Epithelial mesenchymal interactions (EMIs) are a series of programmed, sequential and reciprocal (complex and multiphase) communications between the epithelium and the mesenchyme with its heterotypic cell population, that result in the differentiation of one or both cell populations.
Odontogenesis is the process of tooth development, which involves both ectodermal and mesenchymal components, being the key elements in the development of teeth.
In order for the tooth to form, an interactive mechanism between these heterotypic cellular populations is required.
For these interactions to occur there should be some or other form of messenger system between epithelium and mesenchyme, further underlining the importance of cell signaling networks and intricacies of physiological growth of an individual.
In the process of embryonic development the ectoderm is composed of surface ectoderm, neural crest and neural tube.
The presentation discusses about tooth enamel in detail including its formation, characteristics, structure and histological features along with its clinical considerations. It is well supported with diagrams for better understanding of the text.
Suggestions and feedback will be well appreciated.
The presentation discusses about tooth enamel in detail including its formation, characteristics, structure and histological features along with its clinical considerations. It is well supported with diagrams for better understanding of the text.
Suggestions and feedback will be well appreciated.
A Complete presentation explaining the complete morphology of Maxillary first molar, for the benefit of people like me who tried and failed to find everything in one package
It is a presentation in detail about the strongest structure of the oral cavity "ENAMEL". It is a simple topic but people find it difficult to learn about it. I hope my presentation is a simple method to learn about it. I would like to thank my professors for assign me this project and i learn't a lot from it and still learning my basics daily.
PHYSICAL PROPERTIES
CHEMICAL PROPERTIES
STRUCTURE OF ENAMEL
DEVELOPMENT OF ENAMEL
EPITHELIAL ENAMEL ORGAN
AMELOGENESIS
LIFE CYCLE OF AMELOBLASTS
AGE CHANGES IN ENAMEL
DEFECTS OF AMELOGENESIS
CLINICAL IMPLICATIONS
I prepared this presentation during the first year of my MDS. This will give you a basic idea and necessary information about the pulp of the teeth and its histology. Hope you guys find it useful.
A Complete presentation explaining the complete morphology of Maxillary first molar, for the benefit of people like me who tried and failed to find everything in one package
It is a presentation in detail about the strongest structure of the oral cavity "ENAMEL". It is a simple topic but people find it difficult to learn about it. I hope my presentation is a simple method to learn about it. I would like to thank my professors for assign me this project and i learn't a lot from it and still learning my basics daily.
PHYSICAL PROPERTIES
CHEMICAL PROPERTIES
STRUCTURE OF ENAMEL
DEVELOPMENT OF ENAMEL
EPITHELIAL ENAMEL ORGAN
AMELOGENESIS
LIFE CYCLE OF AMELOBLASTS
AGE CHANGES IN ENAMEL
DEFECTS OF AMELOGENESIS
CLINICAL IMPLICATIONS
I prepared this presentation during the first year of my MDS. This will give you a basic idea and necessary information about the pulp of the teeth and its histology. Hope you guys find it useful.
Genetics in Tooth Development
Introduction
The Molecular Program of Tooth Development
Primary Epithelial Band
Dental Lamina
Vestibular Lamina
Initiation of the Tooth
Genes expressed during tooth development
Developmental signals controlling the position and the number of tooth germs along the oral surface
Homeobox code model
Instructive Signals for Patterning
Tooth Type Determination
Regionalization of Oral and Dental Ectoderm
Bud Stage
Bud-to-Cap Transition
Signaling centres
Applied aspects
Tooth development proceeds with reciprocal inductive interactions between stomadeum ectoderm and underlying ectomesenchymal cells in a strictly controlled temporal and spatial order.
Well studied at the molecular biologic level, over 300 genes and 100 growth and differentiation factors are implicated in the control of cellular differentiation and crosstalk in dental development that result in structures containing combination of mineralized tissues (enamel, dentine, cementum), soft connective tissues (dental pulp, periodontal ligament), blood vessels, nerves and lymphatics.
Tooth development proceeds with reciprocal inductive interactions between stomadeum ectoderm and underlying ectomesenchymal cells in a strictly controlled temporal and spatial order.
Well studied at the molecular biologic level, over 300 genes and 100 growth and differentiation factors are implicated in the control of cellular differentiation and crosstalk in dental development that result in structures containing combination of mineralized tissues (enamel, dentine, cementum), soft connective tissues (dental pulp, periodontal ligament), blood vessels, nerves and lymphatics
Epithelial-Mesenchymal Transition: At the Crossroads of Development and Tumor...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.for more details please visit
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Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.
Dental anomalies are caused by complex multifactorial interactions between genetic, epigenetic and environmental factors during the long process of dental development.
This process is multilevel, multidimensional and progressive. It involves multiple interactions and critical stages
Dental anomalies are caused by complex multifactorial interactions between genetic, epigenetic and environmental factors during the long process of dental development.
This process is multilevel, multidimensional and progressive. It involves multiple interactions and critical stages
The multifactorial factors influenc cleft Lip-literature review Abu-Hussein Muhamad
Congenital cleft-Lip and cleft palate have been the subject of many genetic
studies, but until recently there has been no consensus as to their modes of
inheritance. In fact, claims have been made for just about every genetic
mechanism one can think of. Recently, however, evidence has been
accumulating that favors a multifactorial basis for these malformations. The
purpose of the present paper is to present the etiology of cleft lip and cleft palate
both the genetic and the environmental factors. It is suggested that the genetic
basis for diverse kinds of common or uncommon congenital malformations may
very well be homogeneous, whilst, at the same, the environmental basis is
heterogeneous.
Lymphomas are primary malignancies of lymph nodes and the peripheral lymphatics.
Neoplastic proliferative process of the lymphopoietic portion of the lymphoid system that involves cells of either the lymphocytic or histiocytic series in varying degrees of differentiation & occurs in an essentially homogenous population of a single cell type.
The first lymphoma type recognised was by Dr Thomas Hodgkin in 1832. In 1865 Dr Samuel Wilks recognised additional cases, rediscovered the report by Hodgkin, and designated this neoplasm as ‘Hodgkin disease’.
Hodgkin lymphoma (HL) represents about 10% of all lymphomas.
HL is distinct from other non-Hodgkin lymphomas, clinically by the contiguous spread of tumour along the lymphoid system, and morphologically by the presence of a spectrum of neoplastic cells, including mononuclear Hodgkin (H) cells, classic multinucleated Reed–Sternberg (RS) cells, and mummified (degenerating) cells against an inflammatory background.
The background inflammatory cells actively attracted by HL tumour cells may include T cells, B cells, histiocytes, plasma cells, neutrophils, eosinophils and mast cells.
The etiology of HD is unknown. Infectious agents, especially the Epstein-Barr virus (EBV), may be involved in the pathogenesis.
In as many as 50% of HD cases, the tumor cells are EBV-positive. EBV positivity is higher with mixed cellularity Hodgkin disease (60–70%) than the nodular sclerosis Hodgkin disease (15–30%).
Epstein–Barr virus (EBV), also called human herpes virus 4 (HHV-4), is a member of the herpes family and is one of the most common viruses in humans.
In immunocompetent hosts, EBV-infected B cells are in a resting state under host T-cell immune surveillance.
In hosts with immune dysfunction, EBV-infected cells in the reservoir may be reactivated and proliferate.
In EBV-infected cells, based on the viral proteins expressed, three latency transcription programs of EBV are designated: growth program (latency III) with expression of EBV nuclear antigens 1–6 (EBNA1-6), latent membrane proteins (LMP1, 2A and 2B); default program (latency II) expressing EBNA1, LMP1 and LMP2A; and latency program (latency I), with none or only expression of LMP2A.
In EBV-positive cases, usually all HRS cells are positive, indicating that the infection was an early event in lymphoma development.
The EBV+ HRS cells typically show an EBV latency II gene expression profile, meaning expression of the viral proteins EBV nuclear antigen 1 (EBNA1) and latent membrane proteins 1 and 2a (LMP1 and LMP2a).
EBNA1 is essential for replication of the episomal viral genome in proliferating cells. LMP1 mimics an active CD40 receptor and hence stimulates NF- B and PI3K/AKT activity.
As BCR and CD40 signalling are main survival signals for GC B cells, EBV infection of GC B cells may be a way how GC B cells with destructive mutations survive and become HRS precursor cells.
The non-Hodgkin lymphomas include a diverse and complex group of malignancies of lymphoreticular histogenesis and differentiation.
In most instances, they initially arise within lymph nodes and tend to grow as solid masses.
The non-Hodgkin lymphomas most commonly originate from cells of the B-lymphocyte series, with an estimated 85% of European and American lymphoid neoplasms having this derivation.
Tumors with a T-lymphocyte derivation are less common, whereas true histiocyte-derived lymphomas are even rarer.
Genetic abnormalities like nonrandom chromosomal and molecular rearrangements play an important role in the pathogenesis of many lymphomas and correlate with histology and immunophenotype.
Most lymphomas do not have a familial pattern; however, coexistence of multiple breast cancers, ovarian cancer, sarcomas, and lymphomas in a family may suggest an inherited abnormality in tumor suppressor genes.
Environmental factors also seem to play a role in the development of NHL. Certain chemicals have been linked to the development of NHL include a variety of pesticides and herbicides (e.g. organophosphates, chlorophenols), solvents and organic chemicals (e.g. benzene, carbon tetrachloride), and wood preservatives.
Thus certain workers like pesticide applicators, workers in the petroleum, rubber, plastics, and synthetic industries have a slightly increased risk of NHL.
Patients who receive cancer chemotherapy and/or radiation therapy are at increased risk of developing NHL.
Several viruses have been implicated in the pathogenesis of NHL, including the Epstein-Barr virus in Burkitt’s lymphoma (especially in endemic areas of Africa), sinonasal lymphoma in Asia and South America, and lymphomas in immunocompromised patients; HTLV-1 Human T-lymphotropic Virus in adult T-cell lymphoma/leukemia; and human herpesvirus 8 (HHV 8) in body cavity-based lymphomas in patients with HIV infection.
Immunodeficiency states that seem to predispose to NHL include congenital immunodeficiency states (e.g. ataxia telangiectasia, Wiskott–Aldrich syndrome, common variable hypogammaglobulinemia, severe combined immunodeficiency (SCID) as well as acquired immunodeficiency states (e.g. HIV infection, iatrogenic immunosuppression for solid organ or bone marrow transplant recipients).
Connective-tissue disorders, including Sjögren syndrome, rheumatoid arthritis, chronic lymphocytic thyroiditis, and systemic lupus erythematosus (SLE) are also associated with increased risk of NHL.
The microscopic appearance of the lesional cells was used in the past to classify the tumors as either lymphocytic or histiocytic.
With the development of modern immunologic techniques, however, it is now known that many of the lesions that had been classified as histiocytic were in fact neoplasms composed of transformed B lymphocytes. In the early 1980s, a group of American pathologists devised a classification scheme, known as the Working Formulation for Clinical Use.
S. mutans was originally isolated from carious human teeth by Clarke in 1924.
Little attention was paid to this species until the 1960s when it was demonstrated that caries could be experimentally-induced and transmitted in animals artificially-infected with strains resembling S. mutans.
Besides functioning as a resistant structural matrix, insoluble extracellular polysaccharides can act as a diffusion barrier.
The transport of metabolites and salivary buffers into the plaque and the diffusion of acid out of the plaque may be affected by glucan.
Fructans, on the other hand, unlike the mutan homopolymer of glucan, are generally soluble and can be degraded by plaque bacteria, thus serving as a reservoir of fermentable sugars for oral bacteria.
A group of fructans produced by bacteria or created by breaking down other kinds of plant fructans are called levan .
Levans are both more soluble and more readily catabolized than glucans.
Since levan hydrolysis is rapid, it may function as a short-term reservoir for the sustenance of bacterial anaerobic glycolysis in times of relative unavailability of dietary carbohydrate.
Lipoteichoic acid is another extracellular polymer that is found in cultures of S. mutans. These highly negatively charged compounds might contribute to the adhesiveness of bacteria.
In addition to this, S. mutans strains have an ability to store intracellular glycogen amylopectin type polysaccharide, which provides a reservoir of substrate and enables prolonged periods of increased metabolic activity.
Intracellular glycogen and extracellular polysaccharides serve as substrate reservoirs, which the organism may utilize for energy production, as the exogenous supplies of readily metabolized carbohydrate are depleted. In this fashion, both types of polysaccharides may play a role in the survival of organisms and in their potential to prolong acid production via glycolysis well beyond meal time.
It is known that sucrose-adapted S. mutans strains possess significant levels of invertase activity, and this enzyme isknown to hydrolyze sucrose intracellularly to free glucose and fructose.
Invertase is activated by inorganic phosphate and since phosphate accumulation is coupled with acid production, it is probable that one of the several mechanisms by which sucrose degradation is regulated in S. mutans is the activation of invertase by inorganic phosphate.
Cariogenic features of mutans streptococci - Binding to and colonization of teeth
Accumulation on tooth surfaces & participation in the formation of dental plaque.
Production of acid at a high rate.
Tolerance of high concentration of sugar, high ionic strength & highly acidic conditions
Association with dental caries in humans
Causation of dental caries in animals
Transmissible in animals & apparently in man
Reduction or elimination of mutans results in reduction or elimination of dental caries
Sterilization
It is defined as the process by which an article, surface or medium is freed of all living microorganisms either in vegetative or spore state.
Disinfection
It is destruction or removal of all pathogenic organisms or organisms capable of producing infections but not necessarily spores.
The initiation of tooth development begins at 37 days of development
with formation of a continuous horseshoe-band of thickened epithelium
in the location of upper and lower jaws – Primary Epithelial Band
Dental lamina appears as a thickening
of the oral epithelium adjacent to
condensation of ectomesenchyme
20 areas of enlargement or knobs
appear, which will form tooth buds
for the 20 primary teeth
Not all will appear at the same time.
The first to develop are those of the
anterior mandible region
At this early stage the tooth buds
have already determined their crown morphology
Successional lamina: lamina from
which permanent teeth develop
The dental lamina begins to function
at 6th prenatal week and continues to
15th year of birth (3rd molar)
Tooth development is a continuous process, however can be
divided into 3 stages:
1. Bud Stage
2. Cap Stage
3. Bell Stage
4. Hertwigs epithelial root sheath and root formation
The bud stage is represented by the first epithelial incursion into the ectomesenchyme of the jaw.
The epithelial cells show little if any change in shape or function.
The supporting ectomesenchymal cells are packed closely beneath and around the epithelial bud. As the epithelial bud continues to proliferate into the ectomesenchyme, cellular density increases immediately adjacent to the epithelial outgrowth.
This process is classically referred to as a condensation of the ectomesenchyme.
The epithelium of the dental lamina separated from the underlying ectomesenchyme by basement membrane.
Bud stage is characterized by rounded, localized growth of
epithelium surrounded by proliferating mesenchymal cells,which are packed closely beneath and around the epithelial buds
The transition from bud to cap marks the onset of morphologic differences between tooth germs that give rise to different types of teeth.
Differential cellular division in the epithelial bud initiates a change in shape so that now the epithelial outgrowth assumes a more complex outline with a flattened internal portion along which the mesenchymal condensation densifies.
As the tooth bud grows larger, it drags along with it part of the dental lamina; thus from that point on, the developing tooth is tethered to the dental lamina by an extension called the lateral lamina.
At this early stage of tooth development, identifying the formative elements of the tooth and its supporting tissues is already possible.
The epithelial outgrowth, which superficially resembles a cap sitting on a ball of condensed ectomesenchyme , is still referred to widely as the dental organ but actually should be called the enamel organ, because it eventually will form the enamel of the tooth. Henceforth, the term enamel organ is used.
Condensation of the ectomesenchyme immediately subjacent to the tooth bud caused by lack of extracellular matrix secretion by the cells thus preventing separation.
DISEASES OF NERVES AND MUSCLES
Pain is defined as an “unpleasant sensory and emotional
experience that is associated with actual or potential
tissue damage, or described in such terms even in the
absence of any obvious damage.”
Nociceptive pain
on the one hand, is caused by actual tissue injury and inflammation, such as seen with pulpal involvement of a tooth secondary to dental caries, and is an important physiological protective mechanism
Neuropathic pain
on the other hand, is caused by dysfunction of the central and/or peripheral nervous system in the absence of active injury or inflammation, such as post-herpetic neuralgia, that results in neurosensory signs and symptom
CLSSIFICATION
Trigeminal neuralgia
Glossopharyngeal neuralgia
Sphenopalatine ganglion neuralgia
Raeder’s paratrigeminal
Atypical pain/neuralgia
Postherpetic facial neuralgia
Migrainous neuralgia
Occipital neuralgia
Geniculate neuralgia
Superior laryngeal neuralgia
Tympanic plexus neuralgia
Trigeminal neuralgia –Etiology
Dental pathosis—dental pathosis is believed by some investigators to be involved with the onset of trigeminal neuralgia.
Excessive traction—secondary to excessive traction on the various divisions of the fifth nerve, being influenced by maxillo-mandibular relationship.
3 .• Allergic—it can be secondary to an allergic and hypersensitivity reaction causing edema of the trigeminal nerve root.
4• Ischemia—Wolf thought that ischemia at various portions of the trigeminal pathway might be responsible for the paroxysms of pain.
5. Compression distortion phenomenon—Jannetta and others have shown subtle changes of a compression- distortion phenomenon which is usually caused by arterial loops of atherosclerotic vessels. Vessels become elongated with advancing age and withatherosclerotic involvement gain abnormal positions by wedging into the spacebetween the pons and trigeminal nerve. It is postulated that with progressive material elongation, fascicles of adjacent nerves later suffer myelin injury and pain results.
6• Mechanical factors—like pressure due to aneurysms of the intrapetrous portion of the internal carotid artery that may erode through the floor of the intracranial fossa to exert a pulsatile irritation on the ventral side of the trigeminal ganglion.
7• Anomalies of superior cerebellar artery—it is the most recently blamed cause for trigeminal neuralgia. It lies in contact with the sensory root of the nerve and implicated as a cause of demyelination. Surgical elevation of artery or decompression of the sensory root has high success rate in relieving paroxysmal pain in case of idiopathic trigeminal neuralgia.
8• Secondary lesion—conditions such as carcinoma of the maxillary antrum, nasopharyngeal carcinoma, tumors of peripheral nerve root, intracranial vascular anomalies,and multiple sclerosis may be presented with trigeminal pain.
2.Glossopharyngeal neuralgia
The most common causes of glossopharyngeal neuralgia are
intracranial or extracranial
MANDIBULAR LATERAL INCISOR
INTRODUCTION
Lateral incisors generally appear in the oral cavity after central incisors.
Lateral incisors usually erupts during the seventh year of life .
Roots complete: 9 – 10 years
FDI SYSTEM (Federation Dentaire Internationalae)-
Mandibular RIGHT lateral incisor- 42
Mandibular LEFT lateral incisor- 32
UNIVERSAL SYSTEM-
Mandibular RIGHT lateral incisor- 26
Mandibular LEFT lateral incisor- 23
Zsigmondy-palmar system
Mandibular RIGHT central incisor-
2
Mandibular LEFT central incisor-
2
ARCH TRAITS
Lingual fossa are less pronounced on mandibular incisors.
Mandibular lateral incisors have roots that are more triangular in cross section.
Labio-lingual diameter is wider than mesio-distal diameter.
CLASS TRAITS-
Crown shapes are rectangular, longer inciso-gingivally than mesio-distally.
Mesial & distal marginal ridge converge toward the lingual cingulum.
SET TRAIT
There are depression or perikymata on the labial surface of the crown of the incisors.
Mammelons are seen on the incisal edge of newly erupted incisors.
Cervical ridges of anterior permanant teeth are prominent than primary teeth.
TYPE TRAIT
Lateral incisors have distal proximal contact more apical than the mesial contact.
Lateral incisors have disto-incisal angle more rounded than the mesio-incisal angle.
Labial Aspect
Crown is trapezoidal from labial aspect.
Mesial outline is almost straight in line with mesial outline of root.
Distal outline is straight near cervix and become slightly convex as it reaches distoincisal angle.
Distoincisal angle more rounded than mesioincisal angle
Incisal outline formed by incisal ridge is straight but has tendency to slope cervically in distal direction.
Cervical line is curved apically.
Crown is not bilaterally symmetrical
Distal half is slightly larger.
lingual aspect
Its shape is trapezoidal like labial surface.
Crown tapers lingually making lingual surface narrower than labial surface.
Shallow lingual fossa
Lingual surface is smooth devioid of developmental grooves, and is convex near cingulum.
Distal surface bulges from the incisal view
incisal aspect
It is oval labiolingually.
Labiolingual dimension is greater than mesiodistal.
Incisal ridge is at an angle to the line bisecting the tooth labiolingually rather than being perpendicular.
Slightly twisted on its root base from this aspect.
Cingulum twisted (off-center) to the distal
mesial aspect
Mesial aspect is triangular
Labial outline is convex near cervical line
Lingual outline is straight in incisal 3rd
Incisal edge lingual to root axis line
CEJ is curved more on the mesial than the distal
Mesial contact area is at incisal 3rd of crown
Mesial surface is longer than distal surface
developmental disturbances of teeth
DEVELOPMENTAL DISTURBANCES IN NUMBER OF TEETH
DEVELOPMENTAL DISTURBANCES IN SIZE OF TEETH
DEVELOPMENTAL DISTURBANCES IN SHAPE OF TEETH
Anodontia
Supernumerary teeth
Predeciduous dentition
Post permanent dentition
Microdontia
Macrodontia
Gemination
Fusion
Concrescence
Dilaceration
Talon cusp
Taurodontism
Supernumerary roots
DEVELOPMENTAL DISTURBANCES OF GINGIVA
1) Fibromatosis Gingivae(Elephantiasis gingivae, hereditary gingival fibromatosis, congenital macrogingivae)
Fibromatosis gingivae is a diffuse fibrous overgrowth of the gingival tissues.
This condition is manifested as a dense, diffuse, smooth, or nodular overgrowth of the gingival tissues of one or both arches, usually appearing about the time of eruption of the permanent incisors.
Even seen in very young children
It is not painful and shows no tendency for hemorrhage.
The extent of the tissue overgrowth may be such that the crowns of the teeth are nearly hidden even though they are fully erupted with respect to the alveolar bone .
2) Retrocuspid Papilla
It is a small, elevated nodule located on the lingual mucosa of the mandibular cuspids.
Clinical Features
This soft, well-circumscribed, sessile, mucosal nodule, commonly bilateral, is located lingual to the mandibular cuspid, between the free gingival margin and the mucogingival junction.
It is exceedingly common in children.
Found a greater occurrence bilaterally than unilaterally.
The structure appears as an elevated mucosal tag often showing mild hyperorthokeratosis or hyperparakeratosis, with or without acanthosis.
The underlying connective tissue is sometimes highly vascularized and may exhibit large stellate fibroblasts as well as occasional epithelial rests.
Because of its frequency of occurrence, the retrocuspid papilla is often considered to be a ‘normal’ anatomic structure which regresses with age and requires no treatment.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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.
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
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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2. Table of contents
1)Introduction
-Epithelial mesenchymal interactions
-Odontogenesis
2)Epithelial mesenchymal interactions in odontogenesis
-Experimental studies
-Branchial arch formation
-Growth factors
-Role of extracellular matrix
-Initiation of tooth
-The route map of development
3) Conclusion
2
3. Introduction
Epithelial mesenchymal interactions (EMIs)
are a series of programmed, sequential and
reciprocal (complex and multiphase)
communications between the epithelium and
the mesenchyme with its heterotypic cell
population, that result in the differentiation of
one or both cell populations.
3
4. Odontogenesis is the process of tooth
development, which involves both ectodermal and
mesenchymal components, being the key
elements in the development of teeth.
In order for the tooth to form, an interactive
mechanism between these heterotypic cellular
populations is required.
4
5. Epithelial-mesenchymal interactions are the hallmark
of odontogenesis.
EMI mechanisms can be observed in the dentino-
enamel junction of the tooth.
The embryonic development of ectoderm derived
appendages undergoes these interactions to give rise
to a large variety of highly specialized organs.
5
7. For these interactions to occur there should be some or other
form of messenger system between epithelium and mesenchyme,
further underlining the importance of cell signaling networks and
intricacies of physiological growth of an individual.
In the process of embryonic development the ectoderm is
composed of surface ectoderm, neural crest and neural tube.
This will give rise to the epidermis or skin and the oral epithelium.
7
9. 1)Initiation stage
9
The localization, identity, shape and size of the teeth are
determined during early stages of tooth development .
After day 12 of development, first arch epithelium loses
odontogenic potential, which then is assumed by the
ectomesenchyme; thereafter ectomesenchyme can elicit
tooth formation from a variety of epithelia.
Early signals like Bmp4 (incisor region) and FGF8 (molar
region) from oral ectodermal cells elicit the odontogenic
potentialities of the underlying mesenchyme.
10. 10
Numerous transcription factors expressed in the
mesenchyme are then activated, including genes coding
for several homeobox divergent transcription factors (e.g.
msx1 [muscle segment homeobox 1], msx2, dlx1 [distal-
less homeobox 1], dlx2.
Many of these transcription factors, even within the same
family, are coexpressed and participate to functional
redundancy, allowing rescue mechanism in case of
dysfunctions.
11. 11
Tooth development is arrested at the initiation stage when
msx1 and msx2 or dlx1 and dlx2 are inactivated.
It indicates that odontogenesis is initiated first by factors
resident in the first arch epithelium influencing
ectomesenchyme but that with time this potential is
transferred to and is assumed by the ectomesenchyme.
12. 2)Placode Formation
12
One of the key aspects of tooth development is the formation of
ectodermal placodes, thickenings of the epithelium at the
locations of each family of tooth.
Similar placodes initiate the development of all organs
developing as ectodermal appendages, such as the hair, nails,
salivary, mammary and sebaceous glands.
Signalling molecules from the four well-known families Tgfβ,
FGFs, hedgehog and Wnts families participate in placode
development.
14. 3)Experimental studies
The specific features of the EMIs are explained by the
studies on recombinant DNA, which focus on the
combination of two or more sources of tissues/DNA.
These studies often involve the combination of DNA
from different organisms and depend on the ability to
cut and recombine DNA molecules at certain points
identified by specific sequences of nucleotide bases.
14
15. In 2010, Del Moral et al. maintained that the roles
of the epithelium and the mesenchyme in these
signaling process can be determined using studies
on recombinant tissues.
The proliferative response of epithelial cells via the
keratinocyte growth factor was investigated by
studies on recombinant tissues,which provided
some evidence that was used to study the EMIs.
15
18. The experimental procedures in these studies are based on a
culture of the bud stage of the tooth development process to
evaluate the role of EMI molecules.
In 2003, Garant reported that the results from recombinant studies
revealed that the tooth continues to develop in the following two
combinations:
i) dental epithelium with dental mesenchyme and
ii) dental epithelium and skin mesenchyme.
18
20. On the contrary, no tooth development occurred in cultures
obtained with the dental epithelium only,
i) the dental mesenchyme,
ii) the skin epithelium with dental mesenchyme.
For the EMIs to occur, some form of the messenger system is
also required between the epithelium and the mesenchyme.
The messenger system could be anyone of the following seven:
20
21. Factors involved in growth and
development
1. Direct cell-cell communication
2. Matrix vesicles between two cell populations.
3. Ions like K
+
and Ca
2+
.
4. Extracellular matrix component like collagen IV, I, III, fibronectin, tenascin, E-
cadherin, laminin.
5. Molecular diffusion and transfer of information by substances like bone
morphogenetic protein (BMP-2, 4, 6, 7) FGF, EGF, TGF.
6. Autocrine and paracrine regulators.
7. Messenger RNA.
21
22. In 2003, Irma Thesleff reported the genes
involved in signaling tooth development:pitx2,
p21, Msx2, Lef1, Edar, Lhx6, Lhx7, Dix1, Dix2,
Pax9, Gli1, Gli2,Gli3, Barx1 and Runx2.
These genes have a role in the differentiation
and the mineralization during the tooth
development process.
22
23. Therefore EMIs in odontogenesis are considered to be a
programmed series of events, which are controlled by
various genes, growth factors and extracellular
molecules.
Hierarchical and sequential functional interactions
between the epithelium and the mesenchyme are
considered to be a hallmark of embryonic development.
23
24. 4)GROWTH FACTORS
These were primarily important for signaling of
various developmental steps.
The well regarded signals belong to the
families of Fibroblast Growth Factor (FGF),
Epidermal Growth Factor (EGF) and
Transforming Growth Factor (TGF)
24
25. Fibroblast Growth Factor (FGF)
25
FGF belongs to a large family of heparin binding proteins that
were known to mediate the growth and differentiation of cells
from a wide variety of developmental origins.
At the time of odontogenic initiation this expression becomes
restricted to the area of the presumptive dental epithelium and
persists until the beginning of bud stage.
An important role by this factor was found in the differentiation
of ameloblasts as FGF4 and FGF9 were revealed in the inner
enamel epithelium.
26. Epidermal Growth Factor (EGF)
26
EGF is very important for signaling and synergistic
effect of different factors.
It has got a vivid role in development of an embryo
and highly essential for interaction between key
players of development.
EGF signaling would be responsible for activation
of major tissues like submandibular glands.
27. Transforming Growth factor
(TGF)
27
TGF and its receptor Edar were involved in multiple signaling systems
during developmental regulative mechanisms .
Another idea was that TGF-β and Shh signaling from Hertwig's epithelial
root sheath induces the differentiation of root progenitor cells and thereby
has a direct control in modulating and transforming the formation of
odontoblasts.
It was also established that during tooth morphogenesis, TGF-β
signaling controls odontoblast maturation and dentin formation
28. 5)Role of Extracellular Molecules
(Ecm) and Matrix
28
ECM was present in interactions in the morphogenesis and
differentiation of developing tooth including budding of oral
epithelium and condensation of neural crest cells around the
bud.
The interactions mediated by the basement membrane were
regulated by the differentiation of mesenchymal cells into
odontoblasts and these molecules were elaborated at that
time.
The structural components of ECM and components affect
cellular structure.
29. 29
Also, they were involved in regulation of interactions. The first
extra cellular matrix molecule to appear during embryonic
development is basement membrane.
Their function includes mediation of signals for sustained and
proper development.
By binding to specific matrix receptors on the cell surface, the
extracellular matrix molecules exert their effects on the cells
and structural components, thereby completing the circle of
organized events that finalizes the nature in which these
events turn out .
30. 7)THE ROUTE MAP OF DEVELOPMENT
Growth does not occur in one cycle.
Multiple channels of cell network co-exist to promote
signal propagation between cells, suggesting a type
of cell to exhibit its functional capacities.
Teeth develop as ectodermal appendages in
vertebrate embryos and their early development
resembles morphologically as well as molecularly.
30
31. Interactions between the ectoderm and underlying
mesenchyme constitute a central mechanism
regulating the morphogenesis of all these organs.
During tooth initiation the ectoderm thickens and
forms a placode that buds to the underlying
neural-crest derived mesenchyme.
31
32. Paracrine signal molecules of several conserved families
mediate cell communication during tooth development.
Most of them belong to the transforming growth factor β (TGFβ),
fibroblast growth factor (FGF), Hedgehog and Wnt families.
Although the signals mostly regulate interactions between the
ectoderm and mesenchyme, they also mediate communication
within one tissue layer.
32
33. Ectodysplasin, a recently identified signal molecule
in the tumor necrosis factor (TNF) family, and its
receptor Edar mediate signalling between
ectodermal compartments in tooth germs.
A characteristic feature of tooth development is the
reiterated appearance of transient signalling centers
in the epithelium during key morphogenetic steps.
33
35. These signalling centers express more than ten different
signal molecules including SHH (sonic hedgehog) and
several BMPs (bone morphogenetic proteins, belonging
to the TGFβ superfamily), FGFs and Wnts.
The first signalling centers appear in the dental placodes
when epithelial budding begins.
Subsequently, at the bud-to-cap transition, the enamel
knot signalling centers appear.
35
36. These regulate the advancing morphogenesis of
the tooth crown and control the initiation of the
secondary enamel knots at the sites of epithelial
foldings that mark cusp formation.
An early signalling event in tooth development is
the induction of the odontogenic mesenchyme by
BMPs and FGFs from the epithelium.
36
37. Tissue recombination studies have shown that epithelial
signals induce in the mesenchyme the competence to
instruct subsequent tooth morphogenesis.
BMPs and FGFs induce the expression of several
mesenchymal transcription factors, many of which are
necessary for the continuation of tooth development.
37
38. The first epithelial signals induce in the mesenchyme
the expression of reciprocal signal molecules,
including activin, FGF and BMP4 which act back on
the epithelium and regulate the formation of the dental
placode.
In addition, Wnts and the TNF signal ectodysplasin,
secreted by ectodermal cells, regulate placode
development.
38
40. The placodal signals then regulate budding of the
epithelium and condensation of the mesenchymal
cells.
They maintain the expression of earlier induced
transcription factors in the mesenchyme and induce
the expression of new genes such as the transcription
factor Runx2 and the signal Fgf3, which regulate
epithelial morphogenesis from bud to cap stage.
40
41. 41
Runx2-deficient mice show arrested tooth development at
the bud stage.
The Wnt signalling pathway is involved in the tooth
replacement cycle with the development of the primary and
then permanent dentition.
This signalling pathway also leads to the formation of
supernumerary teeth through the multiplication of signalling
centres via budding from the dental epithelium.
42. At this time mesenchymal BMP4 is required for
the formation of the enamel knot at the tip of the
bud.
It induces the expression of p21, which is
associated with the exit of the knot cells from the
cell cycle.
42
43. The Edar receptor is also induced in the enamel
knot, making the cells responsive to the TNF
signal ectodysplasin, which is expressed in the
flanking epithelium of the tooth bud.
Ectodysplasin-edar signalling regulates the
formation and perhaps the signalling activity of the
enamel knot.
43
44. 44
The underlying condensing mesenchyme controls the growth
and folding of the epithelium.
Mesenchymal signals induce, within the enamel organ, the
formation of signalling centres called enamel knots –
transitory structures which produce numerous signalling
molecules at the cap stage.
The primary enamel knot is indispensable to crown
development. These signals pass towards the mesenchyme
and within the epithelium regulate tooth shape.
45. 45
Shh is one signal essential for epithelial
proliferation, but its direct action seems to
target the mesenchyme, where it induces a
feedback loop signal towards the epithelium.
Wnt and Bmp signalling regulate the formation
of enamel knots.
46. Signals from the enamel knot affect both epithelial
and mesenchymal cells and subsequent reciprocal
interactions between the mesenchyme and
epithelium are responsible for the maintenance of
the enamel knot as well as for the subsequent
morphogenesis of the epithelium.
46
47. An SHH signal from the enamel knot is needed for the
growth of the epithelial cervical loops flanking the enamel
knots.
The enamel knot signals also regulate the patterning of the
tooth crown by influencing the initiation of the secondary
enamel knots that express most of the same signal
molecules as the primary enamel knots.
47
49. They form in an exact sequence and
determine the sites where the epithelial sheet
folds and cusp development starts.
Their development is regulated by signals from
earlier formed primary and secondary enamel
knots together with mesenchymal signals.
49
51. Conceivably this involves mechanisms of lateral
inhibition and activators and inhibitors.
Recently a gene network model was presented that
can reproduce both the reiteration of the epithelial
signalling centers and their gene expression patterns
as well as the resulting tooth morphologies of
different mammalian species (Salazar-Ciudad and
Jernvall, 2002)
51
52. It is obvious that the signalling networks regulating
tooth morphogenesis are much more complex.
For example, there are numerous specific inhibitors of
signals that have central roles in modulating locally the
signalling activities.
Also, the different signalling pathways are integrated at
various levels and have synergistic as well as
counteractive effects.
52
53. Nevertheless, the model illustrates the general principle
of the development of multicellular organisms, namely
that the cells and tissues communicate via conserved
signal molecules which are used reiteratively during
advancing morphogenesis.
The variation in cellular responses to the same signals
in different tissues and at different times is caused by
the different histories of the cells determining their
competence to receive and respond to the signals.
53
55. Dental Anomalies
55
Acquired dental anomalies are relatively common and
provide real markers of gene–environment relationships,
pointing to pre- and post-natal pathological developmental
pathology, easily accessible and readable via fixed teeth
morphology and appearance throughout mineralization.
Missing teeth (anomalies of tooth number) concern tooth
agenesis, hypodontia, oligodontia and anodontia and are
associated with mechanisms regulating tooth patterning as
well as the transition from the bud to the cap stage.
56. 56
In the mouse, inactivation of different genes leads to the arrest of tooth
development.
Genes shown to be involved in arrest of tooth development in mice include
dlx1, dlx2, lef1, pax9, pitx2, runx2 and the activin-coding gene .
In humans, mutations in these same genes, MSX1, PAX9 and PITX2, also
result in missing teeth according to specific patterns.
57. Conclusion
The completion of epithelial mesenchymal interactions and
transitions brings about varied changes in the developing
embryo and tooth development, thereby increasing the
potential of individual cell to grow and substantiate the
necessary development required for tooth formation.
The complex mechanism involved are to be studied
exhaustively in order to overcome the difficulties arising due
to the improper knowledge of pathogenesis of a specific
odontogenic lesion thus jeopardizing treatment options.
57
58. The expansive field of dentistry requires genetic research and
molecular level of contemplation to highlight the significance of
biological processes, thus reflecting on the overall management
protocols.
A paradigm shift is needed in this regard to appropriately digress
the meshwork of intricacies associated with any developmental
scenarios.
The “end of the tunnel” should surely be reached once sufficient
knowledge and expertise is gained in further increasing our
knowledge on several new pathways and factors attached to
developmental scenarios.
58
59. References
59
Epithelial-mesenchymal signalling regulating tooth
morphogenesis Irma Thesleff(2003) Journal of Cell Science
116, 1647-1648
Reiterative signaling and patterning in mammalian tooth
morphogenesis. Jernvall, J. and Thesleff, I. (2000). Mech.
Dev. 92, 19-29
The role of growth factors in tooth development. Thesleff, I.
and Mikkola, M. (2002). Int. Rev. Cytol. 217, 93-135.
Odontogenesis, Anomalies and Genetics. Bloch-Zupan, A.,
Sedano, H. O., & Scully, C. (2012). Dento/Oro/Craniofacial
Anomalies and Genetics, 1–8.
60. 60
Epithelial – Mesenchymal Interactions in Tooth Development
and the Significant Role of Growth Factors and Genes with
Emphasis on Mesenchyme – A Review.Puthiyaveetil J S V,
Kota K,chakkarayan R,chakkarayan J, thodiyil A K P. J Clin
and Diag Res. 2016 Sep, Vol-10(9): ZE05-ZE09
The epithelial-mesenchymal interactions: insights into
physiological and pathological aspects of oral tissues.A.B.
Rajendra Santosh and T.J. Jones. Oncology Reviews 2014;
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Tencate’s oral histology 9th edition