Exam 2 SG.pdf

1 Exam 2 Worksheet 1. Oral Pathologies · Aphthous Ulcers and Mucocele: Und...

1 Exam 2 Worksheet 1. Oral Pathologies · Aphthous Ulcers and Mucocele: Understand the presentation and characteristics of aphthous ulcers. Aphthous ○ Presentation: Tend to be clustered, recurrent and associated with immunologic disorders (celiacs, IBS, Bechets). The lesions appear as single or multiple, shallow, hyperemic, mucosal ulcerations covered by a thin exudate and rimmed by a narrow zone of erythema. Initially mononuclear but becomes neutrophil-rich upon secondary bacterial infection. ○ Characteristics: Painful, affecting up to 40% of the population, (first two decades of life mostly). Lesions typically resolve spontaneously in 7 to 10 days but sometimes persist for weeks, particularly in immunocompromised patients. Mucocele: Common salivary gland lesion as a result of blockage or rupture of gland with saliva leakage. However, most often found on the lower lip as the result of trauma, occurring at all ages. Due to the salivary connection, the mucocele can change in size specifically around meals. It is filled with mucin and macrophages. Characteristics: Lower lip swelling, full of fluid, with a blue translucent hue. Presents as Sialadenitis (literally the word for inflammation), Therefore could then be traumatic, viral or bacterial in nature. VERSUS HSV Canker (Aphthous) Mucocele Fluid filled, could be several small or Clustered and recurrent. Initially Fluid filled due to salivary gland fused together to make a large lesion, single could be multiple shallow rupture, changes size, primarily painful, burning sensation, located rimmed with narrow erythema. internal lower lip. Macrophage and around the lips and mouth, Neutrophil rich. Inside the mouth mucin rich. · Oral Infections: Be familiar with common pathogens associated with oral infections, like Candida albicans or Strep pharyngitis, and how they present (e.g., gray to white membrane that is easily scraped off). Why might some of the symptoms manifest differently with various pathogens? Candida albicans- “Thrush” most common infection in the oral cavity. Can be pseudomembranous, erythematous, or hyperplastic (hyperplasia). Thrush in pseudomembranous form appears as superficial, gray to white membrane easily scraped off revealing erythematous inflammatory base. Remains superficial. Promoted by antibiotics that kill off the good bacteria in the mouth. HSV- Most often HSV-1 but HSV-2 (genital herpes) can be found orally as well. Most that are infected will harbor latent virus. Reactivation will cause recurrent stomatitis. ○ For children typically the initial infection is within the first 2-4 years. Asymptomatic normally however will present as vesicles of oral mucosa, lymphadenopathy, fever and anorexia ○ For adults recurrent acute herpes pharyngitis could occur Strep Pharyngitis- Commonly caused by Strep A (streptococcus pyogenes) which secretes an exotoxin that causes Scarlet Fever and fever. S. pyogenes expresses M protein that allows them to evade phagocytosis creating an exterior capsule. Also secretes a phage-encoded pyrogenic exotoxin that causes fever and rash in scarlet fever. Rheumatic fever can be caused by antistreptococcal M protein antibodies and T cells that cross-react with cardiac proteins. ○ s/s: Fiery red tongue with prominent papillae (raspberry tongue); white-coated tongue through which hyperemic papillae project (strawberry tongue). Think red bumpy tongue. ß-hemolytic strep- can lead to erysipelas, impetigo, rheumatic fever, TSS (toxic shock syndrome), and glomerulonephritis. Infectious mononucleosis- caused by EBV “Kissing” disease. ○ s/s: fever, sore throat, lymphadenitis, severe fatigue, lymphadenopathy · Periodontal Diseases: Review the causes, symptoms, and differences between gingivitis, periodontitis, and other oral inflammatory conditions. Gingivitis: inflammation of the oral mucous and surrounding tissues. ○ Causes: Accumulation of dental plaque and calculus due to poor oral hygiene. The plaque is a combination of bacteria (acid producing increasing caries), salivary proteins and desquamated epithelial cells. ○ s/s: erythema, edema, bleeding, changes in contour, and loss of soft tissue adaptation to the teeth. Periodontitis: inflammatory process that affects the supporting structures of the teeth. Also is a main cause of endocarditis and abscesses in the lung and brain. ○ Causes: inflammatory process that affects the supporting structures of the teeth, periodontal ligaments (destruction of these loss of teeth), alveolar bone, and cementum. Can be caused by immunodeficiency disorders (AIDS, Chron’s, DM, Downs, Sarcoidosis) ○ s/s: similar s/s of gingivitis. Irritation Fibroma (Fibrous Proliferative Lesion): “traumatic” fibroma. Submucosal nodular mass of connective tissue that occurs primarily on the buccal mucosa along the bite line or the gingiva ○ Cause: repetitive trauma ○ s/s: lump/mass in buccal/inner cheek area that is hard/fibrous. No exudate. Clinical exam based on location for dx Pyogenic Granuloma (Fibrous Proliferative Lesion): “pregnancy tumor” exophytic (arising from outer surface) inflammatory lesion that is highly vascular that can have an alarming rapid growth. Appears in children, young adults, and pregnant women.  2 ○ Cause: Several underlying mechanisms responsible such as hypertrophy, hyperplasia, neoplasia, and pooling of the fluid. Making it difficult to approach clinically. ○ s/s: Erythematous and hemorrhagic mass, can regress or mature into dense fibrous masses. Peripheral Ossifying Fibroma (Fibrous Proliferative Lesion): gingival growth that is more than likely reactive rather than neoplastic. Peak in young females. ○ Cause: long standing pyogenic granulomas can turn into these. Or they can arise on their own. 15-20% recurrence ○ s/s: red, ulcerated nodular lesions. Harder than the other lesions, hence ossified. · Behcets Disease: Describe the pathophysiology of Behcet disease and its typical clinical manifestations. All my info is essentially from Mayo clinic and NIH since we did not talk about this one at all and it is not described in the book… APPARENTLY JUST KNOW THAT IT IS INCREASING YOUR LIKELIHOOD FOR CANKER SORES DUE TO ITS PATHO??? Patho: Rare auto-inflammatory disease that causes blood vessel inflammation throughout the body. Cell mediated immune response Clinical manifestations: 99% have mouth sores (similar to canker, are also recurring). Also causes eye inflammation, skin rashes and lesions, and genital sores. Eye irritation causing blurred vision and blindness. Can develop pulmonary and arterial aneurysms which is specific to behcets. · Hairy Leukoplakia: Explain the association between Epstein-Barr virus and hairy leukoplakia. Understand the presentation and characteristics. What are the long-term health implications of the disorder? EBV connection: is a distinctive oral lesion on the lateral border of the tongue caused by EBV that usually occurs in immunocompromised patients. EBV RNA transcripts and proteins can be detected within the lesional cells. Presentation/characteristics: White confluent patches of fluffy (“hairy”), hyperkeratotic thickenings, almost always situated on the lateral border of the tongue. Superimposed candidal infection can add to the “hairiness.” Lesions cannot be scraped off. Long term effect: The change to the cells promotes the growth of cancer in the region of the affected cells. Since the cells are harbored in B cells, when reactivated allows for cancer development. 2. Ear Conditions · Cholesteatoma: Understand what cholesteatomas are, how they develop, and their clinical significance. Cholesteatoma: Non neoplastic cystic lesions associated with chronic otitis media, cholesterol spicules may be present. ○ How they develop: thought that chronic inflammation and perforation of the eardrum, with ingrowth of the squamous epithelium or metaplasia of the secretory epithelial lining of the middle ear, promote the formation of a squamous cell nest that becomes cystic. ○ Clinical significance: can erode into the ossicles, labyrinth, adjacent bone, or surrounding soft tissue and sometimes produce visible neck masses. Worsening or permanent hearing loss. · Otosclerosis: Abnormal bone presentation in the middle ear Patho: bone reabsorption followed by fibrosis and vascularization of the temporal bone, new bone anchoring occurs on the footplate to the staples, slow progression over decades leading to marked hearing loss. Etiologies: age and familial link. Autosomal dominant transmission. Clinical manifestations: both ears, normally marked hearing loss, severity low in young individuals · Otitis Media: Recognize the most common pathogens for necrotizing otitis media in diabetic patients: Individuals with diabetes, otitis media caused by P. aeruginosa is especially aggressive and can spread widely, resulting in destructive necrotizing otitis media. What are the presenting symptoms? Acute: Ear tugging, fluid leaking from the ear (otorrhea), fever, tympanic changes (bulging, hyperemia, decreased mobility) Chronic: otalgia (ear pain), conductive hearing loss, aural fullness (sensation of ear blockage) · (NOT EARS BUT OKAY???) Blepharitis: chronic inflammation at the eyelid level. Anterior blepharitis- affecting the outside front of the eyelid where eyelashes are attached. Clinical presentation: chronic red eye, dry eyes, irritation Pathogens related to anterior blepharitis: May be ulcerative-staphylococci. Or seborrheic in association with seborrhea (excess grease/flakiness) of the scalp, brows, and ears. 3. Ophthalmology · Glaucoma: Understand the pathophysiology of open-angle glaucoma and its primary cause. How does pathology differ from closed angle glaucoma? Glaucoma Definition Risk Factors Patho Signs and Symptoms Open-Angle a chronic, progressive, Older Age Although open-angle Glaucoma and irreversible Family history glaucomas can have Peripheral vision loss multifactorial optic Black race numerous causes, 60 to neuropathy Systemic or topical 70% of cases in the characterized by an steroids United States have no open angle of the High intraocular identifiable cause and anterior chamber, pressure are termed primary  3 typical optic nerve High BP open-angle glaucoma. Central vision head changes, retinal DM Both eyes usually are difficulty nerve fiber layer affected, but typically thinning, and not equally progressive loss of Intraocular pressure Cloudy vision peripheral vision. The (IOP) can be elevated exact cause of primary or within the average open-angle glaucoma range Difficulty seeing in (POAG) is unknown, changing lighting but there are several risk factors and conditions potential causes High intraocular Closed-Angle a rare eye condition pressure. Is caused by disorders Eye pain Glaucoma that occurs when fluid of the iris, the lens, and Age over 55. is blocked from retrolenticular draining out of the eye, Black, Asian or structures Vision changes causing a rapid Hispanic heritage. increase in pressure Family history of Halos glaucoma. Certain medical Headache conditions, such as diabetes, migraines, high blood pressure N/V and sickle cell anemia. Corneas that are thin in Redness the center. Swelling The main feature distinguishing primary closed-angle glaucoma from primary open-angle glaucoma is that the angle, the site of aqueous outflow in the eye, is obstructed by apposition of the iris, resulting in an anatomically closed angle. CAG is worse as people can lose their vision within one day of developing symptoms Cataracts: Understand the pathophysiology and etiology. What clinical manifestations may be present? Lenticular opacities that may be congenital or acquired. Clouding of the lens of the eye. Proteins break down the lens and causes things to look blurry, hazy, and less colorful. Develop overtime slowly Surgical removal à procedure restores vision Accumulation of urochrome pigment may render the lens nucleus brown and distorting one’s perception of blue. Patho Most cataracts develop when aging or injury changes the tissue that makes up the eye's lens. Proteins and fibers in the lens begin to break down. This causes vision to become hazy or cloudy. Some disorders passed down from parents that cause other health problems can increase your risk of cataracts. Etiology Aging (nuclear sclerosis-opacification of the lens nucleus) Congenital – babies born with cataracts; children can develop them but does not affect eyesight, if it does it needs to be removed. Secondary cataracts – due to another disease, diabetes. Can also be from steroid use. Traumatic cataracts - injury Clinical Manifestations Having blurry vision Seeing double or a ghosted image out of the eye with cataract Being extra sensitive to light (especially with oncoming headlights at night); Halos Having trouble seeing well at night, or needing light when you read Seeing bright colors as faded or yellow instead Retinal detachment and Macular Degeneration: Why does it occur? What is happening within the eye? How will the patient present? Retinal detachment – separation of the neurosensory retina from the RPE (retinal pigment epithelium); etiology based on the presence or absence of a break in the retina.  4 Why it occurs: Retinal tears may develop after vitreous collapses and the posterior hyaloid exerts traction on points of abnormally strong adhesion to the retinal internal limiting membrane. Liquefied vitreous humor then seeps through the tear and gains access to the potential space between the neurosensory retina and RPE. Two different types of retinal breaks: rhegmatogenous retinal detachment and nonrhegmatogenous retinal detachment ○ Rhegmatogenous retinal detachment – full-thickness retinal defect – tear or break in the retina that allows fluid to pass into the subretinal space, separating the retina from the retinal pigment epithelium; surgical correction required Patient presentation: Floaters, flashes of light (photopsia), curtain over vision, blurred vision ○ Vitreous detachment – vitreous gel that fills the eye separates from the retina (normal with aging) Patient presentation: Floaters, flashes of light, visual disturbance ○ Nonrhegmatogenous retinal detachment – detachment without retinal break – fluid accumulation under the retina (exudative) or pulling of the retina by scar tissue (tractional); significant exudation and any condition that damages the RPE and permits fluid to leak from the choroidal circulation under the retina (e.g., choroidal tumors and malignant HTN) Patient presentation: Gradual vision loss, visual fields defects (peripheral or central), blurry vision, minimal or no flashes/floaters Macular Degeneration – common causes of irreversible vision loss in patients over 65 YO; results in central vision loss due to damage to the macula. (2 forms – Wet (neoangiogenesis) and Dry (absence) AMD) Why it occurs: DUE TO AGING there is accumulation of cellular debris (drusen) between RPE and Bruch’s membrane, obstructing nutrient transport and waste removal, thinning choroidal BV, and triggering inflammation What happens: ○ Atrophic or “dry” AMD – slow, progressive vision loss due to atrophy of the outer retina, choriocapillaris deterioration, and death of photoreceptors. No treatment available. ○ Neovascular or “wet” AMD – rapid progression due to choroidal neovascularization, (abnormal BV growth is presence of vessels) under the macula, triggered by vascular endothelial growth factor (VEGF). Vessels may leak and exude blood by RPE cells into macular scars causing rapid vision loss Patient presentation: ○ Dry AMD – gradual central vision loss, difficulty seeing fine details, and possible blind spots ○ Wet AMD – sudden onset of central vision distortion or loss, dark spots, and rapid decline in visual acuity Retinoblastoma: Know the genetic basis and first clinical signs of retinoblastoma Cause: Retinoblastoma is caused by the mutational inactivation of both alleles of the RB1 gene located on chromosome 13q14. The RB1 gene encodes the retinoblastoma protein, which normally functions as a tumor suppressor by regulating the cell cycle. Mechanism: When both alleles of the RB1 gene are inactivated, it leads to a loss of tumor suppression, allowing uncontrolled proliferation of retinal cells and the development of a malignant tumor within the retina. Clinical signs: ○ Leukocoria (Cat’s Eye Reflex): The most common and characteristic sign, where a white reflection is seen through the pupil instead of the normal red reflex. This occurs due to light reflecting off the tumor behind the lens. ○ Strabismus (Misaligned Eyes): Eyes look crossed or misaligned, often due to the tumor affecting normal visual development. ○ Other Symptoms: Some children may also present with a red or painful eye, decreased vision, or complete loss of vision if the tumor grows large or invades nearby structures. Retinal arteriosclerosis: etiology and clinical manifestations Etiology: caused by chronic hypertension or other conditions leading to the thickening and stiffening of the arteriolar walls within the retina à reduced ability of the vessels to regular blood flow, leading to retinal ischemia and damage Clinical manifestations: thickened arteriolar wall on ophthalmoscope; can see narrowed vessels and copper and silver wiring (opaquer, blood column’s color changes form bright red to copper color, and in severe cases, a silver color); “cotton-wool spots” – fluffy white lesions that are microinfarctions of the nerve fiber layer Proliferative Diabetic Retinopathy: Study the pathological changes, including increased growth of weak vessels that can rupture and bleed. Associated with diabetes mellitus Growth of new, fragile blood vessels, that sprout on the surface of the retina or optic nerve head (neovascularization). The weak new blood vessels are prone to rupture and leads to bleeding into the vitreous body (vitreous hemorrhage). Fibrous tissue can grow on surface of the retina, leading to traction and potential retinal detachment. Lead to progressive vision loss due to bleeding, and retinal detachment. Difference from nonproliferative diabetic retinopathy – microvascular damage vs. proliferative is neovascularization à severe vision loss due to bleeding and retinal detachment Anterior Blepharitis and Chalazion: What are the common etiologies and treatment strategies? What is the clinical presentation? How would you differentiate the two?  5 Anterior Blepharitis – inflammation of the OUTSIDE front part of the eyelid where eyelashes attach, may be caused by: Staphylococcal infection (bacterial) or seborrhea (scalp, brows, and ears) Clinical presentation: ○ Red ○ swollen eyelids ○ hyperemic lid margins with telangiectasias ○ crusting of eyelashes upon awakening ○ excessive tearing ○ Eyes: itching, dry, frothy tears. irritation, redness,” gritty” or “sandy” sensational burning, foreign body sensation, and blurred vision Treatment: regular cleaning of eyelids with warm compresses and diluted baby shampoo; topical antibiotics or corticosteroid eye drops Chalazion – granulomatous inflammation of a meibomian gland, often following internal hordeolum (blocked or infected oil gland) Clinical presentation: ○ Hard, non-tender swelling on the UPPER or LOWER eyelid ○ Localized swelling and redness of the adjacent conjunctiva Treatment: ○ Warm compresses and gentle massage ○ Intralesional steroid injection or surgical removal Difference overview: Anterior Blepharitis involves diffuse inflammation of the eyelid margins with symptoms of irritation, redness, crusting, and a "gritty" feeling in the eyes. It is often associated with skin conditions like seborrhea. Chalazion presents as a localized, hard, non-tender lump on the eyelid with no significant symptoms of irritation or infection of the eyelid margins. The swelling is usually due to a blocked oil gland. Pterygium and Pinguecula: Recognize this benign conjunctival growth and its potential impact on vision. Pterygium Pinguecula Triangular, fibrovascular tissue growth from the conjunctiva onto the Small, yellowish submucosal elevation on the conjunctiva near the cornea limbus Location: originates on the conjunctiva at the lumbus, may extend Location: located at the limbus, typically on the nasal side of the into the cornea conjunctiva Etiology: sun damage/exposure Etiology: sun damage/exposure Impact on Vision: No threaten on vision but can be irritating or Impact on Vision: does not invade cornea but can cause irritation or foreign body sensation dryness Complications: benign Complications: no risk Management: lubricating eye drops; surgery if vision if threatened Management: artifical tears or cosmetic reasons 4. Genetic Disorders- Understand Inheritance patterns General definitions related to genetic disorders (For example, aneuploidy, mosaicism) ON SEPARATE SHEET 5. Respiratory and Immune Responses · Allergic Rhinitis: Study the cellular response mechanisms in allergic rhinitis. IgE-mediated immune reaction Hypersensitivity to one of the large group of allergens (plant pollens, animal allergens, and dust mites) Dominant chemical mediator with Type 1 hypersensitivity, which are HISTAMINES, which causes patient’s symptoms (mucosal edema, erythema, eosinophil-rich leukocytic infiltrates) Immediate reaction → vasodilation, vascular leakage, smooth muscle spasm or glandular secretions  6 ○ Caused by excessive Th2 cells which stimulates IgE production and promotes inflammation. For allergic rhinitis, a second, late-phase reaction sets in 2-24 hours later; characterized by infiltrate rich in eosinophils, neutrophils, basophils, monocytes, and CD4+ T cells. SENSITIZATION and ACTIVATION of Mast Cells ○ Mast cells are THE cells for immediate hypersensitivity; they are bone marrow- derived cells found near blood vessels, nerves, and subepithelial tissues - causes the immediate hypersensitivity ○ Triggered when IgE antibodies bound to the high-affinity FcεRI receptors on mast cells cross-link with specific antigens (basophils). Other triggers include complement proteins (C3a, C5a - these are anaphylatoxins and mimic anaphylaxis), certain drugs (codeine, morphine, adenosine, melittin - in bee venom), and physical stimuli (heat, cold, sunlight). ○ When mast cells, sensitized with IgE antibodies, encounter the same antigen, they release preformed and newly synthesized mediators, causing immediate hypersensitivity and initiating late-phase reactions (leukocyte infiltration, epithelial damage, and bronchospasm) · Respiratory Distress in Newborns: Know the causes of respiratory distress in preterm infants. (p. 459) NEONATAL RESPIRATORY DISTRESS SYNDROME (hyaline membrane disease) ○ Etiology: deposition of hyaline proteinaceous material in peripheral airspaces ○ Patho: Pulmonary Immaturity and Surfactant Deficiency: Surfactant production by type II alveolar cells accelerates after the 35th week of gestation. In preterm infants, surfactant deficiency causes the lungs to collapse with each breath, requiring increased effort for breathing. Progressive Atelectasis and reduced lung compliance leads to protein- and fibrin-rich exudation into alveolar spaces, forming hyaline membranes that impaired gas exchange, resulting in carbon dioxide retention and hypoxemia. ○ Clinical presentation: Rapid Onset: Breathing difficulty often within 30 minutes; cyanosis develops in a few hours if untreated. Physical Exam: Fine rales over lung fields. Imaging: Chest X-ray shows uniform reticulogranular densities (“ground-glass” appearance). Prognosis: If survival is achieved beyond 3-4 days with therapy, the prognosis significantly improves. ○ Complications Retinopathy of Prematurity: Vision impairment from abnormal retinal development. Bronchopulmonary Dysplasia: Chronic lung disease due to prolonged mechanical ventilation. Other Complications: Patent Ductus Arteriosus, Intraventricular Hemorrhage, Necrotizing Enterocolitis. · Croup: Etiology and characteristic findings in clinical presentation LARYNGOGEPIGLOTTITIS ○ Caused by RSV (respiratory syncytial virus), haemophilus influenzae, or β-hemolytic streptococci ○ Sudden swelling of the epiglottis and vocal cords in infants and young children - MEDICAL EMERGENCY ○ Croup (Laryngotracheobronchitis) Affects children (6 mo. - 3 years) with peak incidence in the 2nd year of life Seasonal - peaks in late autumn (September - December) and winter, with a smaller spring peak. It is self-limiting and influenced by weather. Characterized by inspiratory stridor due to airway narrowing ○ Supraglottitis (acute epiglottitis) Onset: acute, within 2-6 hours Symptoms: Severe sore throat Drooling due to difficult swallowing High fever Inspiratory stridor (noisy breathing) Prefers to sit upright, greater inspiratory stridor than expiratory Hot Potato voice (muffled voice) Flushed face and toxic appearance ○ Incidence: Epiglottis reduced following the introduction of the HIB vaccine  7 6. Neoplastic and Pre-Neoplastic Conditions · Squamous Cell Carcinoma: Recognize the risk factors and common presentations of HPV-associated squamous cell carcinoma in the head and neck. Squamous Cell Carcinoma (SCC): 95% of cancers of the head and neck are SCCs. Primary cause: HPV infection (primary cause), tobacco, and alcohol use. Common Sites: Oropharynx, tonsils, tongue, pharynx. SCC (especially on the tongue) are seen in those who are younger than 40 years old, with no risk factors. They are nonsmokers and are not infected with HPV, is unknown North America/Europe: middle-aged persons who are chronic tobacco and alcohol use India and Asia: chew betel quid and paan Actinic radiation (sunlight) and pipe smoking predisposes cancer to the lower lip SCC of the Oropharynx HPV-Associated SCC Prevalence: Up to 80% of SCCs in the oropharynx (tonsils, base of the tongue, pharynx) are linked to oncogenic variants of Human Papillomavirus (HPV), particularly HPV-16. Epidemiology: The incidence of HPV-associated oropharyngeal SCC has more than doubled over the past two decades. Risk Factors: Younger individuals, increased number of oral sexual partners. Characteristics: ○ Location: Oropharynx (e.g., tonsillar crypts, base of tongue). ○ Histology: Nonkeratinizing, basaloid cells forming nests and lobules within sheets of lymphocytes. ○ Clinical Outcomes: Generally favorable with better prognosis. Pathology: The anatomical sites (tonsillar crypts, base of tongue, oropharynx) are less accessible, complicating early detection. Cytologic screening for premalignant lesions is challenging. HPV-Negative Keratinizing SCC Location: Commonly on the ventral surface of the tongue, floor of the mouth, lower lip, soft palate, and gingiva. Preceding Lesions: Often preceded by premalignant lesions, such as leukoplakia and erythroplakia. Risk Factors: Older age, tobacco and alcohol use. Characteristics: ○ Histology: Keratinizing starts as dysplastic lesions. ○ Clinical Outcomes: Poor prognosis with a high risk of metastasis. Pathogenesis of SCC SCC development is driven by mutations and epigenetic changes that affect oncogenes and tumor suppressor genes. · Pyogenic Granuloma: What are the exam findings and is this a lesion of concern? How does it differ from other fibromas? Pyogenic Granuloma: Exophytic inflammatory lesion (lesions that appear on outer surface) on gingiva; may regress or mature into fibrous masses. ○ Erythematous and hemorrhagic exophytic mass arising from the gingival mucosa. Found on gingiva of children, young adults, and pregnant women - due to hormones Also called the “pregnancy tumor” ○ Can go away by itself, if not, complete surgical removal ○ Red to purple, frequently ulcerated ○ Can develop into peripheral ossifying fibroma Differences from Other Fibromas: Irritation Fibroma: Submucosal hard nodular mass resulting from repetitive trauma, commonly on the buccal mucosa or gingiva. Peripheral Ossifying Fibroma: Reactive gingival growth that can arise from a long-standing pyogenic granuloma or periodontal ligament cells. It is red, nodular, and requires surgical removal due to the potential for recurrence.  8 FIBROUS Description Demographics Treatment PROLIFERATIVE LESIONS 1. Irritation Fibroma Submucosal nodular mass (hard nodular mass) or (Traumatic fibroma fibrous connective tissue stroma due to repetitive or focal fibrous trauma hyperplasia) 2. Pyogenic Granuloma Exophytic inflammatory lesion (lesions that appear on Children, young adults, Can go away by itself, if not, outer surface) on gingiva; may regress or mature into and pregnant woman - complete surgical excision fibrous masses due to hormones 3. Peripheral Ossifying Common gingival growth reactive nodular lesions Young females COMPLETE surgical excision Fibroma with recurrence rates of 15-20% down to periosteum is required Leukoplakia vs. Erythroplakia: Understand the differences in malignant transformation risk between these two conditions. Leukoplakia vs. Erythroplakia: Malignant Transformation Risk 1. Leukoplakia: ○ Description: White patch or plaque in the oral cavity that cannot be scraped off; may be solitary or multiple with sharply defined borders. ○ Appearance: Can be thickened, smooth, wrinkled, fissured, raised, or verrucous. ○ Histology: Shows a range from hyperkeratosis with thickened epithelium to dysplasia and carcinoma in situ. ○ Prevalence and Risk: Affects 3% of the global population; considered precancerous but has a lower risk of malignant transformation compared to erythroplakia. 2. Erythroplakia: ○ Description: Red, velvety, eroded lesion in the oral cavity; often associated with tobacco use and more common in males. ○ Malignant Transformation Risk: Higher risk of malignant transformation than leukoplakia. ○ Histology: Rarely shows orderly maturation; around 90% show severe dysplasia, carcinoma in situ, or invasive carcinoma. Features an intense inflammatory reaction with vascular dilation, contributing to the red appearance. 7. Congenital and Pediatric Conditions *ON SEPARTE SHEET Transcervical (Ascending) Infections Wilms Tumor