Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine, Al-Azhar University. Ameloblastoma is benign slow-growing but locally invasive neoplasm of odontogenic origin. In 2005, the WHO has classified ameloblastomas into multi cystic, unicystic and peripheral subtypes. The clinical picture, radiographic findings and differential diagnosis are presented. Treatment of ameloblastomas is primarily surgical. There has been some debate regarding the most appropriate method for removing. These range from conservative to radical modes. Some authors advocate conservative approach and thought that ameloblastoma are essentially benign in nature and should be treated as such. However, this conservative approach result in recurrence rates of 55% to 90%of the cases. Currently, the standard of care for ameloblastoma includes en bloc resection with 1-2 combine margin and immediate bone reconstruction. Despite the medical nature of a surgical resection, it may actually involve less morbidity than extensive hard and soft tissue resection with associated extensive morbidity that may be warranted in case of recurrence following inadequate primary treatment.
Odontogenic keratocyst (OKC) is the cyst arising from the cell rests of dental lamina. It can occur anywhere in the jaw, but commonly seen in the posterior part of the mandible. Radiographically, most OKCs are unilocular when presented at the periapex and can be mistaken for radicular or lateral periodontal cyst.
Dr. Ahmed M. Adawy, Professor Emeritus, Dep. Oral & Maxillofacial Surgery. Former Dean, Faculty of Dental Medicine, Al-Azhar University. Ameloblastoma is benign slow-growing but locally invasive neoplasm of odontogenic origin. In 2005, the WHO has classified ameloblastomas into multi cystic, unicystic and peripheral subtypes. The clinical picture, radiographic findings and differential diagnosis are presented. Treatment of ameloblastomas is primarily surgical. There has been some debate regarding the most appropriate method for removing. These range from conservative to radical modes. Some authors advocate conservative approach and thought that ameloblastoma are essentially benign in nature and should be treated as such. However, this conservative approach result in recurrence rates of 55% to 90%of the cases. Currently, the standard of care for ameloblastoma includes en bloc resection with 1-2 combine margin and immediate bone reconstruction. Despite the medical nature of a surgical resection, it may actually involve less morbidity than extensive hard and soft tissue resection with associated extensive morbidity that may be warranted in case of recurrence following inadequate primary treatment.
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostoticii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformansc. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitisb. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibromab. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular typeii. Psammomatoid type
d. Gigantiform cementomas
Fibro-osseous lesions of the jaws
Fibrous dysplasia
Cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Periapical cemento-osseous dysplasia
Florid cemento-osseous dysplasia
Ossifying fibroma
Juvenile aggressive ossifying fibroma
Cherubism
Fibro-osseous lesions (FOL) are characterized by replacement of normal bone architecture by collagen fibers and fibroblasts containing calcified tissue.
They include a wide variety of lesions of developmental, dysplastic and neoplastic origins with clinical and radiographic presentation and behavior.
Because of the histological similarities between diverse diseases, proper diagnosis requires correlation of history, clinical and radiographic findings.Fibrous Dysplasia
2. Reactive (dysplastic lesions arising in the tooth-bearing area (presumably of periodontal origin).
a. Periapical cemento-osseous dysplasia
b. Focal cemento-osseous dysplasia
c. Florid cemento-osseous dysplasia
3. Fibro-osseous neoplasms (widely designated as cementifying fibroma, ossifying fibroma or cemento-ossifying fibroma.Bone dysplasias
a. Fibrous dyspla i. Monostoticii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformansc. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitisb. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibromab. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma i. Trabecular typeii. Psammomatoid type
d. Gigantiform cementomas
Differential diagnosis of oral and maxillofacial lesionsAhmed Adawy
A wide variety of lesions from the soft and hard tissues may arise in the orofacial region. Clinical diagnosis is a cognitive process of applying logic and knowledge in a series of step-by-step decisions, to create a list of possible diagnosis.
Most deep fungal infections have their primary foci in the lungs, therefore those presenting with distant organs or skin involvement should be managed aggressively as untreated or severe disease can lead to severe scarring, disfigurement and even death.
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
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.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
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.
3. Ulcerative lesion in oral cavity:
А) Erosion
B) Aphtha
C) Ulcus
D) Rhagada
E) Fistula
F) Vulnus
4. Aphtha
Aphthous ulcer is a small painful
ulcer in the mouth, approximately
2 to 5 mm in diameter. It usually
remains for five to seven days and
heals within two weeks with no
scarring.
5. Ulcus (ulcer)
An ulcer is a tissue defect which has
penetrated the epithelial-connective
tissue border, with its base at a deep
level in the submucosa, or even
within muscle
6. Ulcerative lesions
Facts :
• Ulcer - a local defect, or excavation of the surface of an organ or tissue,
produced by sloughing of necrotic inflammatory tissue.
• Oral ulceration is a break in the oral epithelium, exposing nerve endings
in the underlying connective tissue.
• It results in pain and soreness of the mouth especially with spicy food and
citrus fruits.
• Patients vary in the degree to which they suffer and complain of the
soreness.
7. Ulcerative lesions
Main causes of oral ulceration
1. Local Causes
2. Aphthae
3. Infections
4. Drugs
5. Malignant disease
6. Systemic disease
12. Many drugs can cause mouth ulcers
as a side effect. Common examples
are alendronate (a bisphosphonate,
commonly prescribed for
osteoporosis), cytotoxic drugs (e.g.
methotrexate, i.e. chemotherapy),
non steroidal anti-inflammatory
drugs, nicorandil (may be prescribed
for angina) and propylthiouracil (e.g.
used for hyperthyroidism). Some
illegal drugs can cause ulceration,
e.g. cocaine
Drug-induced neutropenia
15. 5- Malignant diseases
Ulcerative lesions
i) Oral squamous cell carcinoma
Rarely, a persistent, non healing mouth ulcer may be a cancerous lesion.
Malignancies in the mouth are usually carcinomas, but lymphomas,
sarcomas and others may also be possible. Either the tumor arises in the
mouth, or it may grow to involve the mouth, e.g. from the maxillary sinus,
salivary glands, nasal cavity or peri-oral skin. The most common type of
oral cancer is squamous cell carcinoma.
16. 5- Malignant diseases
Ulcerative lesions
Common sites of oral cancer are the lower lip, the floor of the mouth, and
the sides and underside of the tongue, but it is possible to have a tumor
anywhere in the mouth. Appearances vary greatly, but a typical
malignant ulcer would be a persistent, expanding lesion which is totally
red (erythroplasia) or speckled red and white (erythroleukoplakia).
Malignant lesions also typically feel indurated (hardened) and attached
to adjacent structures, with "rolled" margins or a punched out
appearance and bleeds easily on gentle manipulation
17. Advanced oral cancer (T4
N2 M0, stage 4). Note
rolled margins of central
ulcer and surrounding
areas of premalignant
change.
21. Hulusi Behçet
(1889-1948)
Behçet disease is named after Hulusi Behçet (1889–1948), the Turkish dermatologist
and scientist who first recognized the syndrome in one of his patients in 1924 and
reported his research on the disease in Journal of Skin and Venereal Diseases in 1936
22. Behçet's syndrome
• Behçet's disease or Behçet's syndrome is a rare immune-
mediated small-vessel systemic vasculitis that often presents
with mucous membrane ulceration and ocular problems.
Behçet's disease (BD) was named in 1937 after the Turkish
dermatologist Hulusi Behçet, who first described the triple-
symptom complex of recurrent oral aphthous ulcers, genital
ulcers, and uveitis.
• As a systemic disease, it can also involve visceral organs such
as the gastrointestinal tract, pulmonary, musculoskeletal,
cardiovascular and neurological systems. This syndrome can be
fatal due to ruptured vascular aneurysms or severe neurological
complications
Ulcerative lesions
25. According to the International Study Group guidelines, for a patient
to be diagnosed with Behçet's disease, the patient must have oral
(aphthous) ulcers (any shape, size, or number at least 3 times in any
12 months period) along with 2 out of the following 4 "hallmark"
symptoms:
• genital ulcers (including anal ulcers and spots in the genital
region and swollen testicles or epididymitis in men)
• skin lesions (papulo-pustules, folliculitis, erythema nodosum,
acne in post-adolescents not on corticosteroids)
• eye inflammation (iritis, uveitis, retinal vasculitis, cells in the
vitreous)
• pathergy reaction (papule >2 mm dia. 24-48 hrs or more after
needle-prick). The pathergy test has a specificity of 95% to 100%,
but the results are often negative in American and European
patients
Ulcerative lesions
26. There is no specific pathological testing or technique available for the
diagnosis of the disease, although the International Study Group criteria for
the disease are highly sensitive and specific, involving clinical criteria and a
pathergy test.
33. - Are common oral lesions, most of them are caused by physical
trauma. In addition, ulcers may arise with other traumatic causes as:
1. Physical (mechanical)
2. Chemical
Ulcerative lesions
1) Local Causes:
34. Traumatic ulcers :
1- Physical Trauma:
- Physical traumatic ulcers are common oral lesions.
- Common causes of oral ulceration include rubbing on sharp edges of
teeth, fillings, crowns, dentures, orthodontic appliances. Accidental biting
caused by a lack of awareness of painful stimuli in the mouth (following a
local anesthetic e.g. during dental treatment) may cause ulceration
Ulcerative lesions
1) Local Causes:
35. Traumatic ulcers :
1- Physical Trauma:
- Eating rough foods can damage the lining of the mouth. Some people cause
damage inside their mouths themselves, either through an absent minded
habit or as a type of deliberate self harm (factitious ulceration). Examples
include biting the cheek, tongue or lips, rubbing a finger nail, pen or tooth pick
inside the mouth.
- Iatrogenic ulceration can also occur during dental treatment, when incidental
abrasions to the soft tissues of the mouth are common.
Ulcerative lesions
1) Local Causes:
36. 1- Physical Trauma:
Clinical features:
-They are clinically diverse, but usually appear as a single, painful ulcer with
a smooth red or whitish-yellow surface and a thin erythematous halo. They
are usually soft on palpation, and heal without scarring within 6–10 days,
spontaneously or after removal of the cause.
Ulcerative lesions
Traumatic ulcers
1) Local Causes:
37. 1- Physical Trauma:
Clinical features:
- However, chronic traumatic ulcers may clinically mimic a carcinoma.
-The tongue, lip, and buccal mucosa are the sites of predilection.
-The diagnosis is based on the history and clinical features. However, if an
ulcer persists over 10–12 days a biopsy must be taken to rule out cancer.
Ulcerative lesions
Traumatic ulcers
1) Local Causes:
39. Ulcerative lesions
Traumatic ulcers
1- Physical Trauma:
Differential diagnosis Squamous-cell carcinoma and other malignancies,
aphthous ulcer, syphilis, tuberculosis.
Treatment Removal of traumatic factors. Topical steroids may be used
for a short time.
41. Ulcerative lesions
Traumatic ulcers
1- Thermal and electrical burn :
•Thermal burns usually result from placing hot food or beverages in the mouth. This may occur
in those who eat or drink before a local anesthetic has worn off. The normal painful sensation is
absent and a burn may occur. Thermal food burns are usually on the palate or posterior buccal
mucosa, and appear as zones of erythema and ulceration with necrotic epithelium peripherally.
•Electrical burns more commonly affect the oral commissure. The lesions are usually initially
painless, charred and yellow with little bleeding. Electrical burns in the mouth are usually caused
by chewing on live electrical wiring (children). Saliva acts as a conducting medium and an
electrical arc flows between the electrical source and the tissues, causing extreme heat and
possible tissue destruction
42. Ulcerative lesions
Traumatic ulcers
2- Chemical trauma
Caustic chemicals may cause ulceration of the oral mucosa if they are of
strong enough concentration and in contact for a sufficient length of time.
Holding an aspirin tablet next to a painful tooth in an attempt to relieve pulpitis
is common, and leads to epithelial necrosis.
Other caustic medications include hydrogen peroxide, used to treat gum
disease, is also capable of causing epithelial necrosis at concentrations of 1–
3%. Silver nitrate, sometimes used for pain relief from aphthous ulceration,
acts as a chemical cauterant and destroys nerve endings, but the mucosal
damage is increased.
43. Ulcerative lesions
Traumatic ulcers
2- Chemical trauma:
Clinical features:
- It appears as a red, painful erythema that may undergo desquamation,
leaving erosions.
-The lesions heal spontaneously in about a week.
-The diagnosis is made exclusively on clinical grounds.
44. Chemical (Aspirin burn) ulceration:
-The photos show a patient who placed
an aspirin on her gums. Aspirin is an
acid and burned the oral tissues (gums
and cheek).
- Fortunately the mouth heals quickly
and within two weeks healing occurred.
45. Ulcerative lesions
Traumatic ulcers
2- Chemical trauma:
Differential diagnosis
- Thermal burn, traumatic lesions, aphthous ulcers, drug reactions.
Treatment
- Discontinue the application of the causative agent.
46. Ulcerative lesions
Main causes of oral ulceration
1. Local Causes
2. Recurrent Aphthous Stomatitis
3. Infections
4. Drugs
5. Malignant disease
6. Systemic disease
47. 2-Recurrent Aphthous Stomatitis
Ulcerative lesions
- Recurrent aphthous ulcers are among the most common oral mucosal
lesions, with a prevalence of 10–30% in the general population.
-The cause remains unclear. Recent evidence supports the concept that cell-
mediated immune responses play a primary role in the pathogenesis.
- Several predisposing factors have been reported, such as trauma, allergy,
genetic predisposition, endocrine disturbances, emotional stress,
hematological deficiencies, and AIDS.
-Three clinical variations have been recognized: minor, major and herpetiform
ulcers.
-They are very painful and cause the patient a lot of discomfort.
48. Herpetiform recurrent Aphthous Stomatitis
-The herpetiform variation is characterized by small, painful, shallow ulcers, 1–
2 mm in diameter, with a tendency to coalesce into larger irregular ulcers.
- Characteristically, the lesions are multiple (10–100), persist for one or two
weeks, and heal without scarring.
- usually in old age group, common in females.
Ulcerative lesions
2-Recurrent Aphthous Stomatitis
50. Minor recurrent Aphthous Stomatitis
-Minor aphthae are the most common form, and they present clinically as
small, painful, round ulcers 3–6 mm in diameter, covered by a whitish-yellow
membrane and surrounded by a thin red halo.
-The lesions may be single or multiple (two to six), and they heal without
scarring in 7–12 days.
- Mainly found in on the non-keratinized mobile mucosa, lips cheeks, floot of
the mouth.
Ulcerative lesions
2-Recurrent Aphthous Stomatitis
52. Ozone treatment of aphtous ulseration
Treatment is aimed at reducing the pain and swelling and speeding healing, and
may involve systemic or topical steroids, analgesics (pain killers), antiseptics,
anti-inflammatories or barrier pastes to protect the raw area.
53. Major recurrent Aphthous Stomatitis
-The major form is characterized by deep painful ulcers, 1–2 cm in diameter,
that persist for 3–6 weeks and may cause scarring.
- The number of lesions varies from one to five.
- Found in any area of the mucosa, including keratinized dorsum of the
tongue, palate.
Ulcerative lesions
2-Recurrent Aphthous Stomatitis
57. Aphthous ulceration
Minor aphthae
(90 -95 %)
Major aphthae
(5-10%)
Herpetiform ulcers
(1-5%)
Age of onset Childhood or
adolescence
Childhood or
adolescence
Young adult
Ulcer size 2–4 mm 10 mm or larger Initially tiny, but
ulcers coalesce
Number of ulcers Up to about 6 Up to about 6 10–100
Sites affected Mainly vestibule,
labial, buccal
mucosa &
floor of mouth
Any site Any site but often on
ventrum of tongue
Duration of each
ulcer
Up to 10 days Up to 1 month Up to 1 month
58. Ulcerative lesions
Main causes of oral ulceration
1. Local Causes
2. Recurrent Aphthous Stomatitis
3. Infections
4. Drugs
5. Malignant disease
6. Systemic disease
59. Ulcerative lesions
3) Infections
• Many infections can cause oral ulceration:
Agent Example
Viral chickenpox, hand, foot and mouth disease, herpangina, herpetic
stomatitis, human immunodeficiency virus, infectious
mononucleosis
Bacterial acute necrotizing ulcerative gingivitis, syphilis, tuberculosis
Fungal blastomycosis, cryptococcosis, histoplasmosis,
paracoccidioidomycosis
60. Ulcerative lesions
Infectious causes of oral mucosal ulcers
1- Viral
• Vesiculobullous diseases caused by viruses (see lecture №6)
• Human herpesvirus 8 (HHV-8)
• Human Immunodeficiency virus
61. Human Herpes virus-8 (HHV-8)
-The causative microbe for Kaposi’s sarcoma (KS).
-Kaposi sarcoma is a malignant neoplasm of endothelial cell origin.
-Four forms of KS are recognized:
Classic, African (endemic), Immunosuppression-associated (iatrogenic)
and
AIDS-related (epidemic): This has a high incidence among AIDS patients,
primarily involves the skin, lymph nodes, viscera, and frequently the oral
mucosa.
Ulcerative lesions
Infectious causes of oral mucosal ulcers
1- Viral
62. Kaposi’s sarcoma starts as a spot or erythematous or violet plaque which
appears flat. Its habitual location is the palate or the gingiva.
63. Human Herpes virus-8 (HHV-8)
-Clinically: the oral lesions present as multiple or solitary red or brownish-red
patches or elevated plaques or tumors.
- The palate and gingiva are the most common sites affected, followed by
buccal mucosa, tongue, and lips.
- Differential diagnosis: Pyogenic granuloma, peripheral giant-cell
granuloma, hemangioma.
- Treatment: Interferon, chemotherapy, radiotherapy, or surgical excision in
small, localized lesions.
Ulcerative lesions
Infectious causes of oral mucosal ulcers
1- Viral
64. Human Immunodeficiency Virus (HIV)
- A minority of patients with severe HIV disease will develop deep, necrotic
ulcers of unknown aetiology.
- These ulcers are painful, cause profound dysphagia and can arise on any
oral mucosal surface, although the buccal and pharyngeal mucosa ate the
more commonly affected sites.
Ulcerative lesions
Infectious causes of oral mucosal ulcers
1- Viral
65. Human Immunodeficiency Virus (HIV)
-The ulcers typically resolve with systemic thalidomide (e.g. 200 mg daily)
- Small number of patients with HIV disease may have ulcers similar to that of
recurrent aphthous stomatitis (RAS), although whether the frequency of RAS
in HIV is truly increased remains unclear.
Ulcerative lesions
Infectious causes of oral mucosal ulcers
1- Viral
69. Ulcerative lesions
Infectious causes of oral mucosal ulcers
2- Bacterial
i) Acute Necrotizing Ulcerative Gingivitis (ANUG)
-This entity used to be called "Trench Mouth" because of its prevalence in
soldiers fighting in the trenches during world war I.
- Etiology: Fusobacterium nucleatum, Treponema vincentii, and probably other
bacteria play an important role.
- Predisposing factors are emotional stress, smoking, poor oral hygiene, local
trauma, and mainly HIV infection.
72. Ulcerative lesions
Infectious causes of oral mucosal ulcers
2- Bacterial
i) Acute Necrotizing Ulcerative Gingivitis (ANUG)
-Clinical features The characteristic clinical feature is painful necrosis of the
interdental papillae and the gingival margins, and the formation of craters
covered with a gray pseudomembrane.
- Spontaneous gingival bleeding, halitosis, and intense salivation are common.
Fever,
malaise, and lymphadenopathy are less common.
-Rarely, the lesions may extend beyond the gingiva (necrotizing ulcerative
stomatitis).
-The diagnosis is made at the clinical level.
74. Ulcerative lesions
Infectious causes of oral mucosal ulcers
2- Bacterial
i) Acute Necrotizing Ulcerative Gingivitis (ANUG)
- Differential diagnosis Herpetic gingivitis, Desquamative gingivitis,
Agranulocytosis, leukemia.
-Treatment Systemic metronidazole and oxygen-releasing agents topically
are the best therapy in the acute phase, followed by a mechanical gingival
treatment.
75. Ulcerative lesions
Infectious causes of oral mucosal ulcers
2- Bacterial
ii) Syphilis
- Syphilis is a relatively common sexually transmitted disease.
- Etiology Treponema pallidum.
-Clinical features: Syphilis may be acquired (common) or congenital (rare).
- Acquired syphilis is classified as primary, secondary and tertiary.
76. Ulcerative lesions
Infectious causes of oral mucosal ulcers
2- Bacterial
ii) Syphilis
-Clinical features:
-The characteristic lesion in the primary stage is the chancre that appears at
the site of inoculation, usually three weeks after the infection.
- Oral chancre appears in about 5–10% of cases, and clinically presents as a
painless ulcer with a smooth surface, raised borders, and an indurated base.
- Regional lymphadenopathy is a constant finding.
78. Ulcerative lesions
Infectious causes of oral mucosal ulcers
2- Bacterial
ii) Syphilis
- Differential diagnosis Traumatic ulcer, aphthous ulcer, tuberculosis, herpes
simplex, candidiasis, erythema multiforme, lichen planus.
-Treatment Penicillin is the antibiotic of choice. Erythromycin or ephalosporins
are good alternatives.
79. Ulcerative lesions
Infectious causes of oral mucosal ulcers
2- Bacterial
iii) Tuberculosis
-Tuberculosis is a chronic, granulomatous, infectious disease that primarily
affects the lungs.
- Etiology Mycobacterium tuberculosis.
-Clinical features The oral lesions are rare, and usually secondary to
pulmonary tuberculosis.
-The tuberculosis ulcer is the most common feature.
- Clinically, the ulcer is painless and irregular, with a thin undermined border
and a vegetating surface, usually covered by a gray-yellowish exudate.
- The dorsum of the tongue is the most commonly affected site, followed by the
lip, buccal mucosa, and palate.
80. Ulcerative lesions
Infectious causes of oral mucosal ulcers
2- Bacterial
iii) Tuberculosis
- Clinically, the ulcer is painless and irregular, with a thin undermined border
and a vegetating surface, usually covered by a gray-yellowish exudate.
- The dorsum of the tongue is the most commonly affected site, followed by the
lip, buccal mucosa, and palate.
- Differential diagnosis: carcinomas, syphilis, eosinophilic
ulcer, necrotizing sialadenometaplasia, malignant granuloma, major aphthous
ulcer.
- Treatment Antituberculous drugs.