This document discusses various clinical considerations related to tooth development, eruption, and shedding. It begins with an introduction on tooth composition and classifications of developmental defects. It then examines specific defects that can occur during different stages of tooth development, such as anodontia, supernumerary teeth, gemination and fusion during the initiation stage. Enamel hypoplasia, dens invaginatus, taurodontism and amelogenesis imperfecta are among the defects discussed during the apposition stage. Syndromes associated with certain defects and systemic diseases that can cause tooth abnormalities are also reviewed.
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
THEORIES OF ERUPTION
ERUPTION SEQUENCE
PHYSIOLOGY OF TOOTH ERUPTION
CELLULAR BASIS
MOLECULAR BASIS
PRODUCTION OF OSTEOCLAST
ANOMOLIES OF TOOTH ERUPTION
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
THEORIES OF ERUPTION
ERUPTION SEQUENCE
PHYSIOLOGY OF TOOTH ERUPTION
CELLULAR BASIS
MOLECULAR BASIS
PRODUCTION OF OSTEOCLAST
ANOMOLIES OF TOOTH ERUPTION
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.
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.
Ameloblast are the enamel forming cells. Understanding of life cycle of ameloblast aids in the understanding of various developmetal anomalies in particular and various other oral pathologies.
Coronal and radicular pulp
Apical foramen
Accessory canal
Functions of dental pulp
Components of dental pulp
Functions of pulpal extracellular matrix
Organization of cells in the pulp
The principle cells of the pulp
The pathways of collagen synthesis
Matrix and ground substances
Vasculature and lymphatic supply
Innervation of Dentin- pulp complex
Disorders of the dental pulp
Advances in pulp vitality testing
Amelogenesis is the formation of enamel. During amelogenesis, the ameloblast (enamel-forming cells) undergo various stages i.e the life cycle of ameloblast.
For more content check out my blog: www.rkharitha.wordpress.com "a little about everything dental"
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.
Ameloblast are the enamel forming cells. Understanding of life cycle of ameloblast aids in the understanding of various developmetal anomalies in particular and various other oral pathologies.
Coronal and radicular pulp
Apical foramen
Accessory canal
Functions of dental pulp
Components of dental pulp
Functions of pulpal extracellular matrix
Organization of cells in the pulp
The principle cells of the pulp
The pathways of collagen synthesis
Matrix and ground substances
Vasculature and lymphatic supply
Innervation of Dentin- pulp complex
Disorders of the dental pulp
Advances in pulp vitality testing
Amelogenesis is the formation of enamel. During amelogenesis, the ameloblast (enamel-forming cells) undergo various stages i.e the life cycle of ameloblast.
For more content check out my blog: www.rkharitha.wordpress.com "a little about everything dental"
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
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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
2. CONTENTS
Introduction
Classification
Defects occurring during initiation
Defects occurring during proliferation
Defects occurring during morphodiffrentiation
Defects occurring during apposition
Defects occurring during eruption and shedding
Defects of structures due to systemic diseases
References
3. Teeth are specialized structural components of the craniofacial skeleton and are
comprised of - enamel, dentin and cementum.
Developmental defects occur in each of these mineralized tissues, either alone, or in a
combination (syndromic) with defects in other organs or tissues.
INTRODUCTION
4. CLASSIFICATION
Failure of Neural crest cell to migrate Treacher Collins syndrome
Pierre Robin Syndrome
Hemifacial Microsomia
Cranioschiosis,
Achondroplasia
Due to morphodiffrentiation Anodontia, micro/macrodontia
Supernumerary Teeth,
Fusion, Gemination,
Enamel Hypoplasia,
Dense in Dente,Dense Evaginatus,
Talon Cusp, taurodontism
Dilacerations,Concrescence
Amelogenisis imperfecta,
Dentinogenisis imperfecta
Regional odontodysplasia
Dentin dysplasia
5. Systemic diseases Gardner´s syndrome
Ehlers - Danlos syndrome
Fluorosis (mottled enamel)
Tetracycline staining (TTC)
Odontogenic tumors Tumors of odontogenic epithelium or ectomesenchyme
or mixed in origin
Odontogenic cysts OKC, Dentigerous cyst
Endocrinal changes Hypothyroidism, Hypopituitarism
Eruption and Shedding Turner’s hypoplasia
Ankylosis
Eruption cyst
Eruption sequestrum
Retained deciduous
6. ANODONTIA
• Anodontia, also called anodontia vera,
It can be complete or partial.
COMPLETE
PARTIAL
MUTATION OF PAX9 MSX1 AND AXIN2
Defects occurring during Initiation:
True anodontia
Psuedo anodontia.
False anodontiaForms-
7.
8. A- Multiple developmentally missing permanent teeth and several
retained deciduous teeth in a female adult.
B -The panoramic radiograph shows no unerupted teeth in either jaw.
9. Syndromes Associated with Anodontia
● Ankyloglossia superior
● Böök
● Cockayne
● Coffi n-Lowry
● Cranio-oculo-dental
● Crouzon
● Down
● Ectodermal dysplasia
● Ectodermal dysplasia, cleft lip, cleft palate
● Ehlers-Danlos
● Ellis-van Creveld
● Focal dermal hypoplasia
● Freire-Maia
● Frontometaphyseal dysplasia
● Goldenhar
● GorlinGorlin-Chaudhry-Moss
● Hallermann-Streiff
● Hanhart
● Hypoglossia-hypodactylia
● Incontinentia pigmenti
● Johanson-Blizzard
● Lipoid proteinosis
● Marshall-White
● Melanoleukoderma
● Monilethrix-anodontia
● Oral-facial-digital type I
● Otodental dysplasia
● Palmoplantar keratosis, hypotrichosis, cysts of
eyelid
● Progeria
● Rieger
● Robinson
● Rothmund-Thomson
● Sturge-Weber
● Tooth-and-nail
BRAD W. NEVILLE, DOUGLAS D. DAMM, CARL M. ALLEN, JERRY E. BOUQUOT, ORAL AND MAXILLOFACIAL
PATHOLOGY Third Edition
10. SUPERNUMERARY TEETH
OPG OF Patient having numerous Supernumerary
Teeth
Results from continued proliferation of
permanent or primary dental lamina to
form third tooth germ.
Inactivation of Apc or forced activation of Wnt/β-catenin
Supplemental
Rudimentary
Molariform
Conical
Tuberculate
Type
Defects occurring during Initiation…..
12. BRAD W. NEVILLE, DOUGLAS D. DAMM, CARL M. ALLEN, JERRY E. BOUQUOT,ORAL AND
MAXILLOFACIAL PATHOLOGY Third Edition
Syndromes Associated with Hyperdontia
● Apert
● Angio-osteohypertrophy
● Cleidocranial dysplasia
● Craniometaphyseal dysplasia
● Crouzon
● Curtius
● Down
● Ehlers-Danlos
● Ellis-van Creveld
● Fabry-Anderson
● Fucosidosis
● Gardner
● Hallermann-Streiff
● Incontinentia pigmenti
● Klippel-Trénaunay-Weber
● Laband
● Leopard
● Nance-Horan
● Oral-facial-digital types I and III
● Sturge-Weber
● Tricho-rhino-phalangeal
13. MICRODONTIA
(1) True Generalized Microdontia
-all teeth are smaller than normal
(2) Relative Generalized Microdontia
-normal or slightly smaller than normal teeth.
(3) Focal or Localized Microdontia
-common condition
-affects most often maxillary lateral incisor + 3rd molar
-most common form of local microdontia is Peg Lateral
Defects occurring during PROLIFERATION:
14. Kazhila C. Chinsembu ,Teeth are bones: Signature genes and molecules that underwrite odontogenesis
Journal of Medical Genetics and Genomics Vol. 4(2),March 2012
Wnt signaling is required early in tooth germ formation and interference
with signaling via addition of an antagonist results in retarded
development and formation of smaller teeth; mutation of β-catenin
causes formation of larger teeth.
15. MACRODONTIA
(1) True Generalized Macrodontia
-all teeth are larger than normal.
(2) Relative Generalized Macrodontia
-normal or slightly smaller than normal teeth.
(3) Focal or Localized Macrodontia
-the union of one or more teeth results in
single large tooth.
-variant – hemi hypertrophy of face.
Defects occurring during PROLIFERATION……
Kazhila C. Chinsembu ,Teeth are bones: Signature genes and molecules that underwrite odontogenesis Journal of
Medical Genetics and Genomics Vol. 4(2),March 2012
mutation of β-catenin
causes formation of
large teeth
16. GEMINATION
partial or complete cleavage of
single tooth germ.
Large single rooted tooth with one pulp cavity
exhibits “twinning” in crown area.
The etiology of geminated teeth remains unknown.
Possible cause-nutritional deficiency, endocrinal disturbance,infectious/inflammatory processes,
hereditary or congenital diseases, and local traumas and by ionizing radiation is also considered.
PK RAO et al,Twin Tooth on Either Side: A Case Report of Bilateral Gemination, Ann Med Health Sci Res. 2013 Apr-Jun;
3(2): 271–273
Defects occurring during MORPHODIFFERENTIATION……
17. FUSION
• Either complete or incomplete union of two normally separated tooth germs.
• The dentin always confluent in cases of true fusion.
before calcification begins later, when a portion of
the tooth crown has
completed its formation.
If this contact occurs
the two teeth may be
completely united to form a
single large tooth .
there may be union of the
roots only.
Defects occurring during MORPHODIFFERENTIATION……
Sandhya shrivastava et al, FUSION/DOUBLE TEETH,10.5005 jp journals,10011-1200
18. DENS INVAGINATUS(Dens- In- Dente )
• Represents a defect of tooth in which a focal area on the tooth surface is
folded or invaginated pulpally to a variable extent.
• Dens invaginatus is a malformation of teeth probably resulting from an
infolding of the dental papilla before calcifiaction.
• Maxillary lateral incisors, central incisors, premolars, canines and molars
are affected in the order of fashion.
Defects occurring during APPOSITION:
M. Hülsmann, “Dens invaginatus: aetiology, classification, prevalence, diagnosis, and treatment considerations,” International
Endodontic Journal, vol. 30, no. 2, 79–90, 1997.
21. ENAMEL PEARL
Mass of ectopic enamel located in
the furcation area of a molar tooth.
Radiopaque nodule on the mesial surface of the root of the
maxillary third molar.
Another less distinct enamel pearl is present on the distal root
of the second molar.
The formation of ectopic enamel requires the presence of differentiated ameloblasts apical to the CEJ. In humans,
Hertwig's epithelial root sheath (HERS) or its residues, the epithelial rests of Malassez have been implicated as the
likely sources of ectopic ameloblasts.
Defects occurring during APPOSITION….
Shivani sharma et al Enamel pearl on an unusual location associated with localized periodontal disease: A clinical report, J
Indian Soc Periodontol. 2013 Nov-Dec; 17(6): 796–800
22. • Also known as “Eagle’s talon” is an extra cusp on anterior teeth.
Defects occurring during APPOSITION….
24. Hattab FN, Yassin OM, Al-Nimri KS. Talon cusp in the permanent dentition associated with other dental
anomalies: Review of literature and reports of seven cases. J Dent Child 1996;63:368-76.
Hattab et al classified talons cusps as
Type 1, major talon: A morphologically well delineated additional cusp that prominently projects from
the facial or palatal/lingual surface of an anterior tooth and extends at least half the distance from the
CEJ to the incisal edge.
Type 2, minor talon: A morphologically well-defined additional cusp that projects from the facial or
palatal/lingual surface of an anterior tooth and extends more than onefourth, but less than half the
distance from the CEJ to the incisal edge.
Type 3, trace talon: Enlarged or prominent cingula and their variations, which occupy less than one-
fourth the distance from the CEJ to the incisal edge.
Defects occurring during APPOSITION….
25. TAURODONTISM
Taurodontism is an enlargement of the body and pulp chamber of a multirooted tooth, with apical
displacement of the pulpal floor and bifurcation of the roots.
failure of Hertwig's epithelial sheath diaphragm to invaginate at the proper horizontal level.
Shape of the taurodont resembles that of the molar teeth of cud-chewing animals (tauro = bull;
dont = tooth).
Defects occurring during APPOSITION….
Manjunatha BS, Kovvuru SK. Taurodontism –A Review on its etiology, prevalence and clinical considerations. J Clin Exp
Dent. 2010;2(4):e187- 90
26. Illustration exhibiting the classification of taurodontism according
to the degree of apical displacement of the pulpal floor
Defects occurring during APPOSITION….
27. SUPERNUMERARY ROOT
The term supernumerary roots refers to the development of an increased number of roots on a
tooth compared with that classically described in dental anatomy.
A, Gross photograph showing a mandibular molar with
a supernumerary root.
B, Periapical radiograph of the extracted tooth.
A B
• These supernumerary roots may be due to the disturbances
of the Hertwig's epithelial root sheath forming the root.
Kannan SK1, Suganya, Santharam HSupernumerary rootsIndian J Dent Res. 2002 Apr-Jun;13(2):116-9
28. ENAMEL HYPOPLASIA
• Enamel hypoplasia occurs in the form of
pits, grooves, or larger areas of missing enamel.
.
Bilaterally symmetrical pattern of horizontal
enamel hypoplasia of the anterior dentition.
Maxillary central incisors have been restored
previously. (From Neville)
Factors producing injury to ameloblasts during tooth
formation:
Nutritional deficiency (vit. A,C,D)
Diseases like measles, chicken pox, scarlet fever
Congenital syphilis
Hypocalcaemia
Birth injury
Local infection or trauma
Ingestion of chemicals
Defects occurring during APPOSITION….
29. AMELOGENESIS IMPERFECTA
Definition:
Amelogenesis imperfecta is an abnormal formation of the enamel .
color: yellow, brown or grey.
CAUSE: Amelogenesis Imperfecta is due to the malfunction of the proteins in the enamel.
Related gene Protein Variants
AMLEX AMELOGENIN smooth hypoplastic and hypomaturation
ENAM ENAMELIN Hypoplastic (minor pitting to diffuse generalized thin
enamel)
MMP-20 ENAMELYSIN pigmented hypomaturation
KLK4 KALLIKREIN Hypomaturation
DLX3 hypoplastic-hypomaturation
Defects occurring during APPOSITION….
31. DENTINOGENESIS IMPERFECTA(CAPDEPONT’S TEETH)
Dentinogenesis imperfecta (hereditary Opalescent Dentin)
Causes- discoloration (most often a blue-gray or yellow-brown color) and translucent.
Teeth are weaker, prone to rapid wear, breakage, caries and loss.
A B
Defects occurring during APPOSITION….
32. Genes, locus, proteins and associated defects seen in Hereditary Dentinal defects
Aswathy Raj,Deepa.M.S, Ahmed Hasan Farooqi GENETICS AND TOOTH ANOMALIES - AN UPDATE
Oral & Maxillofacial Pathology Journal Vol. 4 No. 1 Jan - June 2013
33. Classified into three basic types:
Shields Type I (associated with Osteogenesis Imperfecta)-
Features- periapical radiolucencies, bulbous crowns, obliteration of pulp chambers, root fractures and amber
translucent tooth color.
Shields Type II (Hereditary Opalescent Dentin)
Features are same as Shields Type I apart from Osteogenesis Imperfecta.
Shields Type III (Brandywine Type)
Teeth have a shell-like appearance with bell-shaped crowns.
Occurs exclusively in a isolated group in Maryland called Brandywine population
Defects occurring during APPOSITION….
35. REGIONAL ODONTODYSPLASIA(ghost teeth)
Regional odontodysplasia is a localized, nonhereditary developmental abnormality of
teeth with extensive adverse effects on the formation of enamel, dentin, and pulp.
Posterior mandibular dentition exhibiting enlarged
pulps and extremely thin enamel and dentin.
Defects occurring during APPOSITION….
36. DENTIN DYSPLASIA
Defects occurring during APPOSITION….
type II (coronal dentin dysplasia)
type I (radicular dentin dysplasia)
Two type –
37. 1. Dentin dysplasia type I (radicular dentin dysplasia)
has been referred to as rootless teeth, because the loss of organization of the root dentin often leads to a
shortened root length.
Posterior dentition exhibiting shortened roots, absence of
pulp canals, and small, crescent-shaped pulp chambers.
FEATURES-Because of the shortened roots, the initial clinical signs
are extreme tooth mobility and premature exfoliation, spontaneously or
secondary to minor trauma. Less frequently, delayed eruption is the
presenting symptom.
Defects occurring during APPOSITION….
39. Dentin dysplasia type II (coronal dentin dysplasia)
The root length is normal in both dentitions.
Radiographically, the dental changes include bulbous crowns, cervical constriction, thin roots, and early
obliteration of the pulp.
the pulp chamber exhibit significant enlargement and apical extension which is described as thistle tube–
shaped or flame-shaped.
Permanent dentition that does not exhibit translucence,
as noted in the deciduous teeth.
The patient also exhibits mild fluorosis of the enamel.
Radiographic appearance of the dentition thistle tube
shaped enlargements of the pulp chambers
Defects occurring during APPOSITION….
40. CONCRESCENCE
• Two fully formed teeth, adhered along the root surface by cementum.
• 2nd molar is frequently involved.
• Clinically radiographic diagnosis is mandatory before attempting tooth extraction.
• Deciduous dentition can result in crowding, abnormal spacing, and delayed or ectopic eruption of the
underlying permanent teeth.
Concrescence. Union by cementum of adjacent
Molars and it’s Radiograph.
Defects occurring during ROOT FORMATION……
The space restriction during development, local trauma,
excessive occlusal force or local infection after development
may be the suspected causative factors.
Dr. Jyoti S. Khedgikar, Dr. Shirish B. Khedgikar Concrescence of a Maxillary First and Second Molar: A Case Report,
Journal of Medical and Dental Science Research Volume 2 Issue 1 (2015)
41. DILACERATION
• Dilaceration refers to an abnormal angulation or a sharp
bend or curve anywhere along the root portion of a tooth
• Occurs due to trauma that displaces the calcified portion
of the tooth germ which alters the angulation of the tooth
during root formation
Root angulation of a mandibular
cuspid. Development has been altered by the presence of an
adjacent compound odontoma.(NEVILLE) (NEVILLE)
Defects occurring during ROOT FORMATION……
42. NATAL TEETH
These are extra teeth that are present at birth.
The most common natal teeth are lower incisors.
Treatment:
These teeth are defective and their removal is
generally recommended, particularly if mobility
poses a threat of aspiration.
These teeth also make feeding difficult.
Disorders of ERUPTION………..
43. NEONATAL TEETH
These are primary teeth that erupt prematurely
(during the first few weeks of life).
Treatment:
These teeth are usually normal primary teeth and
should be retained. An x-ray will be taken if
possible to confirm that these are not extra
teeth.
Disorders of ERUPTION………..
44. ERUPTION CYST (ERUPTION HEMATOMA)
The cyst develops as a result of separation of the dental follicle from around the crown of an
erupting tooth that is within the soft tissues overlying the alveolar bone.
The epithelial lining of eruption cyst is similar to that of the dentigerous cyst (non-
keratinized stratified squamous epithelium), so the eruption cyst is considered a superficial
dentigerous cyst.
This soft gingival swelling contains considerable blood
and can also be designated as an eruption hematoma
Disorders of ERUPTION………..
Preeti Dhawan et al Eruption cysts: A series of two cases Dent Res J (Isfahan). 2012 Sep-Oct; 9(5): 647–650
45. ERUPTION SEQUESTRUM
A small spicule of nonvital bone may be seen radiographically or clinically overlying the crown
of partially erupted permanent posterior tooth.
The process is termed an eruption sequestrum
It’s occurs when the osseous fragment becomes separated from the contiguous bone during
eruption of the associated tooth.
A radiopaque fragment of sequestrating bone
can be seen overlying an impacted third molar.
Disorders of ERUPTION………..
46. Turner’s Hypoplasia
Enamel defects seen in permanent teeth is caused by periapical inflammatory disease of the
overlying deciduous tooth. The altered tooth is called a Turner’s tooth.
Anterior teeth are involved less frequently because crown formation is usually complete before
the development of any apical inflammatory disease.
Extensive enamel hypoplasia of mandibular first bicuspid secondary
to previous inflammatory process associated with overlying first
deciduous molar.
Radiograph of the same
tooth
Disorders of ERUPTION………..
47. ODONTOGENIC TUMORS
I. Tumors of odontogenic epithelium
A. Ameloblastoma
1. Malignant ameloblastoma
2. Ameloblastic carcinoma
B. Clear cell odontogenic carcinoma
C. Adenomatoid odontogenic tumor
D. Calcifying epithelial odontogenic
tumor
E. Squamous odontogenic tumor
II. Mixed odontogenic
tumors
A. Ameloblastic fibroma
B. Ameloblastic fibro-
odontoma
C. Ameloblastic fibrosarcoma
D. Odontoameloblastoma
E. Compound odontoma
F. Complex odontoma
III. Tumors of odontogenic
ectomesenchyme
A. Odontogenic fibroma
B. Granular cell Odontogenic tumor
C. Odontogenic myxoma
D. Cementoblastoma
48. ODONTOGENIC KERATOCYST
odontogenic keratocyst arises from cell rests of the dental lamina.
Multiple odontogenic keratocysts sometimes associated with
nevoid basal cell carcinoma (Gorlin) syndrome
associated with mutations in the gene PTCH, which is part of
the Hedgehog signaling pathway
A
B
ODONTOGENIC CYST
Paul J.W. Stoelinga, Etiology and pathogenesis of keratocysts oral and maxillofacial surgery clinics am 15 (2003) 317-324
49. DENTIGEROUS CYST
The dentigerous cyst is defined as a cyst that originates by the separation of the follicle from
around the crown of an unerupted tooth.
The dentigerous cyst encloses the crown of an unerupted tooth and is attached to the tooth at
the cementoenamel junction.
Central type showing the
crown projecting into the cystic cavity.
Gross specimen of a
dentigerous cyst involving a tooth.
ODONTOGENIC CYST
50. Defects of structure ………….– systemic diseases
Congenital syphilis –
dental follicle infection by T. Pallidum
Diagnostic feature known as Hutchinson Triad
● Hutchinson’s teeth
● Ocular interstitial keratitis
● Eighth nerve deafness
The infection alters the formation of both the
Anterior teeth (Hutchinson’s incisors)
posterior dentition(mulberry molars, Fournier’s molars, Moon’s
molars).
Systemic disease…
51. Defects of structure …………– systemic diseases
teeth varying from bright yellow to dark brown and,
in UV light, showing a bright-yellow fluorescence
TETRACYCLINE
Diffuse brownish discoloration of the permanent dentition.
Systemic disease…
52. Defects of structure………… – systemic diseases
Fluorosis (mottled enamel)
fluoride in drinking water
yellow to dark-brown discoloration
areas of moderate-to-severe enamel fluorosis were termed mottled enamel.
Dentition exhibiting lusterless, white, and opaque enamel.
Systemic disease…
53. References…
NEVILLE, ALLEN, BOUQUOT Oral and Maxillofacial Pathology third edition
Shafer’s text book of oral and maxillofacial pathology seventh edition
Orban’s oral histology and embryology 13th edition.
Aswathy Raj,Deepa.M.S, Ahmed Hasan Farooqi GENETICS AND TOOTH ANOMALIES - AN
UPDATEOral & Maxillofacial Pathology Journal Vol. 4 No. 1 Jan - June 2013
Hattab FN, Yassin OM, Al-Nimri KS. Talon cusp in the permanent dentition associated with
other dental anomalies: Review of literature and reports of seven cases. J Dent Child
1996;63:368-76.
Danker E, Harari D, Rotstein I. Dens evaginatus of anterior teeth. Literature review and
radiographic survey of 15,000 teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
1996;81:472-76
Jan C-C. Hu, James P.,Developmental biology and genetics of dental malformations Orthod
Craniofacial Res 10, 2007; 45–52
Thaleia Kouskoura1 Natassa Fragou1 Maria Alexiou1 Nessy John2 Lukas Sommer2,The genetic
basis of craniofacial and dental abnormalities, Schweiz Monatsschr Zahnmed Vol. 121 7/8/2011
54. Preeti Dhawan et al Eruption cysts: A series of two cases Dent Res J (Isfahan). 2012 Sep-Oct; 9(5):
647–650
Dr. Jyoti S. Khedgikar, Dr. Shirish B. Khedgikar Concrescence of a Maxillary First and Second
Molar: A Case Report, Journal of Medical and Dental Science Research Volume 2 Issue 1 (2015)
Aswathy Raj,Deepa.M.S, Ahmed Hasan Farooqi GENETICS AND TOOTH ANOMALIES - AN
UPDATE Oral & Maxillofacial Pathology Journal Vol. 4 No. 1 Jan - June 2013
Kannan SK1, Suganya, Santharam HSupernumerary rootsIndian J Dent Res. 2002 Apr-Jun;13(2):116-
9
Shivani sharma et al Enamel pearl on an unusual location associated with localized periodontal
disease: A clinical report, J Indian Soc Periodontol. 2013 Nov-Dec; 17(6): 796–800
Sandhya shrivastava et al, FUSION/DOUBLE TEETH,10.5005 jp journals,10011-1200
M. Hülsmann, “Dens invaginatus: aetiology, classification, prevalence, diagnosis, and treatment
considerations,” International Endodontic Journal, vol. 30, no. 2, 79–90, 1997.
Paul J.W. Stoelinga, Etiology and pathogenesis of keratocysts oral and maxillofacial surgery clinics
am 15 (2003) 317-324
Editor's Notes
Here we focus on little about the changes in the tooth germ that lead to the range of congenital tooth abnormalities and the disturbance of the epithelial-mesenchymal interactions.
Also, splitting of a tooth germ or joining of adjacent germs can be responsible for some of the variations in tooth number and shape.
Trauma or infection to the deciduous predecessors have also been implicated in the malformation of permanent teeth.
True partial anodontia (hypodontia or oligodontia)
Studies on the frequency of missing third molars have shown this tooth to be congenitally absent in as many as 35% of all subjects examined, with a frequent absence of all four third molars in the same person .
Other studies have shown that the maxillary lateral incisors and maxillary or mandibular second premolars are commonly missing,
False anodontia-occurs as a result of extraction of all teeth.
Psuedo anodontia-is sometimes applied to multiple unerupted teeth
Supplemental (normal size and shape)
Rudimentary (abnormal shape and smaller size)
Conical (small, peg-shaped),
Tuberculate (barrel-shaped anterior with more than one
cusp)
Molariform (small premolar-like or molar like).
Defined as the size of the tooth which is smaller than the normal.
True- commonly seen in pituitary dwarfism and down syndrome. All the teeth are well formed
Relative-teeth are present in the jaw, which is some what larger than normal. And there is illusion of true microdontia
Defined as the size of the tooth which smaller than the normal.
True- associated with pituitary gigantism
Relative-teeth are present in the jaw, which is some what smaller than normal. And there is illusion of true macrodontia
It has been thought that some physical force or pressure produces contact of the developing teeth and their subsequent.
The tooth may have separate or fused root canals,
Frequently, dens evaginatus is seen in association with, shovel shaped incisors.
Enamel pearls are found most frequently on the roots of maxillary molars (mandibular molars are the second most frequent site).
Radiographically, pearls appear as well-defined, radiopaque nodules along the root’s surface.
Cud is a portion of food that returns from a ruminant's stomach to the mouth to be chewed for the second time
The DLX3 gene is in a group of genes that code for a number of proteins that are critical for craniofacial , Tooth, hair, brain, and neural development;
A, numerous pinpoint pits scattered across the surface of the teeth. The enamel between the pits is of normal thickness, and coloration.
B, Occlusal view of same patient showing diffuse involvement of all maxillary teeth, which would be inconsistent with environmental damage.
A-Dentition exhibiting grayish discoloration with significant enamel loss and attrition.
B-Radiograph of dentition exhibiting bulbous crowns, cervical constriction, and obliterated pulp canals and chambers.
These problems can affect both primary teeth and permanent teeth.
Dentition exhibiting normal thickness enamel, extremely thin dentin, and dramatically enlarged pulps
Radiographically, the altered teeth demonstrate extremely thin enamel and dentin surrounding an enlarged radiolucent pulp,resulting in a pale wispy image of a tooth; hence the term ghost teeth
Subclassifcation of Dentin DysplasiaType I
DDIa: No pulp chambers, no root formation,
DDIb: A single small horizontally oriented and crescent-shaped pulp, roots only a few millimeters in length,
DDIc: Two horizontally oriented and crescent-shaped pulpal remnants surrounding a central island of dentin, significant but shortened root length,
DDId: Visible pulp chambers and canals, near normal root length, enlarged pulp stones that are located in the coronal portion of the canal and create a localized bulging of the canal and root, constriction of the pulp canal apical to the stone,.
The deciduous teeth closely resemble those of dentinogenesis imperfecta.
The eruption cyst is the soft tissue analogue of the dentigerous cyst
Mild sensitivity is noted in the area, especially during eating.
A, Large unilocular radiolucency associated with the right mandibular third molar.
B, Six months after insertion of a polyethylene drainage tube to allow decompression, the cyst has shrunk and the third molar has migrated downward and forward.
Hutchinson’s incisors of congenital syphilis.Dentition exhibiting crowns tapering toward the incisal
edges. tooth resembles a straightedge screwdriver
Mulberry molar of congenital syphilis. Maxillary molar demonstrating occlusal surface with numerous globular
projections.