This document summarizes various dental anomalies and disturbances in development. It describes microdontia, macrodontia, anodontia, supernumerary teeth, disturbances in eruption such as premature/delayed eruption and impacted teeth. It also discusses taurodontism, dens invaginatus, gemination, fusion and other dental anomalies affecting shape and structure. Environmental factors that can affect enamel development are described. Finally it summarizes disturbances in dentin formation including dentinogenesis imperfecta.
Dentin dysplasia (DD) is a rare hereditary disturbance is inherited as an autosomal dominant trait.
unknown etiology that affects approximately 1 :100,000.
In 1972, Witkop classified it into type I and type II which affect both dentitions.DD Type I
Radicular dentin dysplasia
Characterized by:-
1.Both dentitions are affected.
2.Normal appearing crowns
3.No or only rudimentary root development (rootless teeth)
4.Incomplete or total obliteration of the pulp chamber.
5.Teeth may exhibit extreme mobility and exfoliate prematurely.DD type II
coronal dentin dysplasia
Characterized by:-
1.partial pulpal obliteration.
2.Thistle-tube-or flame-shaped coronal pulp chambers
3. Thread-like root canals
4. Usually the absence of periapical radiolucencies.
5. In this type of anomaly, teeth roots are of normal shape and contour.The enamel and the immediately subjacent dentin appear normal.
Deeper layers of dentin show an atypical tubular pattern with an amorphous, atubular area, and irregular organization.
Normal dentinal tubule formation appears to have been blocked so that new dentine forms around obstacles and takes on the characteristic appearances described as “lava flowing around boulders”The radiograph revealed features of dentine dysplasia type I with normal appearance of crown but no root development Autosomal Dominant Disorder:
Manifested in heterozygous states
At least one parent of index case is usually affected
Both males and females are affected.
Clinical feature can be modified by variation in penetrance and expressivity. Some individual inherit the mutant gene but are phenotpically normal. This is reffered to as “incomplete penetrance”.
In many condition the age of onset is delayed.
Inheritance Pattern:
Typical pattern is a heterozygous affected parent with a homozygous unaffected parent.
Every child has one chance in two of having the disease
Both sexes are affected equally..Autosomal Recessive Disorder
Largest category of Mendelian disorder
Usually does not affect the parent of the affected individual, but sibling may show the disease.
Complete penetrance is common.
Onset is frequently early in life.
Usually affect enzymatic proteins.
Pattern Of Inheritance:
Typical pattern is two heterozygous unaffected (carrier) parent.
The triat does not usually affect the parent, but siblings may show the disease
Siblings have one chance in four of being affected
Both sexes affected equally.
Dentin dysplasia (DD) is a rare hereditary disturbance is inherited as an autosomal dominant trait.
unknown etiology that affects approximately 1 :100,000.
In 1972, Witkop classified it into type I and type II which affect both dentitions.DD Type I
Radicular dentin dysplasia
Characterized by:-
1.Both dentitions are affected.
2.Normal appearing crowns
3.No or only rudimentary root development (rootless teeth)
4.Incomplete or total obliteration of the pulp chamber.
5.Teeth may exhibit extreme mobility and exfoliate prematurely.DD type II
coronal dentin dysplasia
Characterized by:-
1.partial pulpal obliteration.
2.Thistle-tube-or flame-shaped coronal pulp chambers
3. Thread-like root canals
4. Usually the absence of periapical radiolucencies.
5. In this type of anomaly, teeth roots are of normal shape and contour.The enamel and the immediately subjacent dentin appear normal.
Deeper layers of dentin show an atypical tubular pattern with an amorphous, atubular area, and irregular organization.
Normal dentinal tubule formation appears to have been blocked so that new dentine forms around obstacles and takes on the characteristic appearances described as “lava flowing around boulders”The radiograph revealed features of dentine dysplasia type I with normal appearance of crown but no root development Autosomal Dominant Disorder:
Manifested in heterozygous states
At least one parent of index case is usually affected
Both males and females are affected.
Clinical feature can be modified by variation in penetrance and expressivity. Some individual inherit the mutant gene but are phenotpically normal. This is reffered to as “incomplete penetrance”.
In many condition the age of onset is delayed.
Inheritance Pattern:
Typical pattern is a heterozygous affected parent with a homozygous unaffected parent.
Every child has one chance in two of having the disease
Both sexes are affected equally..Autosomal Recessive Disorder
Largest category of Mendelian disorder
Usually does not affect the parent of the affected individual, but sibling may show the disease.
Complete penetrance is common.
Onset is frequently early in life.
Usually affect enzymatic proteins.
Pattern Of Inheritance:
Typical pattern is two heterozygous unaffected (carrier) parent.
The triat does not usually affect the parent, but siblings may show the disease
Siblings have one chance in four of being affected
Both sexes affected equally.
Success of any dental procedure is determined by a good isolation. Here is a seminar on how to isolate the oral cavity from fluids and maintain a good dry field while working on a patient
The presentation expalin major anomilies terminology and it's classification according to the site as: jaws, palate, lips gingivae, tongue, salivary gland, line of fusion and teeth
Success of any dental procedure is determined by a good isolation. Here is a seminar on how to isolate the oral cavity from fluids and maintain a good dry field while working on a patient
The presentation expalin major anomilies terminology and it's classification according to the site as: jaws, palate, lips gingivae, tongue, salivary gland, line of fusion and teeth
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Inflammatory gingival hyperplasia is an inflammatory restraint to local irritant correlating with the gingiva; the irritant could be microbial like plaque and calculus.
Clinically present as deep red or bluish, considerably friable and fine with smooth glossy surface and commonly bleed easily [1].
These conditions are presented with the epithelial to mesenchymal transition (EMT), where the basal lamina show disruptions and epithelial cells migrate into connective tissue and change their phenotypes to fibroblast-like cells [12].
Many evidences that CSCs also play a central role in the pathogenesis and progression of carcinomas of the head and neck (HNSCC), including OSCC,have been found.
Early tissue culture studies showed that only a subpopulation of OSCC cells can form expanding tumor colonies, suggesting that human OSCC may contain some form of stem cells and it was subsequently shown that only a small subpopulation of the cells in OSCC corresponds to tumor-initiating cells.
These finding are in accordance with CSCs concept (17,34) that the tumor mass is a mixture of (a) CSCs dividing themselves to feed the tumor's growth, b) transient amplifying cells that divide themselves a few times before maturing into (c) differentiated tumor cells that do not contribute to tumor growth (4).
The isolation of CSCs from oral cancers has mainly been performed with the CD44 marker that was initially used to isolate breast cancer CSCs.
Many evidences that CSCs also play a central role in the pathogenesis and progression of carcinomas of the head and neck (HNSCC), including OSCC,have been found.
Early tissue culture studies showed that only a subpopulation of OSCC cells can form expanding tumor colonies, suggesting that human OSCC may contain some form of stem cells and it was subsequently shown that only a small subpopulation of the cells in OSCC corresponds to tumor-initiating cells.
These finding are in accordance with CSCs concept (17,34) that the tumor mass is a mixture of (a) CSCs dividing themselves to feed the tumor's growth, b) transient amplifying cells that divide themselves a few times before maturing into (c) differentiated tumor cells that do not contribute to tumor growth (4).
The isolation of CSCs from oral cancers has mainly been performed with the CD44 marker that was initially used to isolate breast cancer CSCs.
Clinical Description
Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia representing a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities), to mild CCD, to isolated dental anomalies without other skeletal features [Golan et al 2000]. Most individuals are diagnosed because they have classic features. CCD spectrum disorder affects most prominently those bones derived from intramembranous ossification, such as the cranium and the clavicles, although bones formed through endochondral ossification can also be affected. Cooper et al [2001] recorded the natural history of 90 probands and 56 first- and second-degree relatives; findings highlight the clinical variability of this condition within affected members of the same family who harbor the same pathogenic variant. Roberts et al [2013] reviewed their experience with more than 100 affected individuals in South Africa.
Classic CCD. The most prominent clinical findings in individuals with classic CCD are listed in Suggestive Findings and include: abnormally large, wide-open fontanelles at birth that may remain open throughout life; clavicular hypoplasia resulting in narrow, sloping shoulders that can be opposed at the midline; and abnormal dentition
Further medical problems identified in individuals with CCD spectrum disorder include short stature, skeletal/orthopedic findings, dental complications, ENT complications, endocrine findings, and mild developmental delay.
Molecular Pathogenesis
RUNX2 encodes runt-related transcription factor 2 (RUNX2), a transcription factor involved in osteoblast differentiation and skeletal morphogenesis. RUNX2 is essential for osteoblast differentiation during intramembranous ossification as well as chondrocyte maturation during endochondral ossification [Zheng et al 2005]. RUNX2 contains an N-terminal stretch of consecutive polyglutamine and polyalanine repeats known as the Q/A domain, a runt domain, and a C-terminal proline/serine/threonine-rich (PST) activation domain. The runt domain is a 128-amino-acid polypeptide motif originally described in the Drosophila runt gene that has the unique ability to independently mediate DNA binding and protein heterodimerization [Zhou et al 1999].
The majority of RUNX2 pathogenic variants in individuals with classic CCD affect the runt domain and most are predicted to abolish DNA binding [Lee et al 1997, Mundlos et al 1997, Otto et al 2002]. Pathogenic missense variants cluster at arginine 225 (p.Arg225) of RUNX2, a critical residue for RUNX2 function. In vitro studies have shown that pathogenic missense variants at p.Arg225 interfere with nuclear accumulation of RUNX2.
Hypomorphic RUNX2 alleles with partial loss of protein function, c.90dupC and c.598A>G, are associated with mild CCD, isolated dental anomalies, and significant intrafamilial variability.
Mechanism of disease causation. Loss of function
RUNX2-sp
Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia representing a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities), to mild CCD, to isolated dental anomalies without other skeletal features [Golan et al 2000]. Most individuals are diagnosed because they have classic features. CCD spectrum disorder affects most prominently those bones derived from intramembranous ossification, such as the cranium and the clavicles, although bones formed through endochondral ossification can also be affected. Cooper et al [2001] recorded the natural history of 90 probands and 56 first- and second-degree relatives; findings highlight the clinical variability of this condition within affected members of the same family who harbor the same pathogenic variant. Roberts et al [2013] reviewed their experience with more than 100 affected individuals in South Africa.
Wound healing is a highly dynamic process and involves complex interactions of extracellular matrix molecules, soluble mediators, various resident cells, and infiltrating leukocyte subtypes.
The immediate goal in repair is to achieve tissue integrity and homeostasis
PV is caused by autoantibodies that target cadherins, specifically desmogleins, though there may be some role for desmocollin; thus, this is a type 2 hypersensitivity reaction.[24][25] Acantholysis, or the loss of keratinocyte–keratinocyte adhesion, is interrupted by circulating IgG autoantibodies to intercellular adhesion molecules.[26][27] Acantholysis is seen as a result of the autoantibodies destroying the intracellular connections, leading to bullae that can easily rupture (known clinically as the Nikolsky sign).
A “super-compensation hypothesis” recently submitted by Sinha et al. proposes that additional factors may also play a role in PV.[28] Multiple mechanisms for antibody-induced acantholysis have been suggested, including the induction of signal transduction and the inhibition of adhesive molecule function through steric hindrance, which can trigger cell separation.[29] The pathogenesis of PV has been described in more detail by Hammers et al.[30]
In patients with PV, autoantibodies against desmoglein 1 (Dsg 1) and desmoglein 3 (Dsg 3) is the purported cause.[31] Desmogleins are transmembrane glycoproteins that are an integral part of desmosomes which, in part, are required for cell–cell adhesion via interaction with intermediate filaments. The most common targets of desmoglein for IgG antibodies are the extracellular cadherin domains, which can result in the loss of desmosome-adhesive properties. These signaling pathways trigger endocytosis, depletion, and direct inhibition of Dsg 3 interactions.[32] It is generally believed that the amino portion of the cadherin proteins is most implicated in the pathogenesis of acantholysis leading to PV.[33]
Many animal models have shown that enzymatic inactivation of Dsg 1 and gene deletion of Dsg 3 results in pathology similar to PV.[34][35] This phenomenon was observed to be dose-dependent and suggests that reducing the circulating levels of IgG against Dsg 1 and Dsg 3 can improve patient outcomes.[36] In patients with primarily cutaneous disease, Dsg 1 likely plays a role more superficially, whereas Dsg 3 is more likely to be found in deeper cutaneous structures and mucous membranes.[37][38] The implication is that Dsg 3 can compensate for the absence of Dsg 1 in mucosal structures (thus demonstrating PV in cutaneous lesions only). In contrast, Dsg 1 without Dsg 3 is insufficient to manage mucous membranes or cutaneous lesions alone, implying that Dsg 1 is in lower proportion in mucous membranes.
The binding of antibodies to desmogleins has been confirmed by epitope mapping and is presumed to disrupt desmoglein binding by affecting steric hindrance.[39] Another theory for the pathophysiology of PV is the desmoglein nonassembly depletion hypothesis. This theory suggests that autoantibodies not only bind desmoglein but that they also bind each other, leading to crosslinking and the inability of desmosomes to maintain cell–cell adhesion.[40][41]
PV is caused by autoantibodies that target cadherins, specifically desmogleins, though there may be some role for desmocollin; thus, this is a type 2 hypersensitivity reaction.[24][25] Acantholysis, or the loss of keratinocyte–keratinocyte adhesion, is interrupted by circulating IgG autoantibodies to intercellular adhesion molecules.[26][27] Acantholysis is seen as a result of the autoantibodies destroying the intracellular connections, leading to bullae that can easily rupture (known clinically as the Nikolsky sign).
A “super-compensation hypothesis” recently submitted by Sinha et al. proposes that additional factors may also play a role in PV.[28] Multiple mechanisms for antibody-induced acantholysis have been suggested, including the induction of signal transduction and the inhibition of adhesive molecule function through steric hindrance, which can trigger cell separation.[29] The pathogenesis of PV has been described in more detail by Hammers et al.[30]
In patients with PV, autoantibodies against desmoglein 1 (Dsg 1) and desmoglein 3 (Dsg 3) is the purported cause.[31] Desmogleins are transmembrane glycoproteins that are an integral part of desmosomes which, in part, are required for cell–cell adhesion via interaction with intermediate filaments. The most common targets of desmoglein for IgG antibodies are the extracellular cadherin domains, which can result in the loss of desmosome-adhesive properties. These signaling pathways trigger endocytosis, depletion, and direct inhibition of Dsg 3 interactions.[32] It is generally believed that the amino portion of the cadherin proteins is most implicated in the pathogenesis of acantholysis leading to PV.[33]
Many animal models have shown that enzymatic inactivation of Dsg 1 and gene deletion of Dsg 3 results in pathology similar to PV.[34][35] This phenomenon was observed to be dose-dependent and suggests that reducing the circulating levels of IgG against Dsg 1 and Dsg 3 can improve patient outcomes.[36] In patients with primarily cutaneous disease, Dsg 1 likely plays a role more superficially, whereas Dsg 3 is more likely to be found in deeper cutaneous structures and mucous membranes.[37][38] The implication is that Dsg 3 can compensate for the absence of Dsg 1 in mucosal structures (thus demonstrating PV in cutaneous lesions only). In contrast, Dsg 1 without Dsg 3 is insufficient to manage mucous membranes or cutaneous lesions alone, implying that Dsg 1 is in lower proportion in mucous membranes.
The binding of antibodies to desmogleins has been confirmed by epitope mapping and is presumed to disrupt desmoglein binding by affecting steric hindrance.[39] Another theory for the pathophysiology of PV is the desmoglein nonassembly depletion hypothesis. This theory suggests that autoantibodies not only bind desmoglein but that they also bind each other, leading to crosslinking and the inability of desmosomes to maintain cell–cell adhesion.[40][41]
The primary function of platelets is their role in hemostasis. Briefly, under normal physiological conditions, platelets will adhere to and begin to spread over the surface of subendothelial cells exposed by damage to the vascular endothelium.(1) Adhesion is dependent on the platelet membrane glycoprotein lb complex. The von Willebrand factor (vWF) is required for both adhesion and spreading.
The primary function of platelets is their role in hemostasis. Briefly, under normal physiological conditions, platelets will adhere to and begin to spread over the surface of subendothelial cells exposed by damage to the vascular endothelium.(1) Adhesion is dependent on the platelet membrane glycoprotein lb complex. The von Willebrand factor (vWF) is required for both adhesion and spreading.
Phagocytosis begins with adhesion of the phagocyte surface receptors to the pathogen, which then is internalized into vesicles called phagosomes.
Inside the phagocyte, the phagosome fuses to lysosomes, whose contents are released with consequent digestion and pathogen elimination.
Changes in the oxidase’s gene system components present in phagolysosome membrane lead to disability in respiratory burst and generation of reactive oxygen species (ROS).
Phagocytosis begins with adhesion of the phagocyte surface receptors to the pathogen, which then is internalized into vesicles called phagosomes.
Inside the phagocyte, the phagosome fuses to lysosomes, whose contents are released with consequent digestion and pathogen elimination.
Changes in the oxidase’s gene system components present in phagolysosome membrane lead to disability in respiratory burst and generation of reactive oxygen species (ROS).
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
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
Diagnostic polymerase chain reaction (PCR) is an extremely powerful, rapid method for diagnosis of microbial infections and genetic diseases, as well as for detecting microorganisms in environmental and food samples.
However, the usefulness of diagnostic PCR is limited, in part, by the presence of inhibitory substances in complex biological samples, which reduce or even block the amplification capacity of PCR in comparison with pure solutions of nucleic acids .
In general, diagnostic PCR may be divided into four steps: (1) sampling, (2) sample preparation, (3) nucleic acid amplification, and (4) detection of PCR products
Diagnostic polymerase chain reaction (PCR) is an extremely powerful, rapid method for diagnosis of microbial infections and genetic diseases, as well as for detecting microorganisms in environmental and food samples.
However, the usefulness of diagnostic PCR is limited, in part, by the presence of inhibitory substances in complex biological samples, which reduce or even block the amplification capacity of PCR in comparison with pure solutions of nucleic acids .
In general, diagnostic PCR may be divided into four steps: (1) sampling, (2) sample preparation, (3) nucleic acid amplification, and (4) detection of PCR products
The etiology of a disease refers to the causative trigger(s), whereas pathogenesis refers to the mechanism(s) by which the disease progresses.
In other words, while the microbial biofilm developing on the tooth surface constitutes a necessary etiological factor, its mere presence is insufficient for the initiation of the disease.
Further risk factors, such as host genetics, lifestyle, stress, and systemic conditions, that dictate the immunopathogenesis are crucial for the transition from a healthy to a diseased state.
The etiology of a disease refers to the causative trigger(s), whereas pathogenesis refers to the mechanism(s) by which the disease progresses.
In other words, while the microbial biofilm developing on the tooth surface constitutes a necessary etiological factor, its mere presence is insufficient for the initiation of the disease.
Further risk factors, such as host genetics, lifestyle, stress, and systemic conditions, that dictate the immunopathogenesis are crucial for the transition from a healthy to a diseased state.
More from Romissaa ali Esmail/ faculty of dentistry/Al-Azhar university (20)
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
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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.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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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
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5. Microdontia involving one or two teeth is far
more common than the generalized types.
Individual teeth most frequently affected by
microdontia are the maxillary lateral incisors (peg
laterals) and the maxillary third molars .
6. The crowns often exhibit a conical shape.
Supernumerary teeth are commonly smaller
than normal, and their crowns are often
conical.
7. When all teeth in both arches are measurably
larger than normal, the condition is termed
true generalized macrodontia (seen in rare
conditions such as pituitary gigantism).
8. The term relative generalized macrodontia is used
to describe a condition in which the mandible, the
maxilla, or both are somewhat smaller than normal
but the teeth are normal in size. Rhizomegaly, also
termed radiculomegaly, is an uncommon type of
macrodontia in which the root or roots of a tooth
are considerably longer than normal.
9.
10.
11. Total anodontia is a rare condition in which the
patient has no deciduous and no permanent teeth.
It usually occurs in association with a generalized
disorder such as hereditary ectodermal dysplasia.
it is inherited disase in some families as an X-
linked recessive disorder affecting essentially
males, and in other families as an autosomal
recessive disorder affecting males and females.
12. The gene for the X-linked variety has been
mapped to the long arm of the X chromosome
(Xq12- q13.1). A gene from this region has been
found to encode a transmembrane protein that is
expressed in keratinocytes, hair follicles, and
sweat glands. All features are basic to defects in
the development of the ectodermally derived
structures (hair, sweat glands, teeth).
13. The more common form of anodontia is partial
anodontia, hypodontia or oligodontia, and involves
one or more teeth .
The most common congenitally absent teeth are the
third molars, followed by the maxillary lateral
incisors and the second premolars.
A close correlation exists between congenital
absence of a deciduous tooth and congenital absence
of the permanent successor, suggesting some genetic
influence.
14.
15.
16. They are far more common in the maxilla
(90%) than in the mandible (10%).
A supernumerary tooth located between the
maxillary central incisors, termed a mesiodens is
the most common, followed by maxillary fourth
molars (paramolars) and maxillary lateral incisors.
17. In the mandible the most common
supernumerary teeth are premolars.
A supernumerary tooth may resemble the
corresponding normal tooth or it may be rudimentary
and bear little or no resemblance to its normal
counterpart.
18. Supernumerary teeth may be single or
multiple and erupted or impacted. Multiple
supernumerary teeth, which are generally
impacted, are characteristically seen in
cleidocranial dysplasia and Gardner syndrome.
21. Premature Eruption: Erupted deciduous teeth
present at birth are termed natal teeth .
Deciduous teeth that erupt during the first 30 days
of life are termed neonatal teeth.
Premature eruption usually involves only one or
two teeth, most commonly the deciduous
mandibular central incisors.
22. Natal teeth and neonatal teeth are usually part
of the normal complement of deciduous teeth; they
are not supernumerary teeth and should therefore
be retained if possible.
Premature eruption of permanent teeth is usually a
consequence of premature loss of the preceding
deciduous teeth.
23. In the event that the entire permanent dentition
is obviously erupting prematurely, the possibility
of an endocrine dysfunction such as
hyperthyroidism should be considered.
24. Delayed Eruption: This occurrence is
relatively uncommon and is usually
idiopathic or associated with certain
systemic conditions such as rickets,
cleidocranial dysplasia, or cretinism.
25. Local factors such as gingival fibromatosis,
in which dense fibrous connective tissue
impedes tooth eruption, can result in delayed
eruption of the deciduous dentition.
Treatment of the systemic condition or the
causative local factors may alleviate the
eruption.
26. In conditions such as cleidocranial dysplasia,
the pathophysiologic basis for non eruption is
unclear and no known treatment exists.
Delayed eruption of permanent teeth may
result from the same local and systemic
conditions that give rise to the delayed eruption
of deciduous teeth.
27. Examples of physical barriers that impair tooth
eruption and result in impaction include dental
crowding, supernumerary teeth, some odontogenic
cysts, and odontogenic tumors (particularly
odontomas).
28. The most common impacted teeth are the mandibular
and maxillary third molars and maxillarycuspids,
mandibular second premolars and supernumerary
teeth. Mesioangular impactions of third molar are the
most common type.
An impacted tooth that is totally surrounded by bone is
completely impacted , whereas one that is partly in
bone and partly in soft tissue is partially impacted.
29. Partially impacted teeth, particularly mandibular
third molars, may communicate with the oral cavity
via an inconspicuous periodontal pocket on the
distal aspect of the adjacent second molar, thus
predisposing the impacted tooth to pericoronal
infection and dental caries.
Individual teeth that fail to erupt for no apparent
reason have sometimes been termed embedded
teeth; however, this term is rarely used
30.
31. The common complications of impacted
teeth are root resorption of adjacent normal
teeth, infection and associated pain, a
predisposition to dentigerous cyst formation, and
external resorption of the impacted tooth.
External resorption in an impacted tooth usually
begins in the occlusal area of the crown and
radiographically resembles dental caries.
32. It may arise from the small area of slightly
thickened cortical bone that occupies the area of
the central occlusal fossa of molars or may rep-
resent a miniature complex odontoma present
in the follicular soft tissue overlying the tooth
33. Although most eruption sequestra are
spontaneously exfoliated and therefore require
no treatment, they may occasionally remain in
the alveolar mucosa for several days and may be
brought to the attention of a dentist. In this
event, they can be easily removed.
34.
35.
36. Although occasional examples of dilaceration result
from trauma during tooth development , most
cases are the result of continued root formation
during a curved or tortuous path of eruption. In
some instances the cause of the bent or curved root
is idiopathic .
37.
38. Taurodontism, meaning bull-like teeth, is a
developmental disturbance that primarily affects
molars. Both the permanent and deciduous teeth
may be affected, although involvement of the
permanent teeth appears to be more common.
39. It recognized radiographically and characterized
by teeth that exhibit an overall rectangular shape,
minimal constriction and definition of the cervical
margin, and an apically displaced furcation that
results in an extremely large pulpal chamber that
exhibits an exaggerated apical- occlusal height
and short pulpal canals
40. The unusual root shape probably results from late
invagination of Hertwig’s root sheath, the
mechanism that determines the shape of the tooth
roots. Taurodontism may also occur in patients with
amelogenesis imperfecta, and Down syndrome.
Taurodontism requires no treatment but can
be a complicating factor during root canal treatment
procedures.
41.
42. Dens invaginatus, also termed dens in dente, is
a developmental abnormality that primarily
affects the permanent maxillary lateral incisors.
43. Mild cases is characterized by the presence of an
invaginated lingual pit that extends for varying
distances into the substance of the tooth.
The extent of the invagination is not always clinically
visible. The external pit on the lingual surface is often
inconspicuous on clinical examination but
may be visible in a periapical radiograph .
44. In its most extreme form the deep invagination
results in a bulbous expansion of the affected
root, a form termed a dilated odontoma . As a
result, most teeth with deep invaginations
quickly develop pulpitis, pulpal necrosis, and
inflammatory periapical disease in what
clinically appears to be an intact tooth.
45. Early radiologic diagnosis and prophylactic
restorative treatment of the abnormality are
essential if pulpal and periapical diseases are
to be prevented. Treatment of the more
severe forms of dens invaginatus is
usually extraction.
46.
47.
48. Occasionally, teeth exhibit supernumerary cusps.
The most common example of this phenomenon is
the Carabelli cusp, which develops on the
mesiolingual surface of permanent maxillary first
molars. This particular supernumerary cusp usually
presents no clinical problems and is therefore
represent a normal anatomic variation.
Supernumerary Cusps :
49. however, certain teeth exhibit supernumerary
cusps that result in clinical problems that may
require treatment. Examples of such
supernumerary cusps are dens evaginatus and
talon cusps
50. Dens evaginatus is a developmental
abnormality that primarily affects premolar
teeth. It is characterized by the development of
an abnormal globe-shaped projection of enamel
in the region of the central groove, between the
buccal and lingual cusps of premolars,
51. The clinical significance of dens evaginatus is that
it can interfere with tooth eruption and result in
incomplete eruption or tooth displacement.
Because this extra cusp contains a pulp horn,
attrition or fracture can result in pulp exposure
leading to pulpal inflammation and its sequelae.
52. Talon cusp: It is seen on the lingual aspect of
maxillary central incisors, is called a talon cusp,
because its unusual shape resembles an eagle’s
talon. This is abnormal cusp arises from the
cingulum portion of the tooth and usually
extends to the incisal edge as a prominent
projection of enamel .
53. If the cusp interferes with normal occlusion,
preventive care that includes endodontic
and restorative treatment of the affected
tooth may be required to achieve normal
tooth form. Simple reduction of the cusp should
not be attempted, because the cusp contains a
prominent pulp horn.
54.
55.
56.
57.
58.
59. Supernumerary Roots :
It is common occure in mandibular
premolars cuspids,and maxillary and
mandibular third molars.
60.
61. Gemination is characterized by the partial
division or twinning of a single tooth germ,
resulting in a tooth that exhibits two separate or
partly separated crowns and a single root and
root canal . Gemination can affect the deciduous
and permanent dentitions .
62. Fusion can be complete or incomplete.
If fusion begins before calcification, then the
union will involve all components of the tooth,
including enamel, dentin, cementum, and pulp.
63. If the union begins at a later stage of tooth
development, the affected teeth may have separate
crowns and the fusion may be limited to the roots.
Fusion can be differentiated from gemination by
counting the teeth in the area.
The clinical implications of fusion include esthetic
considerations, crowding when fused to
a supernumerary tooth, and periodontal
disease.
66. Concrescence is a type of fusion that occurs
after root formation is complete.
The condition is thought to
occur as a result of traumatic injury to the area or
crowding with interseptal bone loss, resulting in
close approximation of the tooth roots.
67. Concrescence can occur before or after tooth
eruption and primarily involves the
permanent maxillary molars.
The clinical implications of concrescence relate
primarily to the importance of its radiographic
diagnosis before attempting tooth extraction.
68.
69.
70. Hypercementosis
Teeth with these shapes are difficult to extract
without surgically removing significant amounts of
the surrounding bone. Hypercementosis is more
common in teeth that are subjected to either
increased or decreased occlusal forces, on the teeth of
patients with Paget disease or hyperpituitarism, and
on adjacent teeth in areas of chronic
inflammation.
71.
72. Cervical Enamel Projection :
Focal apical extensions of the coronal enamel
beyond the normally smooth cervical margin
(cementoenamel junction) and onto the root of
the tooth.
73. This occur primarily on maxillary and mandibular
molars. Their clinical significance relates to
the fact that they could contribute to
periodontal pocket formation, which might
progress to periodontal disease. The cervical
enamel projection is also thought to play a role in
the development of the paradental cyst
74. Cervical enamel projections differ from the
ectopic droplets of enamel that primarily occur
in the bifurcation or tri- furcation areas on the roots
of molars . These are termed enamel pearls.
Treatment is not recommended, because it often
leads to the development of root caries, external
resorption, or pulpitis.
75.
76.
77.
78.
79. The environmental factors are bacterial and viral
infections (e.g., syphilis, scarlet fever), inflammation,
nutritional deficiencies (e.g., vitamins A, C, D;
calcium), chemical injuries (e.g., fluoride), and
trauma. Enamel defects resulting from environmental
factors usually affect either the deciduous or the
permanent dentition . Environmental factors often
damage both types of hardtissues.
80. A common form of focal
enamel hy poplasia of known cause is Turner tooth,
which results from localized inflammation or trauma
during tooth development. Typical examples of this
phenomenon occur when a deciduous tooth develops a
caries- or trauma-related abscess that damages the
underlying developing permanent successor.
81.
82. they are manifested clinically as a horizontal line of
small pits or grooves on the enamel surface that
correspond to the time of development and the
duration of the insult
83. congenital syphilis affects the incisal edges of the
permanent incisors and the occlusal surfaces of
the permanent first molars. The notched,
screwdriver-shaped incisors are termed
Hutchinson incisors, whereas the globular
occlusal surfaces of the first molars are termed
mulberry molars.
84. Enamel hypoplasia that results from
hypocalcemia secondary to vitamin D deficiency is
usually of the pitted type.
A well-recognized example of chemically induced
generalized enamel hypoplasia results from the
ingestion of fluoride.
85. Although total fluoride intake will vary with total
water consumption, fluoride-induced enamel
hypoplasia (fluoride mottling) Increased
fluoride levels interfere with ameloblastic function,
which adversely affects both enamel matrix
formation and enamel matrix calcification.
Regardless of the degree of fluoride mottling,
affected teeth are largely resistant to dental caries.
86.
87.
88. It affect both the primary and permanent
dentitions. These disorders are confined to the
enamel; the other components of the teeth are
normal.
89. Three basic types of amelogenesis imperfecta :
(1) The hypoplastic type (focal or generalized),
which exhibits decreased enamel matrix formation
caused by a disturbance in the functioning of the
ameloblasts;
(2) The hypocalcified type, which exhibits a
severe defect in mineralization of the enamel matrix.
90. Both dentitions are commonly affected to some
degree. In the X-linked subtypes the clinical
appearance differs between males and females.
(3) The hypo- maturation type, which
exhibits a less severe alteration in
mineralization with focal or generalized areas
of immature enamel crystallites .
91.
92.
93.
94.
95.
96. Generalized disturbances in dentin formation are
usually hereditary and include conditions
such as dentinogenesis imperfectaand
(DI) dentin dysplasia (DD).
97.
98.
99. Type I: DI that occurs in patients afflicted with
osteogenesis imperfecta (OI)This type is usually
inherited as an autosomal dominant trait. Although
the teeth have the same opalescent color as in type II .
Type II: DI that is not associated with OI.
the common term for this type of DI is hereditary
opalescent dentin. It is the most common type
and is inherited as an autosomal dominant
trait.
100. Type III: DI (Brandywine type) is rare and
inherited as an autosomal dominant trait; it occurs
in a racial isolate in the state of Maryland.
Clinically, it is the same as type I and type II
except that patients exhibit multiple pulpal
exposures in the deciduous dentition.
101. In all three subtypes of DI, teeth of both
dentitions are affected with variable clinical
appearances. The teeth are opalescent with the color
ranging from bluish-gray to brown to yellowish.
The dentin is abnormally soft, providing
inadequate structural support to the overlying
enamel. Although the enamel is normal, it
fractures or chips away easily, exposing the occlusal
and incisal dentin .
102.
103.
104. Radiographic features :
The teeth in DI subtypes I and II are similar
and exhibit bulb-shaped crowns with constricted
cementoenamel junctions and thin roots .
Depending on the age of the patient, the teeth will
exhibit varying stages of obliteration of the pulp
chambers and pulp canals .
105. The cementum, periodontal ligament,
and supporting alveolar bone appear
normal.
The teeth in DI type III may be similar to those
seen in types I and II, or they may exhibit
extremely large pulpal chambers surrounded by
a thin shell of dentin.
106.
107.
108.
109. Type I (radicular DD): type I is far more
common than type II. All teeth in both
dentitions are affected.
The color of the teeth is usually within the
normal range .
In some cases the crowns of the teeth may
exhibit a slight bluish or brownish
translucency in the cervical region.
110. The teeth usually exhibit a normal
eruption pattern, although occasional delayed
eruption has been reported.
Affected teeth often exhibit increased
mobility and may exfoliate prematurely.
111. RADIOGRAPHIC FEATURES :
The roots of the teeth are usually short, blunt, bulged,
conic, or absent.
The mandibular molars commonly have characteristic
W-shaped roots.
In the deciduous dentition, teeth often exhibit
total obliteration of the pulpal chambers and
canals.
The permanent teeth may also exhibit pulpal
obliteration.
112.
113. Type II (coronal DD):
Both the primary and permanent dentitions are
affected in this type of DD.
Clinically the deciduous teeth exhibit a
bluish-gray, brownish, or yellowish color
and have the same translucent, opalescent
appearance that is seen in DI. In contrast, the
permanent teeth have a normal clinical
appearance.
114. RADIOGRAPHIC FEATURES :
The deciduous teeth of DD exhibit
obliterated pulpal chambers and canals.
The pulpal obliteration occurs after tooth
eruption.
The roots of the deciduous and permanent
dentitions are of normal shape and length.
115. The pulp chambers in the permanent
teeth are abnormally large, rather than
obliterated, and exhibit a radicular
extension that imparts a thistle or flame
shape to the root portion of the pulp. Pulpal
calcifications (pulp stones) are visible in
most of the coronal pulp chambers and the
root pulp canals are narrowed .
116.
117.
118. Regional odontodysplasia (ROD), or ghost teeth, is a
sporadically occurring nonhereditary disturbance
of tooth development characterized by the
defective formation of enamel and dentin in
addition to abnormal pulp and follicle
calcifications teeth exhibit a delay or a total failure to
erupt.
The teeth are considerably deformed with a soft
leathery surface and are discolored, yellowish-brown .
119. RADIOGRAPHIC FEATURES
The teeth have been described as ghost teeth
because of the marked decrease in radiodensity.
The enamel and dentin are very thin and
indistinct; the pulpal chambers are extremely
large . Pulp stones may occasionally be visible.
120.
121.
122. Hypophosphatasia is inherited in the majority
of cases as an autosomal recessive condition.
Hy pophosphatasia is a disorder of bone
mineralization caused by a deficiency in
alkaline phosphatase in serum and
tissues.
123. The cause of hypophosphatasia is a basic defect
in the gene encoding for tissue nonspecific
alkaline phosphatase (TNSALP).
Delayed formation and eruption of the
dentition, premature loss of primary teeth,
and the spontaneous loss of permanent
teeth are characteristically seen in
hypophosphatasia