopathy)
• Hypercalcemia
• Hyperuricemia
• ↑ESR level
• Bence Jones protein in the urine → 60–85%
• Unusual protein which coagulates when the urine is heated to
40°–60° C and then disappears when the urine is boiled. It
reappears as urine is cooled.
117. Treatment and Prognosis.
• Bisphosphonate therapy → reduction of osteoclastic
activity and bone mineralization maintenance.
• Chemotherapy
• Extramedullary plasmacytoma → radiation therapy
• Infection, anemia and kidney failure are the most
common immediate causes of death
118. CONCLUSION
• The possibility for the pathologist to correctly diagnose a bone
tumor depends to a large extent on the completeness of the
clinical and imaging information provided.
• Care of the patient requires a multidisciplinary approach
Pathologist
Radiologist
Orthopedic surgeon
Medical oncologist
Radiation oncologist
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