Peripheral and central giant cell granulomaRijuwana77
This document discusses two types of non-epithelial tumours of the oral cavity: peripheral giant cell granuloma and central giant cell granuloma. Peripheral giant cell granuloma originates from the periodontal membrane or alveolar bone and presents as a soft tissue nodule composed of multinucleated giant cells. Central giant cell granuloma is a rare, benign, intraosseous lesion most commonly found in the mandible of young people that causes expansion of the bone and resorption of tooth roots. Both lesions contain proliferation of multinucleated giant cells and other cells and may require surgical excision, with central giant cell granuloma having a higher rate of recurrence.
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
Peripheral giant cell granuloma (giant cell epulisKhin Soe
The document discusses two types of giant cell lesions of the jaw: peripheral giant cell granuloma (PGG) and central giant cell granuloma (CGG). PGG is a reactive lesion caused by local irritation or trauma that occurs on the gingiva. CGG is a benign process that occurs within the jaw bones and can be non-aggressive or aggressive depending on symptoms and growth rate. Both lesions contain multinucleated giant cells and are treated with surgical excision, with CGG having a slightly higher recurrence rate. Key distinguishing features and histological characteristics are provided.
This document discusses pigmented lesions that can occur in the oral cavity. It begins by explaining that pigmentation can be exogenous or endogenous in origin, with the main endogenous pigments being melanin, hemoglobin, hemosiderin and carotene. It then discusses several specific conditions that can cause oral pigmentation, including physiologic pigmentation, Peutz-Jeghers syndrome, Addison's disease, heavy metal exposure, Kaposi's sarcoma, drug-induced pigmentation, postinflammatory pigmentation, smoker's melanosis, vascular lesions, melanotic macules, pigmented nevi, blue nevi, melanoacanthoma, and oral melanoma. Differential diagnosis of pigmented lesions involves considering
Osteomyelitis is an infection of bone that can affect the jaws. It originates from Greek words meaning "bone marrow infection". The infection causes ischemia and necrosis of the infected bone. It can be acute or chronic, suppurative or nonsuppurative. Common causes are odontogenic infections, trauma, surgery, and hematogenous spread. Symptoms include swelling, pain, and draining sinus tracts. Treatment involves antibiotics, surgical drainage, debridement of necrotic bone, and hyperbaric oxygen therapy in some cases.
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.
Temporomandibular joint disorders (TMJDs) can be caused by various factors like dysfunction syndrome, pathological changes, trauma, or developmental abnormalities. Common symptoms include pain, joint sounds like clicking, restricted mouth opening, swelling, and trismus. Investigations involve taking a thorough history, examining for tenderness and sounds, and obtaining imaging like CT or MRI. Management depends on the underlying cause but commonly involves conservative measures like splint therapy, analgesics, muscle relaxants, and physiotherapy. More severe internal derangements may require specialist interventions and occasionally surgery.
Red lesions of the oral mucosa can be caused by a variety of factors including trauma, infections, inflammatory conditions, and systemic diseases. Erythematous candidiasis presents as erythematous patches or areas on the tongue and palate caused by Candida infections. Lichen planus causes erythematous lesions that may be difficult to distinguish from other conditions like erythema multiforme. Reactive lesions like pyogenic granulomas and peripheral giant cell granulomas develop in response to local irritation or trauma. Geographic tongue appears as migrating erythematous lesions surrounded by white borders on the dorsal tongue.
Peripheral and central giant cell granulomaRijuwana77
This document discusses two types of non-epithelial tumours of the oral cavity: peripheral giant cell granuloma and central giant cell granuloma. Peripheral giant cell granuloma originates from the periodontal membrane or alveolar bone and presents as a soft tissue nodule composed of multinucleated giant cells. Central giant cell granuloma is a rare, benign, intraosseous lesion most commonly found in the mandible of young people that causes expansion of the bone and resorption of tooth roots. Both lesions contain proliferation of multinucleated giant cells and other cells and may require surgical excision, with central giant cell granuloma having a higher rate of recurrence.
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
Peripheral giant cell granuloma (giant cell epulisKhin Soe
The document discusses two types of giant cell lesions of the jaw: peripheral giant cell granuloma (PGG) and central giant cell granuloma (CGG). PGG is a reactive lesion caused by local irritation or trauma that occurs on the gingiva. CGG is a benign process that occurs within the jaw bones and can be non-aggressive or aggressive depending on symptoms and growth rate. Both lesions contain multinucleated giant cells and are treated with surgical excision, with CGG having a slightly higher recurrence rate. Key distinguishing features and histological characteristics are provided.
This document discusses pigmented lesions that can occur in the oral cavity. It begins by explaining that pigmentation can be exogenous or endogenous in origin, with the main endogenous pigments being melanin, hemoglobin, hemosiderin and carotene. It then discusses several specific conditions that can cause oral pigmentation, including physiologic pigmentation, Peutz-Jeghers syndrome, Addison's disease, heavy metal exposure, Kaposi's sarcoma, drug-induced pigmentation, postinflammatory pigmentation, smoker's melanosis, vascular lesions, melanotic macules, pigmented nevi, blue nevi, melanoacanthoma, and oral melanoma. Differential diagnosis of pigmented lesions involves considering
Osteomyelitis is an infection of bone that can affect the jaws. It originates from Greek words meaning "bone marrow infection". The infection causes ischemia and necrosis of the infected bone. It can be acute or chronic, suppurative or nonsuppurative. Common causes are odontogenic infections, trauma, surgery, and hematogenous spread. Symptoms include swelling, pain, and draining sinus tracts. Treatment involves antibiotics, surgical drainage, debridement of necrotic bone, and hyperbaric oxygen therapy in some cases.
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.
Temporomandibular joint disorders (TMJDs) can be caused by various factors like dysfunction syndrome, pathological changes, trauma, or developmental abnormalities. Common symptoms include pain, joint sounds like clicking, restricted mouth opening, swelling, and trismus. Investigations involve taking a thorough history, examining for tenderness and sounds, and obtaining imaging like CT or MRI. Management depends on the underlying cause but commonly involves conservative measures like splint therapy, analgesics, muscle relaxants, and physiotherapy. More severe internal derangements may require specialist interventions and occasionally surgery.
Red lesions of the oral mucosa can be caused by a variety of factors including trauma, infections, inflammatory conditions, and systemic diseases. Erythematous candidiasis presents as erythematous patches or areas on the tongue and palate caused by Candida infections. Lichen planus causes erythematous lesions that may be difficult to distinguish from other conditions like erythema multiforme. Reactive lesions like pyogenic granulomas and peripheral giant cell granulomas develop in response to local irritation or trauma. Geographic tongue appears as migrating erythematous lesions surrounded by white borders on the dorsal tongue.
Mandibulofacial dysostosis is a genetic condition caused by the failure of neural crest cells to migrate properly during facial development. It is characterized by underdeveloped bones and tissues of the midface and jaw. Common features include a small lower jaw, high arched palate, cleft palate, unusually large mouth, downward slanted eyes, and varying degrees of vision problems and tooth abnormalities. Treatment focuses on cosmetic surgery to improve facial structure and hearing.
Oral mucosa reflects the health of the whole human body at a first glance.If any disorder is present in the system it will first appear in oral cavity. Here is an overview of certain pigmented lesions.
This document discusses endogenous pigmentation of the oral mucosa. It begins by classifying pigmentation as focal, diffuse, or associated with systemic diseases. Common causes of pigmentation include melanin, hemoglobin, carotene, and hemosiderin. Specific conditions addressed include freckles, oral melanotic macules, oral melanoacanthoma, melanocytic nevi, and malignant melanoma. Diffuse pigmentation can be due to physiologic pigmentation, drugs, smoking, or post-inflammatory changes. Systemic diseases like Addison's disease and Peutz-Jeghers syndrome can also cause oral pigmentation. Histopathology and differential diagnoses are provided for many of the conditions.
This document discusses various types of oral pigmentation. It defines pigmentation as the deposition of pigments in oral tissues. Pigmentation can be endogenous, arising from within the body due to increased melanin or melanocytes, or exogenous, arising from external sources. Endogenous pigmentation includes conditions like freckles and oral melanotic macules. Exogenous pigmentation includes amalgam tattoos. Other causes discussed include drug-induced melanosis, smoker's melanosis, melasma, and systemic diseases. Diagnosis, clinical features, pathology, and treatment are described for different conditions presenting as oral pigmentation.
This document discusses various types of red and white lesions that can occur in the oral mucosa. It describes hereditary lesions including leukodema, white sponge nevus, and hereditary benign intraepithelial dyskeratosis. It also covers reactive/inflammatory lesions such as frictional keratosis. Infectious lesions covered include oral hairy leukoplakia caused by Epstein-Barr virus and various forms of oral candidiasis. Idiopathic "true" leukoplakia and erythroplakia are also discussed. Treatment options are provided for many of the conditions.
Hyperparathyroidism is a condition caused by excess parathyroid hormone that can lead to changes in bone structure and density. Primary hyperparathyroidism is usually caused by a benign tumor of the parathyroid glands and affects females more than males aged 30-60. Symptoms include those related to hypercalcemia like bone pain. Imaging may show features like brown tumors, osteopenia, and a "salt and pepper skull". Surgical removal of the tumor can resolve the condition and reverse changes except for sites of brown tumors.
Oral Lichen Planus is a common chronic inflammatory disease that affects the oral mucosa. It is characterized by T-cell mediated apoptosis of epithelial cells that leads to inflammation. The cause is unknown but believed to be autoimmune in nature. It presents as white reticulated lesions that can be reticular, papular, plaque-like, atrophic, erosive, bullous or ulcerative. Histopathology shows saw-tooth rete pegs and Civatte bodies. Direct immunofluorescence demonstrates a fibrin band in the basement membrane. The erosive form has a risk of malignant transformation. Treatment involves topical corticosteroids and immunosuppressants to reduce symptoms of pain and inflammation.
This document discusses periodontal disease and its effects. It describes the principal fiber groups in the periodontal ligament that help retain teeth. It then discusses signs of periodontal disease like pocket formation, gingival recession, and tooth mobility. Pocket types like gingival and periodontal pockets are defined. Diagnosis involves using a periodontal probe to measure pocket depth and check for furcation involvement. Treatment aims to reduce inflammation and regenerate lost bone and tissues.
A cyst is an epithelium-lined sac containing fluid or semisolid material. In the formation of a cyst, the epithelial cells first proliferate and later undergo degeneration and liquefaction. The liquefied material exerts equal pressure on the walls of the cyst from within. Cysts grow by expansion and thus displace the adjacent teeth by pressure. May can produce expansion of the cortical bone. On a radiograph, the radiolucency of a cyst is usually bordered by a radiopaque periphery of dense sclerotic bone. The radiolucency may be unilocular or multilocular. Odontogenic cysts are those which arise from the epithelium associated with the development of teeth. The source of epithelium is from the enamel organ, the reduced enamel epithelium, the cell rests of Malassez or the remnants of the dental lamina.
The document discusses several types of odontogenic tumors that can occur in the jaws. It focuses on describing ameloblastoma, adenomatoid tumor, and calcifying epithelial odontogenic tumor. Ameloblastoma is a benign but locally aggressive tumor arising from odontogenic epithelium. It commonly presents as a painless swelling in the mandible and radiographs show multilocular radiolucency. Histologically there are follicular or plexiform patterns. Adenomatoid tumor is a rare benign tumor associated with impacted teeth. Calcifying epithelial odontogenic tumor is a rare, locally aggressive tumor that can be mistaken for carcinoma, presenting with calcified masses visible on radiographs.
This document discusses various developmental disturbances that can affect the tongue, including microglossia (small tongue), macroglossia (large tongue), ankyloglossia (tongue tie), cleft tongue, fissured tongue, median rhomboid glossitis (reddish patch on dorsal tongue), benign migratory glossitis (geographic tongue), hairy tongue, lingual varices (dilated veins on tongue), and lingual thyroid nodule (thyroid tissue on tongue). Many of these conditions can cause difficulties with speech, swallowing, or irritation of the tongue. Treatment may include surgery, antifungal medications, or thyroid hormone supplements.
This document discusses red and white lesions of the oral cavity, focusing on oral candidiasis. It describes the various types of oral candidiasis including pseudomembranous, erythematous, chronic plaque-type, and median rhomboid glossitis. Predisposing factors, clinical findings, diagnosis, treatment with antifungal medications or surgery, and prognosis are summarized for each type. Chronic hyperplastic candidiasis may require long-term antifungal therapy or surgery due to risk of recurrence. Overall prognosis is generally good if predisposing factors can be addressed.
This document discusses various types of pigmentation that can occur in the oral cavity. It begins with an introduction and classification of pigmentation as physiologic, pathologic, exogenous, or endogenous. It then describes several types of focal melanocytic pigmentation including freckles, oral melanotic macules, oral melanoacanthomas, melanocytic nevi, and malignant melanoma. It also discusses various types of multifocal and diffuse pigmentation including physiologic, smoker's melanosis, drug-induced melanosis, melasma, and postinflammatory hyperpigmentation. Finally, it covers exogenous pigmentation sources, heavy metal pigmentation, hemoglobin and iron-associated pigmentation, and melanosis associated with
The document discusses various white oral lesions including leukoedema, leukoplakia, lichen planus, and candidiasis. Leukoedema is a common white lesion considered normal variation, while leukoplakia is a premalignant condition defined as a white patch that is not caused by other disease. Lichen planus is a chronic inflammatory disease presenting as bilateral white lesions, and candidiasis is an opportunistic fungal infection caused by Candida albicans.
Necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP) are microbial diseases caused by a mixed bacterial infection and impaired host response. NUG presents with crater-like ulcers and gray pseudomembrane on the gums, accompanied by pain and foul taste. If untreated, NUG can progress to NUP and involve bone loss. Treatment involves removing debris, using antiseptics like chlorhexidine, scaling, and antibiotics in severe cases. Prognosis is good with proper treatment and maintenance of oral hygiene.
This document discusses and classifies various oral white lesions. It describes hereditary lesions including leukoedema, white sponge nevus, and follicular keratosis. Reactive lesions such as frictional keratosis, smokeless tobacco lesions, and nicotine stomatitis are covered. Pre-malignant lesions like actinic cheilitis and idiopathic leukoplakia are also summarized, along with other white lesions including geographic tongue and lichen planus. Non-epithelial lesions like candidiasis, mucosal burns, and lipoma are briefly outlined. The document provides details on histopathological features and treatment for many of the conditions.
This document classifies and describes various oral white lesions. It discusses hereditary lesions such as leukoedema and white sponge nevus. Reactive lesions including frictional keratosis and nicotine stomatitis are covered. Preneoplastic lesions like actinic cheilitis and idiopathic leukoplakia are summarized. Other white lesions such as geographic tongue and lichen planus are also described. Non-epithelial lesions including candidiasis and Fordyce's granules are briefly outlined. Definitions of histopathological features and guidelines for differential diagnosis are provided.
Amelogenesis imperfecta is a hereditary disorder affecting enamel formation. There are three main types - hypoplastic (thin enamel), hypomaturation (improperly mineralized enamel), and hypocalcified (soft enamel). It is caused by defects during the three stages of enamel development: matrix formation, mineralization, and maturation. The condition has various inheritance patterns and clinical presentations depending on the genetic subtype. Treatment aims to restore aesthetics, sensitivity, and function and depends on the severity of enamel defects in each case.
The document defines and classifies different types of gingival enlargement based on etiology and pathologic changes. It describes inflammatory enlargement including chronic, acute, and drug-induced types. It also covers enlargements associated with systemic diseases, neoplastic enlargements including benign and malignant tumors, and false enlargements. Grading systems and detailed clinical, histological, and radiographic features are provided for many conditions.
This document classifies and describes different types of oral lesions. It discusses primary lesions like macules, papules, plaques, nodules, vesicles, bullae, pustules, purpura, petechiae and ecchymoses. It also discusses secondary lesions that result from primary lesions or injury, such as ulcers, erosions, fissures, scars, sinuses, fistulas and crusts. Each type of lesion is defined and examples are provided. Primary lesions represent basic skin reactions while secondary lesions result from modifications or complications of primary lesions.
SKIN CONDITION presentation for medical students.pptxIbrahimKargbo13
This document provides an outline for a course on skin conditions. It begins by listing common skin conditions categorized by symptoms such as itching, pigmentation, crusts, vesicles, pustules, and macules. It then defines dermatology as the study of skin, nails, and hair and discusses the functions and facts about skin. The document outlines important aspects of dermatologic history taking and examination, including describing different types of skin lesions and how their configuration, texture, location, and distribution can provide clues to diagnosis.
Mandibulofacial dysostosis is a genetic condition caused by the failure of neural crest cells to migrate properly during facial development. It is characterized by underdeveloped bones and tissues of the midface and jaw. Common features include a small lower jaw, high arched palate, cleft palate, unusually large mouth, downward slanted eyes, and varying degrees of vision problems and tooth abnormalities. Treatment focuses on cosmetic surgery to improve facial structure and hearing.
Oral mucosa reflects the health of the whole human body at a first glance.If any disorder is present in the system it will first appear in oral cavity. Here is an overview of certain pigmented lesions.
This document discusses endogenous pigmentation of the oral mucosa. It begins by classifying pigmentation as focal, diffuse, or associated with systemic diseases. Common causes of pigmentation include melanin, hemoglobin, carotene, and hemosiderin. Specific conditions addressed include freckles, oral melanotic macules, oral melanoacanthoma, melanocytic nevi, and malignant melanoma. Diffuse pigmentation can be due to physiologic pigmentation, drugs, smoking, or post-inflammatory changes. Systemic diseases like Addison's disease and Peutz-Jeghers syndrome can also cause oral pigmentation. Histopathology and differential diagnoses are provided for many of the conditions.
This document discusses various types of oral pigmentation. It defines pigmentation as the deposition of pigments in oral tissues. Pigmentation can be endogenous, arising from within the body due to increased melanin or melanocytes, or exogenous, arising from external sources. Endogenous pigmentation includes conditions like freckles and oral melanotic macules. Exogenous pigmentation includes amalgam tattoos. Other causes discussed include drug-induced melanosis, smoker's melanosis, melasma, and systemic diseases. Diagnosis, clinical features, pathology, and treatment are described for different conditions presenting as oral pigmentation.
This document discusses various types of red and white lesions that can occur in the oral mucosa. It describes hereditary lesions including leukodema, white sponge nevus, and hereditary benign intraepithelial dyskeratosis. It also covers reactive/inflammatory lesions such as frictional keratosis. Infectious lesions covered include oral hairy leukoplakia caused by Epstein-Barr virus and various forms of oral candidiasis. Idiopathic "true" leukoplakia and erythroplakia are also discussed. Treatment options are provided for many of the conditions.
Hyperparathyroidism is a condition caused by excess parathyroid hormone that can lead to changes in bone structure and density. Primary hyperparathyroidism is usually caused by a benign tumor of the parathyroid glands and affects females more than males aged 30-60. Symptoms include those related to hypercalcemia like bone pain. Imaging may show features like brown tumors, osteopenia, and a "salt and pepper skull". Surgical removal of the tumor can resolve the condition and reverse changes except for sites of brown tumors.
Oral Lichen Planus is a common chronic inflammatory disease that affects the oral mucosa. It is characterized by T-cell mediated apoptosis of epithelial cells that leads to inflammation. The cause is unknown but believed to be autoimmune in nature. It presents as white reticulated lesions that can be reticular, papular, plaque-like, atrophic, erosive, bullous or ulcerative. Histopathology shows saw-tooth rete pegs and Civatte bodies. Direct immunofluorescence demonstrates a fibrin band in the basement membrane. The erosive form has a risk of malignant transformation. Treatment involves topical corticosteroids and immunosuppressants to reduce symptoms of pain and inflammation.
This document discusses periodontal disease and its effects. It describes the principal fiber groups in the periodontal ligament that help retain teeth. It then discusses signs of periodontal disease like pocket formation, gingival recession, and tooth mobility. Pocket types like gingival and periodontal pockets are defined. Diagnosis involves using a periodontal probe to measure pocket depth and check for furcation involvement. Treatment aims to reduce inflammation and regenerate lost bone and tissues.
A cyst is an epithelium-lined sac containing fluid or semisolid material. In the formation of a cyst, the epithelial cells first proliferate and later undergo degeneration and liquefaction. The liquefied material exerts equal pressure on the walls of the cyst from within. Cysts grow by expansion and thus displace the adjacent teeth by pressure. May can produce expansion of the cortical bone. On a radiograph, the radiolucency of a cyst is usually bordered by a radiopaque periphery of dense sclerotic bone. The radiolucency may be unilocular or multilocular. Odontogenic cysts are those which arise from the epithelium associated with the development of teeth. The source of epithelium is from the enamel organ, the reduced enamel epithelium, the cell rests of Malassez or the remnants of the dental lamina.
The document discusses several types of odontogenic tumors that can occur in the jaws. It focuses on describing ameloblastoma, adenomatoid tumor, and calcifying epithelial odontogenic tumor. Ameloblastoma is a benign but locally aggressive tumor arising from odontogenic epithelium. It commonly presents as a painless swelling in the mandible and radiographs show multilocular radiolucency. Histologically there are follicular or plexiform patterns. Adenomatoid tumor is a rare benign tumor associated with impacted teeth. Calcifying epithelial odontogenic tumor is a rare, locally aggressive tumor that can be mistaken for carcinoma, presenting with calcified masses visible on radiographs.
This document discusses various developmental disturbances that can affect the tongue, including microglossia (small tongue), macroglossia (large tongue), ankyloglossia (tongue tie), cleft tongue, fissured tongue, median rhomboid glossitis (reddish patch on dorsal tongue), benign migratory glossitis (geographic tongue), hairy tongue, lingual varices (dilated veins on tongue), and lingual thyroid nodule (thyroid tissue on tongue). Many of these conditions can cause difficulties with speech, swallowing, or irritation of the tongue. Treatment may include surgery, antifungal medications, or thyroid hormone supplements.
This document discusses red and white lesions of the oral cavity, focusing on oral candidiasis. It describes the various types of oral candidiasis including pseudomembranous, erythematous, chronic plaque-type, and median rhomboid glossitis. Predisposing factors, clinical findings, diagnosis, treatment with antifungal medications or surgery, and prognosis are summarized for each type. Chronic hyperplastic candidiasis may require long-term antifungal therapy or surgery due to risk of recurrence. Overall prognosis is generally good if predisposing factors can be addressed.
This document discusses various types of pigmentation that can occur in the oral cavity. It begins with an introduction and classification of pigmentation as physiologic, pathologic, exogenous, or endogenous. It then describes several types of focal melanocytic pigmentation including freckles, oral melanotic macules, oral melanoacanthomas, melanocytic nevi, and malignant melanoma. It also discusses various types of multifocal and diffuse pigmentation including physiologic, smoker's melanosis, drug-induced melanosis, melasma, and postinflammatory hyperpigmentation. Finally, it covers exogenous pigmentation sources, heavy metal pigmentation, hemoglobin and iron-associated pigmentation, and melanosis associated with
The document discusses various white oral lesions including leukoedema, leukoplakia, lichen planus, and candidiasis. Leukoedema is a common white lesion considered normal variation, while leukoplakia is a premalignant condition defined as a white patch that is not caused by other disease. Lichen planus is a chronic inflammatory disease presenting as bilateral white lesions, and candidiasis is an opportunistic fungal infection caused by Candida albicans.
Necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP) are microbial diseases caused by a mixed bacterial infection and impaired host response. NUG presents with crater-like ulcers and gray pseudomembrane on the gums, accompanied by pain and foul taste. If untreated, NUG can progress to NUP and involve bone loss. Treatment involves removing debris, using antiseptics like chlorhexidine, scaling, and antibiotics in severe cases. Prognosis is good with proper treatment and maintenance of oral hygiene.
This document discusses and classifies various oral white lesions. It describes hereditary lesions including leukoedema, white sponge nevus, and follicular keratosis. Reactive lesions such as frictional keratosis, smokeless tobacco lesions, and nicotine stomatitis are covered. Pre-malignant lesions like actinic cheilitis and idiopathic leukoplakia are also summarized, along with other white lesions including geographic tongue and lichen planus. Non-epithelial lesions like candidiasis, mucosal burns, and lipoma are briefly outlined. The document provides details on histopathological features and treatment for many of the conditions.
This document classifies and describes various oral white lesions. It discusses hereditary lesions such as leukoedema and white sponge nevus. Reactive lesions including frictional keratosis and nicotine stomatitis are covered. Preneoplastic lesions like actinic cheilitis and idiopathic leukoplakia are summarized. Other white lesions such as geographic tongue and lichen planus are also described. Non-epithelial lesions including candidiasis and Fordyce's granules are briefly outlined. Definitions of histopathological features and guidelines for differential diagnosis are provided.
Amelogenesis imperfecta is a hereditary disorder affecting enamel formation. There are three main types - hypoplastic (thin enamel), hypomaturation (improperly mineralized enamel), and hypocalcified (soft enamel). It is caused by defects during the three stages of enamel development: matrix formation, mineralization, and maturation. The condition has various inheritance patterns and clinical presentations depending on the genetic subtype. Treatment aims to restore aesthetics, sensitivity, and function and depends on the severity of enamel defects in each case.
The document defines and classifies different types of gingival enlargement based on etiology and pathologic changes. It describes inflammatory enlargement including chronic, acute, and drug-induced types. It also covers enlargements associated with systemic diseases, neoplastic enlargements including benign and malignant tumors, and false enlargements. Grading systems and detailed clinical, histological, and radiographic features are provided for many conditions.
This document classifies and describes different types of oral lesions. It discusses primary lesions like macules, papules, plaques, nodules, vesicles, bullae, pustules, purpura, petechiae and ecchymoses. It also discusses secondary lesions that result from primary lesions or injury, such as ulcers, erosions, fissures, scars, sinuses, fistulas and crusts. Each type of lesion is defined and examples are provided. Primary lesions represent basic skin reactions while secondary lesions result from modifications or complications of primary lesions.
SKIN CONDITION presentation for medical students.pptxIbrahimKargbo13
This document provides an outline for a course on skin conditions. It begins by listing common skin conditions categorized by symptoms such as itching, pigmentation, crusts, vesicles, pustules, and macules. It then defines dermatology as the study of skin, nails, and hair and discusses the functions and facts about skin. The document outlines important aspects of dermatologic history taking and examination, including describing different types of skin lesions and how their configuration, texture, location, and distribution can provide clues to diagnosis.
This document defines and describes various primary and secondary skin lesions seen in veterinary dermatology. It defines primary lesions as those directly associated with the underlying disease process, such as macules, papules, plaques, nodules, tumors, pustules, vesicles, wheals, and cysts. Secondary lesions result from trauma, time, or degree of skin insult and include comedones, crusts, erythema, erosions, ulcers, sinuses/fistulas, self-trauma, scars, fissures, lichenification, hyperpigmentation, and hypopigmentation. Each lesion is concisely defined and an example image provided for illustration.
Primary skin lesions include macules, papules, plaques, nodules, tumors, and wheals. Secondary lesions develop from primary lesions and include scales, crusts, excoriations, fissures, erosions, ulcers, and scars. Special lesions occur under certain conditions and include erythema, telangiectasia, purpura, petechiae, ecchymoses, vibices, and hematomas. The document provides detailed definitions and descriptions of these various skin lesions.
This document describes how to describe skin lesions based on their morphology. It discusses the primary morphology of lesions including whether they are flat or raised, their size, and constituency. It then discusses secondary morphology including color, shape, texture, and location. Specific lesion types are defined such as macules, papules, plaques, nodules, tumors, purpura, ecchymosis, petechiae, urticaria, ulcers, scales, actinic keratoses, target lesions, serpiginous lesions, herpetiform lesions, textures including hyperkeratosis, lichenification, xanthomas, induration, and features such as umbilicated lesions.
This document describes how to describe various skin lesions by their features and type. It discusses primary lesions like macules, papules, plaques, nodules, vesicles, bullae and pustules. It also covers secondary lesions developed from skin diseases like scales, crusts, erosions and fissures. Finally, it provides examples of specific lesions and how they can be classified by their appearance, shape, arrangement and distribution on the body.
This document describes how to describe various skin lesions by their features and type. It discusses primary lesions like macules, papules, plaques, nodules, vesicles, bullae and pustules. It also covers secondary lesions developed from skin diseases like scales, crusts, erosions and fissures. Finally, it provides examples of specific lesions and how they can be classified by their appearance, shape, arrangement and distribution on the body.
The skin is composed of three layers: the epidermis, dermis, and hypodermis. The epidermis contains keratinocytes and dendritic cells. It has multiple layers including the basal, spinous, granular, clear, and horny layers. The dermis contains fibrous and cellular connective tissue with nerve and vascular networks. The hypodermis contains adipose tissue and larger blood vessels and nerves. The skin has several functions including serving as a barrier, regulating temperature, sensation, vitamin D synthesis, and as a blood reservoir. Primary skin lesions include macules, papules, vesicles, pustules, nodules, and plaques. Secondary lesions develop from primary lesions and include scales
The document discusses different types of skin lesions and diseases that can affect the skin. It defines and provides examples of various primary skin lesions like macules, papules, vesicles, and pustules. It also discusses secondary skin lesions that result from primary lesions, such as ulcers, scales, crusts, and erosions. Finally, it lists common skin diseases and their typical symptoms and locations on the body.
This document provides information on examining the skin and describing cutaneous lesions and diseases. It discusses examining the skin, genitalia, mucous membranes, and skin appendages. It describes the key aspects to cover when discussing each disease, including definition, etiology, epidemiology, pathogenesis, clinical picture, investigations, treatment, prognosis and fate. It then describes various primary cutaneous signs like macules, papules, plaques, nodules, vesicles, and pustules. It also covers secondary lesions including scales, crusts, erosions, ulcers, fissures, and scars. The diagnosis of skin diseases is based on the objective physical characteristics and distribution of lesions seen on examination.
Primary skin lesions include macules, papules, plaques, nodules, wheals, angioedema, vesicles, bullae, pustules, cysts, and abscesses. Secondary lesions result from primary lesions and include crusts, excoriations, erosions, ulcers, and scars. Special lesions are diagnostic of particular diseases such as burrows, comedones, milia, and telangiectasia.
This document defines and describes various skin lesions and conditions. It defines erythema, plaques, papules, macules, vesicles, bullae, pustules, abscesses, wheals, angioedema, nodules, tumors, papillomas, petechiae, purpura, ecchymoses, hematomas, comedones, telangiectasia, poikiloderma, scales, keratoses, crusts, ulcers, erosions, excoriations, fissures, sinuses, scars, atrophy, lichenification, and striae. Each term is precisely defined based on appearance, size, composition, and other distinguishing features.
1. The document summarizes various systemic diseases that can manifest themselves through changes in the skin, including hyperlipidemia, gastrointestinal diseases, carcinoid syndrome, diabetes mellitus, liver disease, HIV/AIDS, sarcoidosis, mastocytosis, amyloidosis, acromegaly, hypopituitarism, hypothyroidism, hyperthyroidism, Cushing's syndrome, porphyria, rheumatoid arthritis, Reiter's disease, and myelodysplastic syndrome.
2. Common skin manifestations of these diseases include xanthelasma, xanthoma, erythema nodosum, pyoderma gangrenosum, cutaneous metastases, recurrent skin infections, nec
This document provides guidance on examining patients presenting with skin diseases. It details the important aspects of history taking including primary and secondary lesions, subjective and objective symptoms, and pertinent questions regarding duration, site, evolution, and associated symptoms. Physical examination involves detailed description of lesions including morphology, distribution, and configuration. Key signs related to macules, papules, plaques, vesicles, pustules, and other eruption types are defined. The document emphasizes close examination of nails, hair, and mucosal surfaces to identify relevant findings.
This document provides information on different types of skin lesions seen at various ages and their characteristics. It discusses primary skin lesions such as macules, papules, nodules, tumors, plaques and vesicles/bullae. It also discusses secondary skin lesions that develop due to scratching or infection, such as scales, crusts, excoriations, erosions and ulcers. The document examines characteristics of various specific lesions like moles, freckles, lentigines, comedones, petechiae, purpura and ecchymoses. It concludes with discussing eczematous lesions and conditions like atrophy, hyperkeratosis and scarring.
Dermatitis is an inflammation of the skin that causes redness, swelling and itchiness. There are many types of dermatitis including atopic dermatitis, contact dermatitis and seborrheic dermatitis. Contact dermatitis occurs when the skin comes into contact with an irritant or allergen and can be either irritant or allergic in nature. Symptoms vary depending on the type but may include a rash, blisters, dry cracked skin and itchiness. Treatment involves identifying and avoiding triggers, using moisturizers and topical or oral medications like corticosteroids and antihistamines.
This document discusses the clinical presentation and diagnosis of various skin lesions. It describes key characteristics of macules, papules, plaques, nodules, vesicles, pustules, wheals, erosions, cysts, scaling, crusting, and other lesions. Highlighted are examples like iris-type lesions seen in conditions like erythema multiforme and granuloma annulare. The document emphasizes the importance of assessing lesion type, distribution, evolution over time, and correlating physical exam findings with patient history for accurate diagnosis of skin conditions.
This document provides guidance on diagnosing skin diseases. It outlines the key steps which include taking a thorough history, examining the patient for symptoms and signs of skin abnormalities, and performing relevant investigations. The history should explore symptoms of itching, pain, tingling and include questions on duration, triggers, and associated symptoms. The examination classifies primary skin lesions based on features like size, morphology, arrangement and distribution. Secondary lesions resulting from trauma or evolution are also described. Common diagnostic tools like magnifying lenses, glass slides for diascopy, and wood lamps are listed.
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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
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4. Primarylesions
Examples are
Macule
Patch
Papule
Plaque
Vesicle
Bulla
Pustule
Nodule
Purpura
Petechiae
Ecchymosis
striae
These are basic reaction patterns with
definite morphology
5. Secondarylesions
Examples
Erosion
Ulcer
Fissure
Crust
Sinus
Scar
Atrophy
These are lesions arising from primary lesion as a
result of traumatic injury or the external factors
8. Macule
Well circumscribed, flat lesion, size is less
than 1 cm and it is noticeable because of
their colour change from normal skin
colour.
Macules are flat, nonpalpable lesions
usually < 10 mm in diameter. Macules
represent a change in color and are not
raised or depressed compared to the skin
surface.
Examples
Red macule
Presence of vascular lesions
Inflammation
Brownish black
The presence of melanin, hemosiderin
10. Patch
Well circumscribed, flat lesion,
size is more than 1 cm.
Examples
Red
Haemangioma
Purpura, ecchymosis
Inflammation
Brownish black
The presence of melanin,
haemosiderin and drugs
13. Papule
Solid lesions raised above the skin
surface, which is less than 1cm in
diameter.
Papules are elevated lesions
usually < 10 mm in diameter that
can be felt or palpated.
Examples
White
Papulular lichen planus
Yellowish white
Fordyces granules
Red
Petechiae
Apthous
Erethema multiforme
15. Plaque
Solid, raised lesions, which is
more than 1cm in diameter.
Plaques are palpable lesions > 10
mm in diameter that are elevated
or depressed compared to the
skin surface. Plaques may be flat
topped or rounded
Examples
White
Leukoplakia
Lichen planus
candidiasis
Red
Erythroplakia
Black
Melanoma
19. Bulla
Bullae are clear fluid-filled
blisters > 10 mm in diameter.
These may be caused by
burns, bites, irritant contact
dermatitis or allergic contact
dermatitis, and drug reactions.
Classic autoimmune bullous
diseases include
pemphigus vulgaris and bullous
pemphigoid. Bullae also may
occur in inherited disorders of
skin fragility.
21. Pustule
Pustules are vesicles that
contain pus.
Pustules are common in
bacterial infections and
folliculitis and may arise in
some inflammatory disorders
including pustular psoriasis.
23. Nodule
Nodules are firm papules or
lesions that extend into the
dermis or subcutaneous tissue
. Examples include
cysts,
lipomas,
and fibromas.
25. Purpura
Purpura is a larger area of
hemorrhage that may be
palpable.
Palpable purpura is considered
the hallmark of
leukocytoclastic vasculitis.
Purpura may indicate a
coagulopathy.
Large areas of purpura may be
called ecchymoses or,
colloquially, bruises.
30. Erosion
Erosions are open areas of skin
that result from loss of part or
all of the epidermis.( without
involving connective tissue)
Erosions can be traumatic or
can occur with various
inflammatory or infectious skin
diseases.
An excoriation is a linear
erosion caused by scratching,
rubbing, or picking.
32. Ulcer
Ulcers result from loss of the
epidermis and at least part of
the dermis.
Break in continuity of
epithelium involving connective
tissue.
Causes include
Vesiculobullous and ulcerative
lesions
39. Sinus
Blind tract leading from the
surface down to the tissues.
It is lined by granulation
tissue, which maybe
epithelialized
Examples
Intraoral sinus
Periapical abscess
Periodontal abscess
Extraoral sinus
Periapical abscess
Osteomyelitis
Tuberculosis
41. Scar
Scars are areas of fibrosis that
replace normal skin after
injury.
Some scars become
hypertrophic or thickened and
raised.
Keloids are hypertrophic scars
that extend beyond the original
wound margin.
43. Atrophy
Atrophy is thinning of the skin,
which may appear dry and
wrinkled, resembling cigarette
paper.
Atrophy may be caused by
chronic sun exposure, aging,
and some inflammatory and
neoplastic skin diseases,
including cutaneous T-cell
lymphoma and lupus
erythematosus.
Atrophy also may result from
long-term use of potent topical
corticosteroids.