AIDS is defined as a condition indicative of a defect in cell-mediated immunity occurring in a person with no known cause for immunodeficiency other than the presence of HIV.
CDC defined AIDS as
“The occurrence of one or more group of life-threatening opportunistic infections, malignancies, neurologic diseases and other specific illness in patients with HIV infection or with CD4 counts less than 200/cu mm”
Oral manifestation of bleeding disorders and dental management of the same
also for more
https://youtu.be/aaJ6gpQohcs
https://youtu.be/REMKSUty0cE
https://youtu.be/fv3_tWZPJIU
https://youtu.be/GeZIbCwqKYU
if you want me to make ppt on some topic do let me know on the comment section of my youtube channel
AIDS is defined as a condition indicative of a defect in cell-mediated immunity occurring in a person with no known cause for immunodeficiency other than the presence of HIV.
CDC defined AIDS as
“The occurrence of one or more group of life-threatening opportunistic infections, malignancies, neurologic diseases and other specific illness in patients with HIV infection or with CD4 counts less than 200/cu mm”
Oral manifestation of bleeding disorders and dental management of the same
also for more
https://youtu.be/aaJ6gpQohcs
https://youtu.be/REMKSUty0cE
https://youtu.be/fv3_tWZPJIU
https://youtu.be/GeZIbCwqKYU
if you want me to make ppt on some topic do let me know on the comment section of my youtube channel
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.
Science Cabaret by Dr. Rodney Dietert "How to train your super organism..via ...Kitty Gifford
Attendees (and their microbes) at this event enjoyed a lively discussion on how we might better interact with our environment to support a healthier life for ourselves and our children. Think with your microbes about why we have to suffer from ever-increasing numbers of debilitating chronic diseases (asthma, food allergies, diabetes, autoimmune conditions, obesity, heart disease and cancer).
with Dr. Rodney Dietert, Cornell University Professor, Department of Microbiology and Immunology
Dr. Rodney Dietert is an internationally-known author, lecturer, scientist, book series editor, and educator. He is the author of Strategies for Protecting Your Child’s Immune System, and Science Sifting: Tools for Innovation in Science and Technology.
Richard Frye, MD, PhD, FAAP, FAAN, CPI, will discuss:
*The enteric (gut) microbiome has an important influence on health and disease states in humans.
* The enteric microbiome influences the human host using chemical mediators, some of which can directly affect mitochondrial function
* Short chain fatty acids produced by gut bacteria not only modulate mitochondrial function and cellular regulatory pathways, but can also be used as mitochondrial fuels.
Human nutrition, gut microbiome and immune system S'eclairer
Dr Zahida Chaudnary talks with the students about nutrition, gut microbiomes, and nutrition as we look at diseases and how your body reacts to what you eat.
Check out the slideshow by itself here.
Want an audio version? Subscribe to our Podcast on iTunes!
Want to join us for the live discussion? Check out our Social Media in the noon hour every Monday as we sit down on Google Hangout OnAir! Follow us on Twitter, Facebook, or Google+ to get updated with the link when we start!
Many systemic diseases are reflected in the oral mucosa, maxilla, and mandible.
Mucosal changes may include ulceration or mucosal bleeding.
Immunodeficiency can lead to opportunistic diseases such as infection and neoplasia.
Bone disease can affect the maxilla and mandible.
Systemic disease can cause dental and periodontal changes.
Drugs prescribed for a systemic disease can affect oral tissue.
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
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
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.
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
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Oral manifestations of systemic diseases
1. Oral manifestations of
systemic diseases
Done by
Dr. Mohammed Sa’ad (B.D.S)
AL Imam Ali ( A.S ) General Hospital
Maxillofacial Surgery Department
2. Introduction
• Careful examination of the oral cavity may
reveal findings indicative of an underlying
systemic condition, and allow for early diagnosis
and treatment. Examination should include
evaluation for mucosal changes, periodontal
inflammation and bleeding, and general
condition of the teeth.
3. GIT Diseases
• Gastrointestinal diseases refer to diseases involving
the gastrointestinal tract, namely the esophagus,
stomach, small intestine, large intestine and rectum,
and the accessory organs of digestions, the liver,
gallbladder, and pancreas.
4. • Crohn's disease, also known as Crohn
syndrome and regional enteritis, is a type of
inflammatory bowel disease (IBD).
• Ulcerative colitis is a form of inflammatory
bowel disease (IBD) that causes inflammation
and ulcers in the colon.
• Gastroesophageal reflux is a chronic symptom
of mucosal damage caused by stomach acid
coming up from the stomach into the
esophagus.
• Chronic liver disease in the clinical context is a
disease process of the liver that involves a
process of progressive destruction and
regeneration of the liver parenchyma leading to
fibrosis and cirrhosis.
5. • Crohn disease
– diffuse labial, gingival or mucosal swelling
– „cobblestoning“ of buccal mucosa and
gingiva
– aphtous ulcers
– mucosal tags
– angular cheilitis
– oral granulomas
• Ulcerative colitis
– oral signs are present in periods of
exacerbation of disease
– aphtous ulceration or superficial
hemorrhagic ulcers
– angular stomatitis
– pyostomatitis vegetans, pyostomatitis
gangrenosum
cobblestoning of
the gut mucosa
GIT diseases
pystomatitis vegetans
6. • Gastroesophageal reflux
– reduction of the pH of the oral cavity below
5,5 – enamel damage
– damage of the dentin – higher sensitivity (to
temperature..), caries
• Chronic liver diseases
– jaundice
– petechiae or gingival bleeding (hemostasis
disorder)
GIT diseases
7. Hematologic Diseases
• Hematologic diseases are disorders which
primarily affect the blood
• Anemia is usually defined as a decrease
in the amount of red blood cells (RBCs) or
hemoglobin in the blood.
• Leukemia is a group of cancers that
usually begins in the bone marrow and
results in high numbers of abnormal white
blood cells.
12. Connective tissue disease
• connective tissue disease is any disease that has the
connective tissues of the body as a target of pathology.
• Sjögren's syndrome is a chronic autoimmune disease
in which the body's white blood cells destroy the
exocrine glands.
• Kawasaki disease is an autoimmune disease in which
the medium-sized blood vessels throughout the body
become inflamed.
• Scleroderma is a chronic systemic autoimmune disease
characterised by hardening (sclero) of the skin (derma).
• Lupus erythematosus is a systemic autoimmune
disease in which the body’s immune system mistakenly
attacks healthy tissue.
13. • Sjögren syndrome
– autoimmune disease
– men : women - 1 : 9, 50 years and older
Main signs
– sicca syndrome
– keratoconjuctivitis sicca
– xerostomia
Oral signs
– decrease in saliva
• xerostomia
– dry, red, wrinkled mucosa
• difficulty in swalloving and eating
• disturbance in taste and speech
• increased dental caries
• infections
• atrophy of the papilae
• candidiasis
Connective-tissue diseases
14. • Kawasaki disease
– vasculitis of medium and large arteries
Oral signs
– swelling of papilae on the surface of the
tongue (strawbery tongue)
– intense erythema of the mucosal
surfaces
– cracked, cherry red, swolen and
hemorrhagic lips
Connective-tissue diseases
15. • Scleroderma
– diffuse sclerosis of the skin, GIT,
heart muscle, lungs, kidney
Oral signs
– pursed lips – dificult to open the
mouth
– esophafeal sclerosis →
gastroesophageal reflux – damage
of enamel
– pale, rigid mucosa
– teleangiectasias
– decreased mobility of tongue
– salivary hypofunction
Connective-tissue diseases
Limited mouth opening and decreased
tongue mobility
Gingival retraction
17. Pulmonary diseases
• Cystic fibrosis, also known as mucoviscidosis,
is a genetic disorder that affects mostly the
lungs but also the pancreas, liver, kidneys and
intestine.
• Sarcoidosis, is a disease involving abnormal
collections of inflammatory cells (granulomas)
that can form as nodules in multiple organs.
19. • Sarcoidosis
Oral signs
– multiple, nodular, painles ulcerations of the
gingiva, bucal mucosa, labial mucosa and palate
– tumorlike swelling of salivary glans
– swelling of the tongue
– xerostomia
– facial nerve palsy
Pulmonary diseases
20. Cutaneous diseases
• Psoriasis is a long lasting disease
characterized by patches of abnormal
skin.
• Acanthosis is diffuse epidermal
hyperplasia.
21. • Psoriasis
Oral signs
– fissured tongue
– small white papules
– red and white plagues
– bright red patches
• Acantosis nigricans
– hyperpigmentation, papillomatosis
Oral signs
– gingival hyperplasia
– gingiva, tongue, lips - papilomas
Cutaneous diseases
22. Endocrine diseases
• Diabetes mellitus, is a group of metabolic
diseases in which there are high blood sugar
levels over a prolonged period.
• Thyroid disorders is the condition that occurs
due to excessive or insufficient production of
thyroid hormone by the thyroid gland.
• Cushing's syndrome is a collection of signs
and symptoms due to prolonged exposure to
cortisol.
• Addison’s disease is a rare, chronic endocrine
system disorder in which the adrenal glands do
not produce sufficient steroid hormones.
24. • Hypoparathyroidism
Oral signs
– candidiasis
– upper lip twitching
• Hyperparathyroidism
Oral signs
– loss of the lamina dura surrounding the
roots of the teeth
– decrease of trabecular density
– osseous lesions „brown tumor“
Endocrine diseases
25. • Cushing´s syndrome
Oral signs
– fatty tissue deposition – „moon face“
– osteoporosis → pathological fractures of
the mandible, maxilla or alveolar bone
– delayed healing of fractures and also sof
tissue injuries
• Addison´s disease
Oral signs
– „bronzing“ hyperpigmentation of the skin
– oral mucosal melanosis – buccal mucosa,
tongue
Endocrine diseases
moon face
hyperpigmentation
26. Renal diseases
• Uremic stomatitis a rare form of
stomatitis that occurs with renal failure.
27. • Uremic stomatitis
– rare
– in undiagnosed and untreated chronic renal
failure
– irritation and chemical injury of mucosa by
ammonia or ammonium compounds
Signs
– painful plagues and crusts – bucal mucosa, the
floor or dosrum of the tongue, floor of the mouth
– Type I
• generalized or localized erythema
• exudate
• pain, burning, xerostomia, halitosis, gingival
bleeding, candidiosis
– Type II
• ulceration
• secondary infection
• anemia
Renal diseases
29. REFERENCES
1. U.S. Department of Health and Human Services. Oral health in America: a report of the Surgeon General. Rockville, Md.: U.S. Department of
Health and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000.
2. Janket SJ, Baird AE, Chuang SK, Jones JA. Meta-analysis of periodontal disease and risk of coronary heart disease and stroke. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 2003;95(5):559-569.
3. Xiong X, Buekens P, Fraser WD, Beck J, Offenbacher S. Periodontal disease and adverse pregnancy outcomes: a systematic review. BJOG.
2006;113(2):135-143.
4. Demmer RT, Jacobs DR Jr, Desvarieux M. Periodontal disease and incident type 2 diabetes: results from the First National Health and
Nutrition Examination Survey and its epidemiologic follow-up study. Diabetes Care. 2008;31(7):1373-1379.
5. Moazzez AH, Alvi A. Head and neck manifestations of AIDS in adults. Am Fam Physician. 1998;57(8):1813-1822.
6. Gonsalves WC, Chi AC, Neville BW. Common oral lesions: Part I. Superficial mucosal lesions. Am Fam Physician. 2007;75(4):501-507. 7.
Neville BW, Damm DD, Allen CM, Bouquot JE. Pernicious anemia. In: Oral and Maxillofacial Pathology. 3rd ed. St. Louis, Mo.: Saunders
Elsevier; 2009:829-831.
8. Schiّdt M. Oral manifestations of lupus erythematosus. Int J Oral Surg. 1984;13(2):101-147.
9. Nico MM, Vilela MA, Rivitti EA, Lourenço SV. Oral lesions in lupus erythematosus: correlation with cutaneous lesions. Eur J Dermatol.
2008;18(4):376-381.
10. Callen JP. Oral manifestations of collagen vascular disease. Semin Cutan Med Surg. 1997;16(4):323-327.
11. Jessop S, Whitelaw DA, Delamere FM. Drugs for discoid lupus erythematosus. Cochrane Database Syst Rev. 2009;(4):CD002954.
12. Sirois DA, Fatahzadeh M, Roth R, Ettlin D. Diagnostic patterns and delays in pemphigus vulgaris: experience with 99 patients. Arch
Dermatol. 2000;136(12):1569-1570.
13. Hyams JS. Extraintestinal manifestations of inflammatory bowel disease in children. J Pediatr Gastroenterol Nutr. 1994;19(1):7-21.
14. Pittock S, Drumm B, Fleming P, et al. The oral cavity in Crohn’s disease. J Pediatr. 2001;138(5):767-771.
15. Coenen C, Bِrsch G, Müller KM, Fabry H. Oral inflammatory changes as an initial manifestation of Crohn’s disease antedating abdominal
diagnosis. Report of a case. Dis Colon Rectum. 1988;31(7):548-552.
16. Talbot T, Jewell L, Schloss E, Yakimets W, Thomson AB. Cheilitis antedating Crohn’s disease: case report and literature update of oral
lesions. J Clin Gastroenterol. 1984;6(4):349-354.
17. Plauth M, Jenss H, Meyle J. Oral manifestations of Crohn’s disease. An analysis of 79 cases. J Clin Gastroenterol. 1991;13(1):29-37. 18.
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