The document provides an overview of tooth development from prenatal development through adulthood. It discusses the key stages of development including initiation of tooth buds during the 6th week of prenatal development, proliferation of the dental lamina forming tooth buds by the 8th week, and the subsequent stages of crown and root formation through odontogenesis. Tooth eruption begins around 6 months of age for primary teeth and continues in a sequential pattern until adulthood when all 32 permanent teeth have erupted.
Introduction
Evolutionary Concept of dentition
Prenatal development of human dentition
Eruptive tooth movement
Phases of occlusion development
Pre-dental period
Deciduous dentition period
Mixed dentition period
Permanent dentition period
Transient malocclusions
Andrews six keys of occlusion
References
Introduction
Evolutionary Concept of dentition
Prenatal development of human dentition
Eruptive tooth movement
Phases of occlusion development
Pre-dental period
Deciduous dentition period
Mixed dentition period
Permanent dentition period
Transient malocclusions
Andrews six keys of occlusion
References
Development of dentition. /certified fixed orthodontic courses by Indian dent...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.
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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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
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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Letter to MREC - application to conduct studyAzreen Aj
Application to conduct study on research title 'Awareness and knowledge of oral cancer and precancer among dental outpatient in Klinik Pergigian Merlimau, Melaka'
QA Paediatric dentistry department, Hospital Melaka 2020Azreen Aj
QA study - To improve the 6th monthly recall rate post-comprehensive dental treatment under general anaesthesia in paediatric dentistry department, Hospital Melaka
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
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
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
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.
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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!
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.
2. CONTENTS
• Overview of prenatal development
• Facial development
• Dentition period - primary, mixed, permanent
• Tooth development & eruption (odontogenesis)
• Common dental disturbances
3. OVERVIEW OF PRENATAL DEVELOPMENT
• In human, prenatal development begins at the start of
pregnancy & continues until birth of the child
**pregnancy → birth
• Prenatal development consists of 3 periods :
1. Preimplantation period
2. Embryonic period
3. Fetal period
4. Periods of prenatal development
Preimplantation period
(1st week)
Embryonic period
(2nd-8th week)
Fetal period
(3rd-9th month)
6. Developmental disturbances during prenatal development
• preimplantation & embryonic period (1st trimester of pregnancy) is the most
critical period of development
• developmental disturbances during this period may cause major congenital
malformations of embryo (birth defects) which evident at birth
• any teratogens can cross placenta & present during active differentiation of
organ or tissue which may lead to tissue malformations
• tissue malformations can be due to :
*genetic factors → chromosome abnormalities
*environmental factors → infections (:rubella, syphilis), radiation, chemicals,
drugs (alcohol, thalidomide, tetracycline)
7. FACIAL DEVELOPMENT
• Facial development begin to form during 4th week of prenatal period
(within embryonic period)
• During 4th week, face & neck begin to develop with the primittive
eyes, ears, nose, oral cavity & jaw areas
• Facial development derives from 5 facial processes that form during
4th week :
→single frontonasal process
→paired maxillary & mandibular processes
8. • These facial processes become centers of facial growth :
*frontonasal process → upper part of face
*maxillarry processes → midface
*mandibular processes → lower part of face
12. Pharyngeal / branchial arches
• structures seen during embryonic
development that are precursors for
many structures
• in human embryo, the arches are first
seen during 4th week of
development
• derived from 3 embryonic layers :
→ ectoderm, mesoderm, endoderm
• development of pharyngeal arches
relies on contribution from
ectoderm, mesoderm, endoderm &
neural crest cells
• failure of pharyngeal arches
correctly develop results in
anatomical, developmental defects
14. 1st pharygeal arch
• a.k.a. mandibular arch
• develop during 4th week of prenatal
period
• located bw stomodeum & 1st pharyngeal
groove
• this arch divides into maxillary &
mandibular process :
*maxillary process → maxilla
*mandibular process → mandible
• Meckel's cartilage (located in mandibular
process) act as a “template” of mandible
formation (perichondral ossification)
15.
16. TOOTH DEVELOPMENT & ERUPTION
• Odontogenesis = process of tooth development, eruption & integration with
its surrounding tissues
• 2 types dentitions :
→ primary
→ permanent
• Primary dentition develops during prenatal period - consists of 20 teeth
which erupt & are later shed
• As primary teeth are shed - jaws grow & mature - permanent dentition
(consists of 32 teeth) gradually erupt & replaces primary dentition
• Overlapping period bw primary & permanent dentition → mixed dentition
17. • during odontogenesis, many physiological processes occurs -
initiation, proliferation, differentiation, morphogenesis & maturation
• not all teeth in each dentition begin to develop at the same time
• initial teeth for both dentitions develop in anterior mandibular region
→ anterior maxillary region → progresses posteriorly in both jaws
• this posterior mvt of odontogenesis allows time for the jaws to grow
accomodate the increased number of primary teeth, larger primary
molars & finally overall larger permanent teeth
18. Primary dentition
• Primary tooth buds formation → 6th week of prenatal period
• Primary teeth begin to erupt → 6 mth
• Eruption time for primary teeth → 6 mth – 3 yo
19. • Sequence of primary teeth eruption :
A → B → D → C → E
• Sequence of primary teeth loss :
A → B → D → C → E
Primary dentition
20.
21. • tooth formation occurs as early as 6th week of prenatal period when jaws
have assumed their initial shape - but during this time jaws are small
• development of primary & permanent teeth continues in this period ; jaws
grow follows the need for additional space posteriorly for additional teeth
• alveolar bone height ↑ to accomodate the ↑ length of teeth
• growth of anterior parts of jaws is limited after 1st year of postnatal life
• at birth, usually no teeth visible in mouth
22. Interdental spacing
• Primary teeth generally shows some
degree of interdental spacing
• Spacing in primary dentition is important
for proper alignment of permanent
dentition
• Absent of spaces in primary dentition
can cause crowding in permanent
dentition
23. • Interdental spacing of primary teeth determines chances of
crowding in permanent dentition
,,,,
24. Mixed (transitional) dentition
• Transition from primary to permanent dentition begins with
emergence of :
→perm.mand.central incisors (6 yo)
→1st perm.molars (6-7 yo)
25. Early mixed dentition in a child with full set of primary teeth
& first permanent molars
A. Maxilla B. Mandible
26. Arch dimensions & tooth size
• Important part of dental arch in development occlusion of permanent dentition is
the premolar segment
• In this section, the erupting premolars are smaller in mesiodistal dimension
than primary molars, which they replace
• The difference is related to the Leeway space or amount of space gained by
difference in the mesiodistal dimensions of the premolars and the primary
molars
27.
28. Leeway space = difference in mesiodistal width bw primary teeth (C,D,E) &
permanent teeth (3,4,5)
Arrows indicate mesial movement of the perm.molars after loss of primary molars &
eruption of 2nd perm.premolar
29. Permanent dentition
• Sequences of eruption in maxilla :
6-1-2-4-3-5-7-8 & 6-1-2-4-5-3-7-8
• Sequences of eruption in mandible :
(6-1)-2-3-4-5-7-8 & (6-1)-2-4-3-5-7-8
30.
31. Mechanisms of tooth eruption
• 4 main factors :
-eruption path
-eruption force
-PDL capacity to adapt with eruptive movement
-quality of alveolar bone
32. Eruption path
-available, sufficient, no obstruction
-regulated by dental follicle
-alveolar bone formation & resorption occuring around
erupting tooth are regulated by dental follicle
-disturbance of dental follicle can cause failure / delay /
deflected path of tooth eruption
33. Eruption force
-comes from elongation of roots
*tooth normally erupt when they have reached 2/3 rd root length
-root elongated & pushing against immovable base
*root formation will increase tooth length - must be accommodated by
increase in jaw height & tooth crown moving occlusally
34. PDL capacity to adapt with eruptive movement
-PDL must be able to adapt with eruptive tooth mvt
-in certain conditions (-ankylosis, hypercementosis),
PDL unable to adapt with eruptive tooth mvt causes failure
of tooth eruption
35. Quality of alveolar bone
-alveolar bone malformation can disturb tooth eruption
Eg : osteopetrosis (marble bone disease)
Bones harden, denser
36. Tooth movement
• For teeth to become functional, movement is required to
bring them into occlusal plane
• 3 types of tooth mvt :
1. Pre-eruptive mvt
2. Eruptive mvt
3. Post-eruptive mvt
37. Pre-eruptive movement
• Occurs in primary & permanent tooth germs before they
begin to erupt
• Is a movement required to place teeth within jaw in a
position for eruptive movement
• Combinations of 2 factors :
1. Bodily mvt of tooth germs
2. Jaw growth
38. • When deciduous tooth germs first differentiate, they are
small
• Then, they grow rapidly & become crowded
• This crowding is alleviated by jaw growth
• Permanent tooth germs develop on lingual aspect of
primary teeth in the same bony crypt
39. Eruptive movement
• Tooth move from its position within jaw bone to its
functional position in occlusion
• During eruptive phase, significant developmental
changes occur – formation of roots, PDL, DEJ
• Once tooth erupt into oral cavity, it continues to erupt at
same rate of about 1mm every 3 mths & slowing as it
meets its antagonist in opposing arch
40. • Once it appears in oral cavity, it is subjected to
environmental factos that will determine its final position
in dental arch
Eg : muscle forces from tongue, cheeks, lips
forces of contact of erupting tooth with other erupted teeth
thumbsucking habit
41. Post-eruptive movement
• 3 types :
1. Movements to accommodate with growing jaws
-to keep pace with increasing jaws height
2. To compensate for continued occlusal wear
-compensation occurs by continuous deposition of cementum around tooth apex
3. To accommodate interproximal wear
-compensated by mesial or approximal drift
42. A. Crown formation :
1. Initiation stage
2. Bud stage
3. Cap stage
4. Bell stage
5. Apposition & maturation
stages
B. Root development :
1. Root dentin formation
2. Cementum & pulp formation
3. Periodontal ligament &
alveolar bone development
ODONTOGENESIS
47. -dental lamina grow /proliferate
into bud, penetrating into
growing mesenchyme
-at the end of proliferation
involving primary dentition's
dental lamina, both future max
& mand arch will each have
10 buds
-each of these buds +
surrounding mesenchyme
→ tooth germ & supporting
tissues
BUD STAGE : (8th week of prenatal period)
mesenchyme
ectoderm (oral epithelium)
dental lamina (bud)
48. BUD STAGE
*proliferation of dental
lamina into growing
mesenchyme in the
form of buds, the
future tooth germs
49. -depression in the deepest part of dental
lamina forming cap or enamel organ
*enamel organ → future enamel
*enamel organ derived from ectoderm
-enamel organ will surround mass of
mesenchyme (dental papilla)
*dental papilla → future dentin & pulp
-basement membrane still exists bw enamel
organ & dental papilla → future DEJ
(dentinoenamel juction)
-mesenchyme surrounding enamel organ
→ dental follicle / dental sac
*dental follicle → periodontium (PDL,
cementum, alveolar bone)
CAP STAGE : (9-10th weeks of prenatal period)
enamel organ (cap)
dental papilla
basement
membrane
dental follicle (sac)
50. CAP STAGE
*Tooth germ :
-enamel organ
-dental papilla
-dental sac (follicle)
*developing primordium
of permanent
succedaneous tooth
lingual to primary tooth
germ (in bud stage)
51. -enamel organ differentiate into bell & consists of
4 types of cells :
*OEE (outer enamel epithelium)
*IEE (inner enamel epithelium)
*stellate reticulum
*stratum intermedium
-dental papilla differentiate & consists of
2 types of cells :
*outer cells of dental papilla
*central cells of dental papilla
**outer cells of dental papilla → odontoblasts (secrete dentin matrix)
**central cells of dental papilla → pulp
BELL STAGE : (11-12th weeks of prenatal period)
52. BELL STAGE : (11-12th weeks of prenatal period)
-basement membrane
remains bw IEE & dental
papilla
-dental sac will increases
in amount of collagen
fibers & differentiate into
periodontium during later
period than enamel organ
& dental papilla
53. APPOSITION STAGE :
-enamel, dentin, cementum are
secreted in successive layers as a
matrix
APPOSITION & MATURATION STAGE
MATURATION STAGE :
-dental tissues (matrix) fully
mineralize to mature form
54. Formation of Preameloblasts
• IEE will diffrentiate → preameloblasts
• premaeloblasts will later on secrete
enamel matrix
55. Formation of Odontoblasts & Dentin Matrix
• preameloblasts will induce outer
cells dental papilla to
differentiate into odontoblasts
• odontoblasts will begin
odontogenesis → apposition of
dentin matrix (predentin)
• odontoblasts secrete dentin
matrix before production of
enamel matrix
56. Formation of Ameloblasts, Dentinoenamel Junction &
Enamel Matrix
• after apposition of predentin, basement membrane bw
preameloblasts & odontoblasts disintegrates
• preameloblasts will come into contact with predentin -
will induce preameloblasts diffrentiate into ameloblasts
• ameloblasts begin amelogenesis (apposition of enamel
matrix)
• enamel matrix is secreted from Tome's process (of
ameloblasts)
• enamel matrix in contact with predentin
• mineralization of disintegrating basement membrane
forming DEJ (dentinoenamel junction)
• odontoblasts will leave odontoblastic process in
predentin area - each odontoblastic process is contained
in dentinal tubules
• calcification or maturation of matrix occurs later (different
process for both enamel & dentin)
57. ROOT DEVELOPMENT
• root development takes place after crown is completely
shaped & tooth starting to erupt into oral cavity
• structure responsible for root development is the cervical loop
• cervical loop is the most cervical portion of enamel organ,
consists of IEE (inner enamel epithelium) & OEE (outer
enamel epithelium)
58. • cervical loop will grow deeper into mesenchyme of dental
sac, elongating & moving away from crown area to enclose
more of dental papilla tissue & form Hertwig's root sheath
(HERS)
**cervical loop → HERS
• function of this sheath is to shape the root & induce dentin
formation in root area, so that it is continuous with coronal
dentin
59.
60. ROOT DENTIN FORMATION
• root dentin forms when outer cells of dental papilla (in root
area) are induced to undergo differentiation & become
odontoblasts (under influence of IEE of HERS)
• these cells undergo dentinogenesis & begin to secrete
predentin
• when root dentin formation is completed, the entire HERS will
disintegrates & become epithelial rests of Malassez
61. outer cells of dental
papilla differentiate into
odontoblasts &
apposition of dentin in
root area
when root dentin
formation is completed,
the entire HERS will
disintegrates & become
epithelial rests of
Malassez
62. CEMENTUM & PULP FORMATION
• Cementogenesis (apposition of cementum) occurs after
HERS disintegrates
• induction of dental sac / follicle cells to differentiate into
cementoblasts
• cementoblasts produce cementum matrix (cementoid)
• many cementoblasts become entrapped by cementum matrix
& become mature cementocytes
• as cementum matrix surrounding the cementocytes
becomes calcified or matured → cementum
• central cells of dental papilla → pulp
63. *after HERS
disintegration, dental sac
cells differentiate into
cementoblasts
*cementoblasts produce
cementum matrix
*cementoblasts
entrapped in cementum
matrix & become
cementocytes
64. PERIODONTAL LIGAMENT &
ALVEOLAR BONE DEVELOPMENT
• as crown & root develop, surrounding supporting tissues of tooth are
also developing
• mesenchyme from dental sac / follicle begins to form periodontal
ligament (PDL) adjacent to newly formed cementum
• ends of these fibres insert into outer portion of cementum &
surrounding alveolar bone to support tooth
• mesenchyme of dental sac also begins to mineralize to form tooth
sockets surrounding the PDL
65. PRIMARY TOOTH ERUPTION & SHEDDING
• eruption of primary tooth involves active vertical movement of tooth
• after enamel apposition ceases in crown area, layers of enamel organ
are compressed, forming reduced enamel epithelium (REE)
*enamel organ → REE
• REE fuses with oral epithelium in oral cavity
• REE produce enzymes that cause disintegration of area of fused
tissues, creating a tunnel for tooth movement & eruption into oral cavity
• tissue disintegration causes an inflammatory response known as
“teething” which accompanied by tenderness & edema of local tissues
66. • as tooth erupts, coronal fused tissues detached from the crown, leaving cervical
portion still attached to neck of tooth
• this fused tissue that remain near CEJ after tooth erupts, serves as initial
junctional epithelium (JE) & later replaced by definitive JE as root is formed
• primary tooth is then exfoliated, as permanent tooth erupts lingual to it
• the process of primary tooth loss involves :
→ resorption of alveolar bone bw the two teeth (by osteoclasts)
→odontoclasts resorb primary tooth's root dentin, cementum & small portions of
enamel crown
67. PERMANENT TOOTH ERUPTION
• permanent tooth erupt in a position lingual to roots of
shedding primary tooth
• eruption process = primary tooth
• permanent tooth starts to erupt before primary tooth is fully
shed
68. A. before eruption process begins
- REE covers newly formed
enamel
B. REE fused with oral epithelium
C. disintegration of fused tissue,
leaving a tunnel for tooth
movement & eruption
D. as tooth erupts, coronal fused
tissues detached from the crown,
leaving cervical portion still
attached to neck of tooth
69. COMMON DENTAL DISTURBANCES
Initiation stage :
Hypodontia
*absence of single or multiple teeth
*perm.max.lateral incisor, 3rd molar, mand.2nd premolar
*result from endocrine dysfuntion, systemic disease, excess
radiation
*may be a/w syndrome of ectodermal dysplasia
70. Supernumerary / hyperdontia
*development of one or extra teeth
*extra teeth are initiated from dental lamina
*commonly found → bw maxillary central incisors,
distal to 3rd molars & premolar region
*may cause crowding, failure of normal eruption & disrupt
occlusion
79. Bud stage :
Micro / macrodontia
*abnormally small or large teeth
*cause → abnormal proliferation may cause tooth to be larger or
smaller than normal
*commonly affects perm.Max.lateral incisor & 3rd molars
*complete micro / macrodontia rarely occurs & can be due to
dysfunction of pituitary gland
81. Cap stage :
Dens in dente (dens invaginatus)
*enamel organ invaginates into dental papilla
*a.k.a “tooth within a tooth”
*commonly affects perm.max.lateral incisor ;
***due to external forces applied on lateral incisor tooth bud by developing central incisor or
canine which develops earlier
*may have deep lingual pit in area of invagination - may lead to pulp exposure
+ pathology → may need endodontic therapy
*r/g → tooth within a tooth
84. Germination
*single tooth germ tries to divide into two tooth germs (unsuccessful
division)
*large single-rooted tooth with one pulp cavity
*exhibits “twinning” in crown area
*appearance of splitting / cleft in the incisal surface, resembling 2 crowns
*number of teeth in dentition is normal
*usually occurs in anterior teeth (primary / permanent dentition)
*problem in appearance & spacing
87. Fusion
*union of 2 adjacent tooth germs, possibly due to pressure in the area
*large tooth with 2 pulp cavities
*lack amount of tooth in dentition
*fusion occurs only in crown area, but it can involve both crown & root
*common → anterior teeth
*problems in appearance & spacing
89. Dens evaginatus (extra cusps)
*presence of extra cusp in a form of tubercle
**tubercle usually contain pulp tissue
*arise from occlusal or lingual surface of tooth
*a.k.a Talon cusp (anterior teeth) or Leong’s premolar (premolars)
*causes → trauma, pressure, metabolic disease that affects enamel
organ forming the crown area
93. AMELOGENESIS IMPERFECTA
• hereditary, positive family history
• 2 major types :
→hypoplastic
→hypomineralization / hypomaturation
• affect primary & permanent dentitions
• most of enamel on all teeth is involved
94. Hypoplastic type :
• ↓ volume enamel matrix, normal mineralization
• enamel - thin & hard
• generalized pitting, grooving of enamel
95. Hypomineralization / hypomaturation type :
• enamel matrix volume is normal, ↓ mineralization
• enamel - normal thickness, but soft & porous
• mottled, opaque, yellow-brownish appearance
• rapidly lost by abrasion, attrition exposing the dentin
97. MOLAR-INCISOR HYPOMINERALIZATION (MIH)
• mineralization / maturation of enamel matrix is affected
• enamel - normal thickness, but soft & porous
• cause → disturbance in ameloblasts activity which
disturbs the amelogenesis
• enamel is opaque, yellow-brownish appearance
• enamel easily breakdown, more prone to caries
• localized - affect several teeth (usu.molar & incisor)
99. Cementum formation stage :
Concrescence
*union of root structure of 2 or more teeth by cementum
*common - permanent max.molars
*teeth involved are originally separate but join because of
excessive cementum deposition
*causes - traumatic injury or crowding of teeth in area
during apposition & maturation stage of tooth development
*problems during extraction & endodontic treatment
102. Root formation stage :
Enamel pearl
*causes : displacement of ameloblasts to root area, causing enamel
to be abnormally formed on cemental root surface
*small, spherical enamel projections on root surface, especially at
CEJ or in furcation area on molars
*they may have a tiny dentin & pulp core - appear radiopaque on
radiographs
*it may be confused with a calculus deposit upon exploration of root
surface - but cannot be removed
103. Dilaceration
*distorted root or crown angulation
*results from distortion of HERS due to injury or pressure
*can cause problem during extraction & endodontic therapy
104. Taurodontism
*bull like tooth
*pulp chamber has greater apico-occlusal height than in
normal teeth, with no constriction at level of CEJ
*result in chamber extend apically, beyond neck of tooth
*affects multirooted tooth
*cause → failure of HERS to invaginate at proper horizontal
level
105. Accessory roots
*may be due to trauma, pressure or metabolic disease that
affects HERS
*can affect any tooth, but commonly in permanent 3rd molar
*problems in extraction & endodontic therapy
113. Dentin formation stage :
Dentinogenesis Imperfecta
*type I, II, III
***type I - a/w Osteogenesis Imperfecta
***type II - only teeth affected
*genetic
*affect - primary & permanent dentition
*teeth have normal contour with opalescent, translucent apperance
*↓dentin hardness causing rapid attrition of teeth following enamel loss
*r/g → blunt roots with partial / total obliteration pulp chamber & root canal by
dentin
*HPE → dentinal tubules -↓number, wide, irregular
→√ areas of atubular / abnormal dentin that may partly / totally obliterates
pulp chamber & root canal
121. • Ankylosis - fusion of root dentin to alveolar bone
(delayed exfoliation of deciduous tooth → delayed
tooth eruption)
• Arch length deficiency - space loss → crowding
impactions
125. FLUOROSIS
• ingestion of excess fluoride during period of tooth formation
• severity depends on amount fluoride ingested, duration &
timing of exposure
• generalized mottled appearance of teeth ; yellow-brownish-
black discoloration
• enamel → hypomineralization of subsurface enamel or
hypoplastic pitting
• can affect primary & permanent dentition
127. NATAL & NEONATAL TEETH
• natal teeth = teeth present at birth
• neonatal teeth = teeth erupted within 1st mth of life (day 1-30)
• can be supernumerary or primary mandibular incisors
• problems :
→mobility
→ulceration of tongue
→difficulty in breastfeeding
129. TETRACYCLINE STAINING
• systemic tetracycline therapy of pregnant women during
fetal period of prenatal development
• may result in permanent tetracycline staining in primary
teeth that are developing at that time
• intrinsic yellow-brown staining of teeth
• antibiotic bound to dentin & because the transparency of
enamel, the stain is visible
• can also affect permanent teeth if drug is given during their
development