Developmental Disturbances Of Oral And Para Oral Structures PDF

no Developmental Disturbances Of Oral And Para Oral Structures Basic Sciences Wed. Sep. 4. 2024 1 INTRODUCTION Malformation or defects resulting from disturbance of growth & development are known as Developmental Anomalies Manifestation of defects are evident eit...

no Developmental Disturbances Of Oral And Para Oral Structures Basic Sciences Wed. Sep. 4. 2024 1 INTRODUCTION Malformation or defects resulting from disturbance of growth & development are known as Developmental Anomalies Manifestation of defects are evident either at birth or sometimes after birth The development of tissues is influenced by genetic or environmental conditions. Anomaly is a medical term meaning ‘irregularity’ or ‘different from normal’. Affect normal growth and differentiation of craniofacial structures. First discovered in childhood or early infancy. 5 Malformation: Defect due to localize error in morphogenesis resulting in an abnormal shape or structure, with interference in function. E.g. cleft palate Deformation: An alteration in shape or structure of a previously normally formed part. E.g. torticollis Anomaly: Any deviation from normal. It is same as malformation but there is no interference with function. E.g. peg shaped lateral Anomalad: Malformation and subsequently derived structural changes. E.g. Robin anomalad where hypoplasia of the mandible result in cleft palate and respiratory difficulty. 6 Congenital Developmental Anomalies: Defects which are present at birth or before birth during the intra-uterine life because of either heredity or environmental influences E.g. - Cleft lip & palate Hereditary Developmental Anomalies: Defects are genetically transmitted from the parents to the offspring, where definite genetic location is identified E.g. Downs syndrome –Trisomy 21 Familial Developmental Anomalies: Defects are transmitted from the parents to the offspring, where definite genetic location is not identified E.g. – Diabetes 8 Acquired Developmental Anomalies: Defects develop during intra-uterine life due to some pathological environment condition Can be Prenatal / neonatal / Postnatal E.g.: 1. Congenital Syphilis - Notched incisors - Mulberry molars 2. Fluorides - Enamel hypoplasia r 9  Developmental Disturbances of soft tissue Lip pits:Congenital lip pits. Commissural: common 1-20% ▪ Autosomal D: in some cases ▪ Uni/bilateral blind tracts at angle of lip, up to 4 mm 13 Paramedian lip pits: As deep as 2 cm Double lip: usually congenital ▪ Horizontal folds of mucosal tissue Inner aspect of U > L lip 14 Frenal Tag: ▪ Autosomal D ▪ U labial frenum Fordyce granules: Collection of sebaceous glands Mostly bilateral on Buccal mucosa Yellow spots Histologically: superficial no hair Glands (1-5 lobules) that empty into a duct that opens on the mucosal surface. 15 Retrocuspid Papilla ▪Slightly raised area, about 2-4 mm, often bilaterally ▪Commonly located lingual to the cuspids ▪Attached gingiva ▪incisive papilla ▪Histologically: ▪A focus of fibrovascular tissue ▪With an orthokeratinized no /parakeratinized surface ▪Covers the osseous foramen of a nutrient blood vessel 17 MICROGLOSSIA  It is a rare congenital anomaly manifested by the presence of Rudimentary or small tongue  The condition when tongue being completely absent is known as Aglossia  Patient finds difficulties in eating and swallowing CLASSIFICATION True microglossia Relative microglossia 19 MACROGLOSSIA  It is a condition when patient have an enlarged tongue  True macroglossia and pseudomacroglossia  Pseudomacroglossia includes any of the following conditions,which force the tongue to sit in an abnormal position: Habitual posturing of the tongue, Enlarged tonsils/adenoids  True macroglossia can be congenital or acquired CAUSES FOR CONGENITAL MACROGLOSSIA Over development of the musculature Down syndrome b Beckwith-Wiedemann syndrome 20 Down syndrome (Trisomy 21 syndrome) Flat face Large anterior fontanel Open sutures Small slanting eyes with epicanthal folds Open mouth Cardiac abnormalites Macroglosia High arched palate 21  ANKYLOGLOSSIA (tongue-tie)  It can be defined as a developmental condition characterized by fixation of tongue to the floor of the mouth, causing restricted movement  It can be either complete ankyloglossia or partial ankyloglossia (tongue tie)  Complete ankyloglossia occurs as a result of fusion between the tongue and the floor of the mouth  Partial ankyloglossia occurs as a result of short lingual frenum or due to a frenum which attaches too near to the tip of the tongue 25 CLEFT TONGUE/Bifid Tongue  Complete cleft tongue occurs due to lack of merging of lateral lingual swellings.  Partial cleft tongue occurs due to incomplete merging and failure of groove obliteration by underlying mesenchymal proliferation  Partially cleft tongue occurs more common and is manifested as deep groove in the midline of dorsal surface  Food debris and microorganisms collect in base of cleft and cause irritation 26 FISSURED TONGUE/ SCROTAL TONGUE ▪ Deep fissures may be seen in children or adults but ↑ with age ▪ Down syndrome & Melkersson-Rosenthal Syndrome Histologic Features A biopsy is rarely performed on a fissured tongue because of its characteristic diagnostic clinical appearance; however, histologic examination has shown an increase in the thickness of the lamina propria, loss of filiform papillae of the surface mucosa, hyperplasia of the rete Ipegs, neutrophilic micro abscesses within the epithelium, and a mixed inflammatory infiltrate in the lamina propria. 27 MEDIAN RHOMBOID GLOSSITIS Central papillary atrophy of the tongue / posterior lingual papillary atrophy  It is an asymptomatic elongated erythematous patch of atrophic mucosa on the mid dorsal surface of the tongue. 28 Histological features: Atrophic stratified squamous epithelium mm  Occasionally pseudoepitheliomatous hyperplasia,  Presence of fungal hyphae,  Loss of papillae,elongated rete ridges and lymphocytic infiltration.  Median rhomboid glossitis shows a smooth or nodular surface covered by atrophic stratified squamous epithelium overlying a moderately fibrosed stroma  Fungiform and filiform papillae are not seen, although surface nodules may mimic or perhaps represent anlage of these structures.  A mild to moderately intense chronic inflammatory cell infiltrate may be seen within subepithelial and deeper fibrovascular tissues. 29 BENIGN MIGRATORY GLOSSITIS Geographic tongue, erythema migrans, wandering rash of tongue Filiform papillae Migrate & periods of remission Asymptomatic but acidic & spicy food Histological features: Hyperparakeratosis, spongiosis, acanthosis, elongated rete ridges Red areas-keratin desquamated, neutrophils and lymphocytes in epithelium A thickened layer of keratin is infiltrated with neutrophils, as are lower portions of the epithelium to a lesser extent 30 HAIRY TONGUE BLACK HAIRY TONGUE, LINGUA NIGRA, LINGUA VILLOSA  characterized by marked accumulation of keratin on filiform papillae of the dorsal surface resulting in a hair like appearance Histologic Features. Consist of elongated filiform papillae, with mild hyperkeratosis and occasional rinflammatory cells. Debris accumulation among the papillae and candidal pseudohyphae is not unusual finding. r 31 LINGUAL VARICES  It is a dilated, tortuous vein which is often subjected to increased hydrostatic pressure but is poorly supported by surrounding tissue  Involved veins appear red or purple shotlike clusters of vessels on the ventral surface and lateral borders of tongue as well as in the floor of the mouth r 32 LINGUAL THYROID NODULE ▪ Thyroid tissue at mid-posterior dorsum of tongue ▪ Failure of migration ▪ Clinically: 2-3cm smooth sessile mass ▪ Apparent during puberty or adolescence HISTOPATHOLOGY  Lingual thyroid nodule consist of normal mature thyroid tissue  Occasionally thyroid nodules may exhibit colloid degeneration 33 Thank You 34 4 i r in I r v r r r  Developmental anomalies of Teeth And Jaw Part II Basic Sciences Wed. Sep. 18. 2024 Amelogenesis imperfecta I Also known as Hereditary enamel dysplasia/Hereditary brown enamel/Hereditary brown opalescent tooth Group of conditions caused by defects in the genes encoding enamel matrix proteins Affects both dentition deciduous and permanent Types Amelogenesis imperfecta may set in during any stage of enamel formation. Based on that there are 4 types 1. Hypoplastic type - Defective matrix deposition 2. Hypocalcification type – Defective calcification 1 3. Hypomaturation type- Defective maturation 4. Hypomaturation-hypoplastic with taurodontism Hypoplastic type : I There is defective formation of matrix. Enamel doesn’t form to full thickness on newly erupted developing teeth. Teeth exhibit complete absence of enamel or there may be presence of enamel on some focal areas Enamel thickness is usually below normal Quantity is affected, but quality of formed enamel is normal Tooth appears as though prepared for receiving a prosthetic crown Hypocalcified type There is defective mineralization of the formed matrix. Enamel is so soft that it can be removed by a prophylactic instrument. Hypomaturation type Enamel crystallites remains immature. Enamel can be pierced by explorer point under firm pressure and can be lost by chipping away from the underlying normal appearing dentin. Crowns may or may not show discoloration. If present they may be yellow to dark brown. Hypoplastic type Enamel may appear totally absent or as a thin line Radiodensity of affected enamel is similar to that of normal enamel (greater than dentin) Histologic Features : Hypoplastic type Lack of differentiation of ameloblast cells with little or no matrix formation Hypocalcification type Abnormal matrix structure & mineral G deposition Hypomaturation type Alteration in the enamel rod & rod sheath structures  Environmental enamel hypoplasia Focal enamel hypoplasia Also known as Turner’s hypoplasia Most common form of enamel hypoplasia Occurs due to trauma or infection to deciduous teeth affecting the developing permanent tooth Usually affects single tooth & is called as Turners tooth Hypoplasia ranges from a mild, brownish discoloration to a severe pitting of enamel surface on the labial aspect Frequently involved teeth are permanent maxillary/mandibular bicuspids & maxillary incisors  DENTINOGENESIS IMPERFECTA It is the hereditary developmental disturbance of the dentin in the absence of any systemic disorder. Affected teeth are gray to yellowish-brown Also known as “Hereditary opalescent dentin” & “Capdepont’s teeth” r According to Shields it is classified as Dentinogenesis imperfecta I – It occurs with Osteogenesis Imperfecta with opalascent teeth. Deciduous teeth more severely affected. Dentnogenesis imperfecta II- In this the tooth gives a look as if it has cheesy consistency Both dentition affected Dentinogenesis imperfecta III- It is also like type II with some clinical and radiological variations like multiple pulp exposures periapical radiolucencies and variable radiographic appearance. Both dentition affected Multiple pulpal exposures in deciduous dentition  Histologic Features. Enamel & mantle dentin are normal The dentin, on the other hand, is composed of irregular tubules, with large areas of uncalcified matrix. Remaining dentin is severely dysplastic & exhibits vast areas of inter-globular dentin I Dentinal tubules are short, disoriented, irregular & widely spaced Scanty odontoblasts line the pulp and they can be seen in the defective dentin The DEJ is Smooth  Dentin Dysplasia (Rootless teeth) A hereditary defect characterized by defective dentin formation & abnormal pulpal morphology Type I Radicular dentin dysplasia Also known as “Rootless teeth” Type II (Coronal dentin dysplasia) Type I is more common. Conditions associated with dentin dysplasia Rheumatoid arthritis Sclerotic bone and skeletal anomalies Histologic Features: Type I (radicular). A portion of the coronal dentin is usually normal. n r Apical to this may be areas of tubular dentin, but most of that which obliterates the pulp is calcified tubular dentin, osteodentin, and fused denticles. Type II (coronal) The deciduous teeth exhibit amorphous and atubular dentin in the radicular portion, while coronal dentin is relatively normal. The permanent teeth also show relatively normal coronal dentin, but the pulp has multiple pulp stones or denticles.  REGIONAL ODONTODYSPLASIA Also known as GHOST TEETH/ Odontodysplasia/ odontogenic dysplasia/ odontogenesis imperfecta Its a dental abnormality that involves the hard tissues that are derived from both epithelial (enamel) and mesenchymal (dentin and cementum) components of tooth forming apparatus. The teeth exhibit short roots, open apical foramina, and enlarged pulp chambers. Thickness and defective mineralization quality of enamel and dentin layers have given rise to the term Ghost teeth. The permanent teeth are affected more than primary. Maxillary anterior are affected more than other teeth Histologic Features Abnormal enamel & dentin The widening of the pre-dentin layer The presence of large areas of inter-globular dentin An irregular tubular pattern of dentin. Characteristically, the reduced enamel epithelium around uneruptcd teeth shows many irregular calcified bodies. Large pulp chamber with pulp stones Calcification in follicular connective  Agnathia Also known as Otocephaly, Holoprosencephaly agnathia Characterized by is absence of a portion or the entirety of one or both jaws. It is a very rare condition. Etiology: Failure of migration of neural crest mesenchyme i into the maxillary prominence at the fourth to fifth week of gestation Incidence: less than 10% MICROGNATHIA Also known as Mandibular hypoplasia It is a condition in which a child has a very small lower jaw. Bird face appearance a)True micrognathia b) Pseudo micrognathia 2 types true micrognathia 1) Congenital 2) Acquired Etiology of congenital – unknown But associate with Congenital Heart Disease or Pierre Robin Syndrome Acquired Post natal in origin Causes Ankylosis of joint as result of trauma/infection  CAUSES OF MICROGNATHIA Congenital - Pierre Robin syndrome - Catel Manzke syndrome - Cerebrocostomandibular syndrome Intrauterine acquired conditions – congenital syphillis Chromosomal abnormality - Trisomy 18 - Turners syndrome Autosomal dominant conditions - Treacher Collins syndrome - Pallister Hall Syndrome Autosomal recessive conditions - Cohen syndrome - Craniomandibular dermatodysostosis  Pierre Robin syndrome Also know as Robin sequence, Pierre Robin Anomalad, Robin complexes, Pierre Robin Malformation Cleft palate Micrognathia and glossoptosis Hypoplasia of mandible ‘Bird facies’ Respiratory difficulty Congenital heart defects Occular lesions Mental retardation  MACROGNATHIA Increase in both jaws c Macrognathia can be associated with pituitary gigantism, tumors, and other disorders. This condition could be secondary to other diseases, as in Paget’s disease (overgrowth of cranium & max/mandible) & in Acromegally (mand). Factors favoring mandibular prognathism Long rami Increased mandibular body length/ decreased maxillary length Excess condylar growth Prominent chin button Varying soft tissue contours  FACIAL HEMIATROPHY Also known as Parry Romberg Syndrome, Progressive Facial Hemiatrophy, Progressive hemifacial atrophy Parry and Romberg in 1846 ORAL MANIFESTATIONS Dental anomalies: incomplete root formation, delayed eruption and severe facial asymmetry Eruption of teeth on the affected side may be retarded. Atrophy of half of the upper lip and tongue Deviation of jaws while opening the mouth A characteristic loss in the soft tissues of essentially half the face. Coup de sabre’ –  FACIAL HEMIHYPERTROPHY Also called Friedreich’s Disease Significant unilateral enlargement of the face Represents hyperplasia of tissues rather than hypertrophy Syndromes associated: Neurofibromatosis Beckwith Wiedemann syndrome Albright syndrome ETIOLOGY Unknown, but due to vascular or lymphatic absence, CNS disturbances, chromosomal absence. ORAL MANIFESTATION Dentition is abnormal in three respects – Crown size and root may be large Involve any tooth but most frequently in cuspid, premolar and first molar Bone of maxilla and mandible also enlarged Tongue: commonly involved, shows bizzare pattern of enlargement of papillae Buccal mucosa freq appears velvety and may hang in soft pendulous folds on affected side  Treacher Collins Syndrome(Mandibulo Facial Dysostosis) Convex facial profile Mandibular and midface hypoplasia Underdeveloped or absence of zygomatic bones Downward inclination of palpebral fissures 75% pt: COLOBOMA: notch on outer portion of lower eye lid Occasional facial clefts Palate: high arched with 30% clefts Retrusive chin Deformed pinna  Apert Syndrome (Acrocephalosyndacty) Wheoton in 1894 Apert in 1906 summarized 9 cases ORAL MANIFESTATIONS Maxillary Hypoplasia and V shaped arch Class III Malocclusion and mouth breathing Trapezoid shaped appearance of lips Tile Pulp and Periapical Pathology Basic Sciences Department Wed. Sep. 25. 2024 1 Reversible Pulpitis (Pulp Hyperemia) Definition — reversible pulpitis is a mild to moderate condition of the pulp caused by stimuli in which pulp is capable of returning to the uninflamed state following the removal of stimuli. HISTOLOGICAL FEATURES: Pulp hyperemia (dilation of blood vessels) Edema fluid collection due to damage of vessel wall & allowing extravasations of RBC or diapedesis of WBC Chronic inflammatory cellular infiltrate Reparative secondary dentin may be noted Exudation Inflammatory cell infiltration (neutrophils) Reactions usually remain localized adjacent to the cause 9  Acute irreversible pulpitis Etiology Acute dental caries Pulp exposure Histopathological features Inflammation involves the whole dental pulp Vascular dilatation and edema Inflammatory (granular cells) infiltration Odontoblasts near to the cause are destroyed Formation of a minute pulp abscess In a few days pulp undergoes liquefaction and necrosis 11 Pulp and Periapical pathology / Oral Pathology ACUTE PULPITIS A common condition affecting a tooth accompanied by severe, relentless pain HISTOLOGIC FEATURES: Edema in pulp with vasodilation. Infiltration of polymorphonuclear leukocytes along vascular channels & migrate through endothelium lined structures. Destruction of odontoblasts at pulp dentin border. Acute suppurative pulpitis- Numerous abscess formation cause pulp liquefaction & necrosis. Mononuclear cell inflammatory infiltration Evidence of fibroblastic activity Minute abscess if exist it is localized by granulation tissue 12 Pulp and Periapical pathology / Oral Pathology CHRONIC PULPITIS A common condition affecting a tooth accompanied by dull, bearable pain. HISTOLOGIC FEATURES: Infiltration of mononuclear cells, lymphocytes & plasma cells, with vigorous connective tissue reaction. Capillaries are prominent; fibroblastic activity & collagen fibers in bundles. When granulation tissue formation occurs in wide open exposed pulp surface – ulcerative pulpitis. (with bacterial stains & micro-org. in carious lesion) The dental pulp exhibits an area of fibrosis and chronic inflammation peripheral to the zone of abscess formation. 14 Pulp and Periapical pathology / Oral Pathology Chronic Hyperplastic Pulpitis (pulp polyp) Overgrowth of pulp tissue outside the boundary of pulp chamber as protruding mass. Histological features Hyperplastic tissue is basically granulation tissue, consisting delicate CT fibers & young blood capillaries. EInflammatory cell infilterate,plasma cells, lymphocytes. Fibroblast and endothelial cell proliferation prominent. Stratified squamous type epithelial lining resembles oral mucosa with well formed rete pegs. 15 The polyp surface is covered with stratified squamous epithelium. Epithelium may be derived from gingiva or from freshly desqumated epithelial cell of mucosa or tongue. The polyp consists of granulation tissues It contains delicate connective tissue, fibers and blood vessels Mononuclear inflammatory cell infiltration 16 Pulp and Periapical pathology / Oral Pathology Internal Resorption: Odontoclastoma, Pink Tooth of Mummery Histological Features Resorption is of irregular lacunar variety showing occasional osteoclast or odontoclast hence the term “Odontoclastoma” Pulp tissue exhibits chronic inflammatory reaction 17 Pulp and Periapical pathology / Oral Pathology True Pulp stone: They rare and contains dentin with distint dentinal tubules lined by odontoblasts. It arises as a result of epithelial mesenchymal interaction. False Pulp stone: It contains a concentric layers of mineralized tissue formed by surface accretion around blood thrombi, dying or dead cells or collagen fibers. It arise from degenerating cells of the pulp that eventually get mineralized. 19  Pulp and Periapical pathology / Oral Pathology Apical Periodontitis: It’s a painful inflammation of periodontium as a result of trauma, irritation or infection through the root canal, regardless whether pulp is vital or not. Histopathology An inflammatory reaction occurs in Apical PDL-vascular dilation infiltration of PMNs PMNs (Polymorphonuclear neutrophils) Accumulation of serous exudates distends the PDL and extrudes the tooth slightly PDL shows signs of inflammation to Inflammation is transient, if caused by acute trauma. If irritant not removed, progress into surrounding bone resorption. Abscess formation may occur if it is associated with bacterial infection Acute periapical abscess / Alveolar abscess. 21 Pulp and Periapical pathology / Oral Pathology Chronic Apical Periodontitis : A growth of granulomatous tissue continuous with the Periodontal ligament resulting from the death of the pulp. HISTOLOGIC FEATURES: Hyperemia and edema of the PDL ligament with infiltration of chronic inflammatory cells. Inflammatory and locally increased vascularity of the tissue are associated with resorption of the surrounding bone adjacent to this area. Granulation tissue mass consists proliferating fibroblasts, endothelial cells & numerous immature blood capillaries with bone resorption. Capillaries lined with swollen endothelial cells. 22  Pulp and Periapical pathology / Oral Pathology Periapical Abscess (Dentoalveolar Abcess, Alveolar Abscess, Root end Abscess ) It is an acute or chronic suppurative process of the dental periapical region Histological Features Area of suppuration composed of PMN leukocytes, lymphocytes, cellular debris, necrotic materials & bacterial colonies. Dilatation of PDL and adjacent marrow spaces of the bone Marrow spaces show chronic inflammatory cell infiltrate Tissue around area show suppuration containing serous exudate. Sheet of polymorphonuclear leukocytes intermixed with scattered histiocytes 23 Pulp and Periapical pathology / Oral Pathology Acute Exacerbation of Chronic Periapical Abscess (Phoenix Abscess) Definition -Its an acute inflammatory reaction superimposed on an existing chronic lesion such as cyst or granuloma Histopathology Areas of liquefaction necrosis with disintegration of PMNs and cellular debris 0 This area is surrounded by infiltration of macrophages, lymphocytes and plasma cells 24  Pulp and Periapical pathology / Oral Pathology Periapical Granuloma It is one of the most common of all sequel of pulpitis Histological Features Granulation tissue mass consists proliferating fibroblasts, endothelial cells & numerous immature blood capillaries with bone resorption Bone tissue at the periphery is lined by osteoclast cells with areas of bone resorption Lesion is usually sterile in nature and microrgs not seen unless secondarily infected Capillaries lined with swollen endothelial cells. It is relatively homogenous lesion composed of macrophages, lymphocytes & plasma cells. Plasma cells containing Russels body are found extracellularly. 25 Pulp and Periapical pathology / Oral Pathology OSTEOMYELITIS: The word “osteomyelitis” originates from the ancient Greek words osteon (bone) and muelinos (marrow) Acute Suppurative osteomyelitis: Serious sequela of periapical infection that often results in diffuse spread of infection throughout the medullary spaces, with subsequent necrosis of variable amount of bone. Histological Features Necrotic bone- loss of osteocytes from their lacunae, peripheral resorption and bacterial colonization. o Medullary space→ filled with inflammatory exudates Osteoblasts bordering the bony trabeculae are destroyed Trabeculae may lose their viability and begin to undergo slow resorption 28 Pulp and Periapical pathology / Oral Pathology CHRONIC FOCAL SCLEROSING OSTEOMYELITIS ( CONDENSING OSTEITIS) Unusual reaction of bone to infection HISTOLOGIC FEATURES Dense bony trabeculae with little interstitial marrow tissue Many reversal and resting lines giving pagetoid appearance If interstitial soft tissue is present, it is generally fibrotic and infiltrated with small amount of lymphocytes Osteocystic Lacunae appears empty 31  Pulp and Periapical pathology / Oral Pathology CHRONIC DIFFUSE SCLEROSING OSTEOMYELITIS : is the clinical entity characterized by a nonsuppurative, inflammatory process associated with recurrent swelling, trismus and pain HISTOLOGIC FEATURES Dense, irregular trabeculae of bone bordered by active layer of Osteoblasts; focal Osteoclastic area may be present. Mosaic pattern appearance Trabecular bone with the presence of reparative and reactive new bone formation. There was a marked abundant osteoid and osteoblastic rim. Interstitial soft tissue is fibrotic Proliferating fibroblasts and occasional small capillaries as well as small focal collection of lymphocytes and plasma cells 32 Pulp and Periapical pathology / Oral Pathology CHRONIC OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS: (Garre’s chronic nonsuppurative sclerosing osteitis ,periostitis ossificans) HISTOLOGIC FEATURES Subperiosteal mass is composed of much reactive new bone and osteoid tissue, with Osteoblasts bordering many of trabeculae Trabeculae is perpendicular to cortex and parallel to each other Connective tissue is fibrous and shows sprinkling of lymphocytes and plasma cells 33 Pulp and Periapical pathology / Oral Pathology CELLULITIS/ PHLEGMON Cellulitis is a diffuse inflammation of soft tissues which is not circumscribed or confined to one area, but which, in contrary to the abscess, tends to spread through tissue spaces and along fascial spaces. HISTOLOGICAL FEATURE A microscopic section through an area of cellulitis shows a diffuse exudation of polymorphoneuclear leukocyte and lymphocyte. Considerable serous fluid and fibrins causing separation of connective tissue and muscle fibres. 35 Tile BACTERIAL INFECTIONS Basic sciences Department Wed. Oct. 02. 2024 1 Bacterial Infection / Oral Pathology SCARLET FEVER (Scarlatina) Caused by beta hemolytic streptococci. Oral Manifestation: Reffered as Stomatitis Scarlatina Small, red macules may appear in the hard and soft palate and uvula which are called Forchheimer spots. 7 Bacterial Infection / Oral Pathology In early course of the disease, tongue exhibits a white coating and the fungiform pappila are edematous and hyperemic. This phenomenon has been described clinically as ‘strawberry tongue’. Later, the tongue coating is lost and appears red and glistening and smooth except the pappliae this is called as ‘raspberry tongue’. 8 Bacterial Infection / Oral Pathology Histological features: Neutrophilic infiltrate with spongiosis C Parakeratosis in the epidermis. Necrotic conective tissue. 9 Bacterial Infection / Oral Pathology TUBERCULOSIS Causative Micro organism:- Mycobacterium Tuberculosis Ulcer is commonly tongue followed by palate, lips, gingiva, buccalmuccosa Histological features: Activate T cell causes transformation of macrophages to epitheloid cells and multinucleated giant cells. o Multinucleated giant cells seen in the tubercles are referred to as langhans giant cells. Marked proliferation of fibroblasts and dense collagen fibers are laid down all around the tubercle. 10 Bacterial Infection / Oral Pathology DIPTHERIA Caused by gram +ve bacillus, Corynebacterium diptheriae. Also called Klebs Loeffler bacillus Oral Manifestations Formation of ‘Diptheric Membrane’. In oral cavity, appears as nonspecific ulcers. Histopathology: The initial stage of the disease is characterized by edema and hyperemia of the affected epithelial surface, which is followed by necrosis and the formation of fibrinous suppurative exudates. The pseudomembrane is composed of fibrin, necrotic epithelial cells. The membrane is composed of mostly fibrin over the vocal cords, while on the bronchus, it is composed of both fibrin and neutrophils. 11  Bacterial Infection / Oral Pathology ACTINOMYCOSIS Also known as LUMPY JAW. 3 It shows typical ‘sulfur granules’. HISTOLOGICAL FEATURE Typical lesion is granulomatous with central abscess formation showing colonies of microorganisms within it. Colonies appear to be floating in the sea of PMNS. Peculiar appearance of colonies, with peripheral radiating filaments, termed as RAY FUNGUS. 12 Bacterial Infection / Oral Pathology SYPHILIS (Lues) Caused by Treponema palladium Acquired Syphilis Primary Syphilis:- lesion known as CHANCRE. Lip, tongue, palate, gingiva and tonsil. APPEARANCE:- It is an elevated, ulcerated nodule showing local induration and producing regional lymphadenitis. Lesion on lip may have brownish crustered appearance. 13  Bacterial Infection / Oral Pathology SECONDARY OR METASTATIC STAGE Commences 6 weeks after primary lesion. APPEARANCE:- Oral Lesions called ’mucous patches’ are usually multiple, painless, grayish white plaques overlying an ulcerated surface. Snail track ulcer SITES AFFECTED:- Tongue, gingiva , buccal mucosa 14  Bacterial Infection / Oral Pathology Oral Manifestation: Short maxilla o High palatal arch n o Saddle Nose u oHuthinson’s triad: hypoplasia of incisors, molar teeth,8th nerve deafness and intestinal keratitis. TERTIARY SYPHILIS Classical lesion of tertiary syphillis is ‘GUMMA’. Intraorlly: tongue and palate. Histological features Primary syphilis (primary chancre) demonstrates an acanthotic epidermis which erodes with time to become ulcerated. Under the ulcer bed there is typically a dense lymphocytic response, numerous plasma cells. I 15 Bacterial Infection / Oral Pathology Secondary syphilis shows a psoriasiform hyperplasia with superficial neutrophils Tertiary syphilis shows necrotising granulomatous inflammation. 16 Bacterial Infection / Oral Pathology NOMA (Cancrum Oris, Gangrenous Stomatitis) Initial lesion is painful ulceration,usually of gingiva or buccal mucosa. Rapid spread of the ulcer which necrotises. Characterized by destructive process of orofacial tissues. Histological features: Extensive necrosis and destruction of soft tissues and bones. 17 Bacterial Infection / Oral Pathology ACUTE NECROTISING ULCERATIVE GINGIVITIS (Trench Mouth, Vincent’s Infection) Teeth seem to be slightly extruded, sensitive to pressure, or to have a “woody sensation”, slightly mobile with difficulty in eating. Typical lesion is, Punched out, necrotic, crater like ulceration seen over the interdental papillae Ulceration may develop on the cheeks, lips and the tongue, palate & pharyngeal area. Histological features: Most superficial is a bacterial area of fibrous mesh composed of epithelial cells, leukocytes, and a variety of bacterial cells, including rods, fusiform bacteria, and spirochetes. Deep to that layer exists a neutrophil-rich zone composed of a higher number of leukocytes, spirochetes, and bacterial cells. Next lies a necrotic zone containing disintegrated cells, spirochetes, and fusiform bacteria. The deepest layer contains spirochete infiltration. 18 Bacterial Infection / Oral Pathology Leprosy (Hansen’s disease) Chronic granulomatous infection caused by Mycobacterium leprae. Leprosy manifests in two polar forms, namely, tuberculoid type and lepromatous type. Oral Manifestations: Oral lesions consist of small tumor like masses called lepromas, which develop on the tongue, lips, or hard palate. These nodules show a tendency to break down and ulcerate. Gingival hyperplasia with loosening of the teeth Histologic Features: Typical granulomatous nodule shows collections of epithelioid histiocytes and lymphocytes in a fibrous stroma. Langhans type giant cells are variably present. Sheets of lymphocytes with vacuolated macrophages called lepra cells are scattered throughout the lesions. 19 Bacterial Infection / Oral Pathology BOTRYOMYCOSIS (Bacterial actinophytosis, actinobacillosis) Chronic granulomatous infection Oral Manifestations: Human botryomycosis is usually a localized granulomatous infection of the skin or mucosa. Histologic Features. Chronic granulomatous nodules are characterized by the presence of suppurative foci which contain grains or granules The eosinophilic,peripheral clubs formation typical of actinomycetes is usually not identifiable in this disease. 20 Bacterial Infection / Oral Pathology GRANULOMA INGUINALE (Granuloma venereum, donovanosis) Disease is a progressive, chronic, infectious, granulomatous disease Oral Manifestations: Papules or nodules, which ulcerate to form clean, granular lesions with rolled margins and which show a tendency for peripheral enlargement. Histologic Features. Various forms of granuloma inguinale is one of granulation tissue with infiltration of polymorphonuclear leukocytes and plasma cells. Pathognomonic of the disease is the presence of large mononuclear phagocytes, each containing intra cytoplasmic cysts within which are found the Donovan bodies. These bodies are tiny, elongated, basophilic and argyrophilic rods and are present in profuse numbers within the macrophages. 21 Bacterial Infection / Oral Pathology PYOSTOMATITIS VEGETANS Uncommon inflammatory disease of the oral cavity Oral Manifestations: Oral lesions consist of large numbers of broad based papillary projections, tiny abscesses or vegetations developing in areas of intense erythema. Small projections are red or pink in color. Histologic Features: Papillary projections generally show hyperplastic stratified squamous epithelium with an underlying loose connective tissue which is generally densely infiltrated by large numbers of plasma cells, lymphocytes, and occasional polymorphonuclear leukocytes, sometimes with a preponderance of eosinophils. Tiny areas of focal necrosis and microabscess formation, either intraepithelial or subepithelial, are common features of the lesions. In some instances, focal areas of degeneration and necrosis of the overlying epithelium are present. 22 Bacterial Infection / Oral Pathology CELLULITIS It is a diffuse inflammation of soft tissues which is not circumscribed or confined It is also known as Phlegmon. HISTOLOGIC FEATURES:- Collection of fibrin & serum fluid in the tissue; thus causing separation of CT and muscle fibres. Acute inflammatory cell infiltration / diffuse exudation by PMN leukocytes & lymphocytes. 23 Tile Fungal And Viral infections Basic Sciences Department Wed. Oct. 09. 2024 1 Fungal And Viral infections/ Oral Pathology Pseudomembranous candidiasis The best recognized form of candidal infection is pseudomembranous candidiasis. Also known as thrush. Pseudomembranous candidiasis is characterized by the presence of adherent white plaques that resemble cottage cheese or curdled milk on the oral mucosa. Scraping them with a tongue blade or rubbing them with a dry gauze sponge can remove these plaques. 8  Fungal And Viral infections/ Oral Pathology It may be initiated by exposure of the patient to broad-spectrum antibiotics or by impairment of the patient’s immune system. Site: buccal mucosa, mucobuccal folds, dorsal tongue 9  Fungal And Viral infections/ Oral Pathology Histological features- 1) PAS positive candidal hyphae invading the epithelium. 2) Epithelium may show hyperkeratosis and elongated rete ridges. 3) Collection of neutrophils in the epithelium. 4) Chronic inflammatory cell infiltrate can be seen in the connective tissue immediately subjacent to the infected epithelium. 10 Fungal And Viral infections/ Oral Pathology Erythematous Candidiasis Site -tongue, gingiva,palate Tongue shows depapillation & dekeratinization n Histological features- f 1) Hyperplastic epithelium with superficial necrotic and desquamating parakeratotic layer. 2)Infiltration by both yeasts , hyphae and by inflammatory cells mainly by neutrophils which may accumulate to form micro abscesses 11  Fungal And Viral infections/ Oral Pathology Central papillary atrophy (median rhomboid glossitis) Other forms of erythematous candidiasis are usually asymptomatic and chronic. This category is the condition known as central papillary atrophy of the tongue, or median rhomboid glossitis. Clinically, central papillary atrophy appears as a well-demarcated erythematous zone that affects the midline, posterior dorsal tongue and often is asymptomatic. 12  Fungal And Viral infections/ Oral Pathology Some patients with central papillary atrophy may also exhibit signs of oral mucosal candidal infection at other sites. This presentation of erythematous candidiasis has been termed chronic multifocal candidiasis. The palatal lesion appears as an erythematous area that, when the tongue is at rest, contacts the dorsal tongue lesion, resulting in what is called a “kissing lesion” because of the intimate proximity of the involved areas. Multifocal oral candidiasis characterized by central papillary atrophy of the tongue and other areas of involvement. Same patient showing a “kissing” lesion of oral candidiasis on the hard palate. 13  Fungal And Viral infections/ Oral Pathology Angular cheilitis It is characterized by erythema, fissuring, and scaling Saliva tends to pool in these areas, keeping them moist and thus, favoring a yeast infection. The candidal infection more extensively involves the perioral skin, usually secondary to actions that keep the skin moist (e.g chronic lip licking, thumb sucking), creating a clinical pattern known as cheilocandidiasis (exfoliative lesions of the vermilion zone and perioral skin are due to superficial candidal infection) Angular cheilitis. Cheilocandidiasis. 14  Fungal And Viral infections/ Oral Pathology Denture stomatitis This condition is characterized by varying degrees of erythema, sometimes accompanied by petechial hemorrhage, localized to the denture-bearing areas of a maxillary removable dental prosthesis. The palatal mucosa and tissue-contacting surface of the denture are swabbed and separately streaked onto a Sabouraud’s agar slant. Sabouraud’s agar slanthas been streaked with swabs 15 Fungal And Viral infections/ Oral Pathology Chronic inflammatory changes of the denture bearing mucosa Newton's classification Type I – Pinpoint erythema Type II- Diffuse areas of erythema and edema of palatal mucosa Type III- Nodular hyperplastic areas of mucosa interspersed with normal areas of mucosa Histological features- i 1) Epithelium shows hyperplasia/ atrophy 2) Surface being Para keratinized or non keratinized 3) Leucocytes infiltrate the epithelium forming micro abscesses 16  Fungal And Viral infections/ Oral Pathology Hyperplastic Candidiasis (Candidal leukoplakia) This form of candidiasis is the least common investigators believe that this condition simply represents candidiasis that is superimposed on a preexisting leukoplakic lesion, a situation that may certainly exist at times. Often the leukoplakic lesion associated with candidal infection has a fine intermingling of red and white areas, resulting in a speckled leukoplakia. 17 Fungal And Viral infections/ Oral Pathology Site -buccal mucosa , palate Histological features- f 1) Epithelium is Para keratinized 2) Cells in the Para keratinized layer are separated by edema numerous neutrophils collecting to form micro abscesses 3)Lesions may have an increased frequency of epithelial dysplasia 18 Fungal And Viral infections/ Oral Pathology Histoplasmosis Granulomatous fungal disease caused by Histoplasma capsulatum. Histoplasmosis, the most common systemic fungal infection. Site -gingiva, tongue and palate I The condition usually appears as a solitary, variably painful ulceration of several weeks duration however, some lesions may appear erythematous or white with an irregular surface. The ulcerated lesions have firm, rolled margins, and they may be indistinguishable clinically from a malignancy. 19  Fungal And Viral infections/ Oral Pathology Histological features- Histoplasmosis showing a diffuse infiltrate macrophages more commonly, collections of macrophages organized into granulomas with cytoplasmic microorganisms r Multinucleated giant cells are usually seen in association with the granulomatous inflammation. This medium-power photomicrograph shows scattered epithelioid macrophages admixed with lymphocytes and plasma cells. Some macrophages contain organisms of Histoplasma capsulatum (arrows). This high-power photomicrograph of a tissue section readily demonstrates the small yeasts of Histoplasma capsulatum. (Grocott-Gomori methenamine silver stain.) 20  Fungal And Viral infections/ Oral Pathology Blastomycosis Caused by dimorphic fungus known as Blastomyces dermatidis Blastomycosis is a relatively uncommon disease. These lesions may have an irregular, erythematous or white intact surface, or they may appear as ulcerations with irregular rolled borders and varying degrees of pain. Clinically, because the lesions resemble squamous cell carcinoma, biopsy and histopathologic examination are required. 21  Fungal And Viral infections/ Oral Pathology Histological features- Large yeasts of Blastomyces dermatitidis (arrow) and pronounced host inflammatory response to the organism. Lesional tissue typically shows a mixture of acute inflammation and granulomatous inflammation surrounding variable numbers of yeasts. They are characterized by a doubly refractile cell wall and a broad attachment between the budding daughter cell and the parent cell. Because this benign elongation of the epithelial rete ridges may look like squamous cell carcinoma at first glance under the microscope, careful inspection of the underlying inflamed lesional tissue is mandatory. 22  Fungal And Viral infections/ Oral Pathology CRYPTOCOCCOSIS Relatively uncommon fungal disease caused by the yeast Cryptococcus neoformans. Oral lesions are relatively rare, they have been described either as craterlike, nonhealing ulcers that are tender on palpation or as friable papillary erythematous plaques. 23  Fungal And Viral infections/ Oral Pathology Histological features- Lesion generally show a granulomatous inflammatory response to the organism. The yeast appears as a round-to-ovoid structure, by a clear halo that represents the capsule. Staining with the PAS or Grocott- Gomori methenamine silver method readily identifies the fungus; moreover, a mucicarmine stain uniquely demonstrates its mucopolysaccharide capsule. 24  Fungal And Viral infections/ Oral Pathology ZYGOMYCOSIS (MUCORMYCOSIS; PHYCOMYCOSIS) It involve any one of several areas of the body, but the rhinocerebral form is most relevant to the oral health care provider. Patients may experience nasal obstruction, bloody nasal discharge, facial pain or headache, facial swelling or cellulitis, and visual disturbances with concurrent proptosis. Symptoms related to cranial nerve involvement (e.g., facial paralysis) are often present. If the condition remains untreated, palatal ulceration may evolve, with the surface of the ulcer typically appearing black and necrotic. r 25 Fungal And Viral infections/ Oral Pathology Histological features- Lesional tissue shows extensive necrosis with numerous large (6 to 30 um in diameter), branching, nonseptate hyphae at the periphery. The hyphae tend to branch at 90-degree angles. The extensive tissue destruction and necrosis associated with this disease are undoubtedly attributable to the preference of the fungi for invasion of small blood vessels. This disrupts normal blood flow to the tissue, resulting in infarction and necrosis. A neutrophilic infiltrate usually predominates in the viable tissue. 26  Fungal And Viral infections/ Oral Pathology ASPERGILLOSIS Fungal disease that is characterized by noninvasive and invasive forms. Histological features- Tissue sections of invasive Aspergillus lesions show varying numbers of branching, septate hyphae, 3 to 4 μm in diameter. These hyphae show a tendency to branch at an acute angle and to invade adjacent small blood vessels. 27  Fungal And Viral infections/ Oral Pathology TOXOPLASMOSIS Relatively common disease caused by the obligate intracellular protozoal organism Toxoplasma gondii. Histological features- Histopathologic examination of a lymph node obtained from a patient with active toxoplasmosis shows characteristic reactive germinal centers exhibiting an accumulation of eosinophilic macrophages. The macrophages encroach on the germinal centers and accumulate within the subcapsular and sinusoidal regions of the node. 28 Fungal And Viral infections/ Oral Pathology Herpes Simplex Infection Herpes simplex virus (HSV) includes HSV 1 and HSV 2. More severe primary infection can become latent when HSV remains dormant in neural ganglia. Recurrent event has a shorter duration and milder clinical findings than the primary infection HSV-1 Gingivostomatitis is primary HSV Infection occurs most often in young children but may be seen in older children and adults. Onset usually consists of fever, malaise, drooling, and oral and perioral lesions 33  Fungal And Viral infections/ Oral Pathology Primary Herpetic Stomatitis Herpetic stomatitis is a common oral disease transmitted by droplet spread or contact with the lesions. It affects children and young adults. The most common site of recurrence for HSV-1 is the vermilion border and adjacent skin of the lips. This is known as herpes labialis (“cold sore” or “fever blister”). Multiple small, erythematous papules develop and form clusters of fluid filled vesicles 34  Fungal And Viral infections/ Oral Pathology Histologic Features. Herpetic vesicle is an intraepithelial blister filled with fluid. The virus exerts its main effects on the epithelial cells. Infected epithelial cells exhibit acantholysis, nuclear clearing, and nuclear enlargement, which has been termed ballooning degeneration while others characteristically contain intranuclear inclusions known as Lipschütz bodies. The acantholytic epithelial cells are termed Tzanck cells Multinucleated, infected epithelial cells are formed when fusion occurs between adjacent cells. 35  Fungal And Viral infections/ Oral Pathology Chronic herpetic infection Numerous mucosal erosions, each of which is surrounded by a slightly raised,yellow-white border, in a patient with acute myelogenous leukemia. Herpes simplex. Altered epithelial cells exhibiting ballooning degeneration, margination of chromatin, and multinucleation. 36  Fungal And Viral infections/ Oral Pathology Varicella These may cause localized or systemic manifestations that varies from erythematous lesions vesiculation, ulceration, scarring or severe constitutional symptoms. The varicella-zoster virus (VZV, HHV-3) is ensues, herpes simplex virus (HSV) in many respects. Chickenpox represents the primary infection with the VZ; latency ensues and recurrence is possible as herpes zoster, often after many decades. 37  Fungal And Viral infections/ Oral Pathology The vermilion border of the lips and the palate are the most common sites of involvement, followed by the buccal mucosa. Occasionally, gingival lesions resemble those noted in primary HSV infections. The lesions begin as 3- to 4-mm, white, opaque vesicles that rupture to form 1- to 3-mm ulcerations Histologic Features The cytologic alterations are virtually identical to those described for HSV. The virus causes acantholysis, with formation of numerous free-floating Tzanck cells, which exhibit nuclear margination of chromatin and occasional multinucleation. 38  Fungal And Viral infections/ Oral Pathology HERPES ZOSTER (SHINGLES) After the initial infection with VZV (chickenpox), the virus is transported up the sensory nerves and presumably establishes latency in the dorsal spinal ganglia. Clinically evident herpes zoster occurs after reactivation of the virus, with the involvement of the distribution of the affected sensory nerve. Oral lesions occur with trigeminal nerve involvement and may be present on the movable or bound mucosa. r 39  Fungal And Viral infections/ Oral Pathology The lesions often extend to the midline and frequently are present in conjunction with involvement of the skin overlying the affected quadrant. Facial paralysis has been seen in association with herpes zoster of the face or external auditory canal. Ramsay Hunt syndrome is the combination of cutaneous lesions of the external auditory canal and involvement of the ipsilateral facial and auditory nerves. 40 Fungal And Viral infections/ Oral Pathology Ramsay-Hunts syndrome A special form of zoster infection of the geniculate ganglion, with the involvement of the external ear and oral mucosa, has been termed Hunt’s syndrome (James Ramsay Hunt’s syndrome). The clinical manifestations include facial paralysis as well as pain of the external auditory meatus and pinna of the ear. 41  Fungal And Viral infections/ Oral Pathology INFECTIOUS MONONUCLEOSIS (MONO; GLANDULAR FEVER; “KISSING DISEASE”) Infectious mononucleosis is a symptomatic disease resulting from exposure to Epstein-Barr virus (EBV, HHV-4). Petechiae on the hard or soft palate are present in about 25% of patients. The petechiae are transient and usually disappear within 24 to 48 hours. Necrotizing ulcerative gingivitis (NUG) r 42  Fungal And Viral infections/ Oral Pathology Histologic Features Biopsy specimens of intraoral CMV lesions usually demonstrate changes within the vascular endothelial cells. Scattered infected cells are extremely swollen, showing both intracytoplasmic and intranuclear inclusions and prominent nucleoli. This enlarged cell has been called an “owl eye” cell. Salivary ductal epithelium also may be affected and form “owl eye” cells. 44  Fungal And Viral infections/ Oral Pathology ACUTE LYMPHONODULAR PHARYNGITIS Lesions, characteristic of the disease, are raised, discrete, whitish or yellowish to dark pink solid papules or nodules, surrounded by a narrow zone of erythema. The lesions are not vesicular and do not ulcerate. The lesions characteristically appear on the uvula, soft. Histologic Features. The papules or nodules consist of hyperplastic lymphoid aggregates. In some cases, the overlying epithelium show inclusion of bodies which in some instances are intranuclear but in others, cytoplasmic. 45  Fungal And Viral infections/ Oral Pathology RUBEOLA (MEASLES) Koplik’s spots Candidiasis Necrotizing ulcerative gingivitis (NUG) Appearance of red spots appear 2 days before the onset are known as Koplicks spots r r 46  Fungal And Viral infections/ Oral Pathology Histologic Features Koplik’s spots represent areas of focal hyper parakeratosis in which the underlying epithelium exhibits spongiosis, intercellular edema, dyskeratosis, and epithelial syncytial giant cells. The number of nuclei within these giant cells ranges from three to more than 25. On electron microscopy, the inclusions have been shown to represent microtubular aggregates characteristic of the causative paramyxovirus. Multinucleated cells subsequently have been termed Warthin-Finkeldey giant cells and were thought for a time to be specific for measles. 47  Fungal And Viral infections/ Oral Pathology MUMPS (EPIDEMIC PAROTITIS) Mumps is an infection caused by a virus in the family Paramyxovirus, genus Rubulavirus, which causes a diffuse disease of exocrine glands. The parotid gland is involved most frequently,but the sublingual and submandibular glands also can be affected. Discomfort and swelling develop in the tissues surrounding the lower half of the external ear and extending down along the posterior inferior border of the adjacent mandible. The most frequently reported oral manifestation is redness and enlargement of Wharton’s and Stensen’s salivary gland duct openings. In addition, involvement of the sublingual gland may produce bilateral enlargements of the floor of the mouth. 48  Fungal And Viral infections/ Oral Pathology ORAL HAIRY LEUKOPLAKIA Although EBV is thought to be associated with several forms of lymphoma in HIV-infected patients, the most common EBV-related lesion in patients with AIDS is oral hairy leukoplakia. This lesion clinically presents as a white mucosal plaque that does not rub off and is characterized histopathologically by a somewhat distinctive (but not diagnostic) pattern of hyperkeratosis and epithelial hyperplasia. Most cases of OHL occur on the lateral border of the tongue and range in appearance from faint white vertical streaks to thickened and furrowed areas of leukoplakia, exhibiting a shaggy keratotic surface. r 49  Fungal And Viral infections/ Oral Pathology Histopathologically OHL exhibits thickened parakeratin that demonstrates surface corrugations or thin projections. The epithelium is acanthotic and exhibits a bandlike zone of lightly stained cells with abundant cytoplasm (“balloon cells”) in the upper spinous layer. Close examination of the superficial epithelium reveals scattered cells with peripheral margination of chromatin termed nuclear beading Dysplasia is not noted. Heavy candidal infestation of the parakeratin layer is typical, although the normal inflammatory reaction to the fungus usually is absent. 50 Tile PREMALIGNANT LESIONS AND CONDITIONS Basic Sciences Department Wed. Oct. 23. 2024 1 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology The World Health Organization classifies oral precancerous/potentially malignant disorders into 2 general groups as follows: A precancerous lesion A precancerous condition Precancerous lesion ( Precancer, premalignancy, potentially malignant lesion) A morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart. (WHO 1972) 1. Leukoplakia, 2. Erythroplakia, 3. The palatal lesions of reverse smokers. 7 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Precancerous conditions A generalized state associated with a significantly increased risk of cancer (WHO 1972) 1. Submucous fibrosis 2. Lichen planus, 3. Epidermolysis bullosa, 4. Discoid lupus erythematous. ur 8 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Classification of Precancerous lesions & Precancerous conditions Precancerous lesion Leukoplakia Leukoedema Erythroplakia Carcinoma- in – situ Actinic cheilosis /cheilitis Oral Lesion Associated with use of tobacco Stomatitis Nicotina Snuff Dipper Lesion Precancerous conditions Oral submucosis fibrosis Lichen planus Lichenoid Reaction Discoid lupus erthematosus 9  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Precancerous lesion Leukoplakia: Greek latin ( Leuko = white; plakia= patch ) Def : A whitish patch or plaque that cannot be characterized clinically or pathologically as any other disease and which is not associated with any physical or chemical causative agent except for the use of tobacco. Types Leukoplakia: Homogenous Non Homogenous / Nodular Verrucous /speckled Etiology Local factors: Tobacco Smokeless tobacco ( chewable or snuff) Smoking tobacco ( cigar,bidi,cigarette,pipe) Candidasis Systemic Factors Syphilis Viruses Vitamin deficiency 10  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Clinical classification of leukoplakias HOMOGENOUS LEUKOPLAKIA. Well defined white patch,localized that is slightly elevated Fissured,wrinkled or corrugated appearance. Low potential for premalignancy. NON- HOMOGENOUS LEUKOPLAKIA(Granular or nodular form) Mixed red & white lesion in which keratotic white nodules High malignant transformation –2/3 rd VERRUCOUS LEUKOPLAKIA / SPECKLED Thick white lesion with papillary surfaces Stronger malignant potential than homogenous leukoplakia Proliferative verrucous leukoplakia Hansen et al in 1985 Multiple keratotic plaques with roughened surface projections 11 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology HISTOPATHOLOGY Degree of hyperkeratosis Epithelial thickness (acanthosis/atrophy) Dysplasia and inflammatory cell infiltration Micropically leukoplakia is characterized by: 1. Hyperkeratosis: thickened keratin layer may be parakeratotic or orthokeratotic surface epithelium may be smooth or irregular with papillary projection ( verrucous LKP) 2. Acanthosis: Most of lkp lesion show thickening of spinous layer. Some of lesion show area of epithelial atrophy. 3.Dysplastic features: a. Drop-shaped rete ridges: Normally rete ridge taper to deeper portion or parallel sided with blunt ends. Dysplasia rete ridge become wider ( accommodate the increased cells) b. Basal cell hyperplasia: Normally 1-2 layer basal cell. Dysplasia increased more than 2 layer 12  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology c. Loss of polarity of basal cells: Normally nucleus of basal cell is arranged perpendicular to basement membrane in this f arrengement is lost nuclei are in different angles. Known as loss of polarity. d. Irregular epithelial stratification: Normal epithelium distinct layers (strata) are seen. Disturbance in this arrangement called irregular epithelial stract. e. Loss of intercellular adherence:Normal epithelium cell attached each other Dysplasia cells loses their attachment. f. Cellular and nuclear pleomorphism: Dysplasia epithelium cells shows variation in shape and size. g. Alternation in nuclear cytoplasmic ratio: normally 1:4 or 1: dysplasia 1:1 h. Nuclear hyperchromatism: In this increased or dark staining of nucleus. i. Enlarged nuclei g. Increased number of mitotic figures k. Mitotic figures that are abnormal in form 13 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Leukoedema :is an abnormality of the buccal mucosa which clinically resembles early leukoplakia, but appears to differ from it in certain respects. Histologic Features. Increase i in thickness of the epithelium. Intracellular edema of the spinous and broad rete pegs which appear irregularly elongated. Cytoplasm appears lost, and the nuclei appear absent, clear or pyknotic. Shows only acanthosis with intracellular edema of the spinous cells. 14 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Carcinoma in situ (Intraepithelial carcinima) More common on skin but also occur oral mucous membrane. Histopathology 1. Dysplastic changes from basal layer to superficial layer (Loss of cells and their polarity) 2. Intact basement membrane I 3. Keratin may or may not be found on the surface of the lesion but, if present, is more apt to be parakeratin rather than orthokeratin 4.Certain cytologic alterations may also occur. 15  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Erythroleukoplakia : literally means red patch Defi:“a velvety, red patch that cannot be characterized clinically or pathologically as any other disease” Red area partially ulcerated Histopathologic Features: l The epithelium shows lack of keratin production and is often atrophic, but it may be hyperplastic. Severe degree of dysplasia to ca-in-situ. 16  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Actinic cheilosis/ chilitis: It is cutaneous premalignant lesion Associated with lip as well as other sun exposed surfaces. Resulting long term exposure to solar radiation HISTOPATHOLOGICAL FEATURES Varying degrees of epithelial dysplasia Mild chronic inflammatory cell infiltrate Underlying connective tissue demonstrates a band of amorphous, acellular,basophillic change –SOLAR (ACTINIC) ELASTOSIS 17 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Stomatitis Nicotine (smoker’s palate, stomatitis nicotina palati) Specific white lesion present on hard & soft palate in heavy cigarette,pipes. It is also seen in people who smoke reverse also called reverse smoke palate. Histological Features: Hyperorthokeratosis, epithelial dysplasia and inflammatory cells in the connective tissue. Epithelial dysplasia. 18  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Snuff dipper lesion (snuff pouch,tobacco pouch keratosis, smokeless tobacco keratosis.) Histologic Features. Lesions showed pale staining parakeratin-like surface layers of epithelium, containing round I nuclear remnants, ballooning and vacuolated cells and epithelial hyperplasia. 19  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Oral Submucous Fibrosis Mucosal rigidity of varying intensity due to fibroelastic transformation of juxtaepithelial connective tissue layer” followed by a fibro elastic changes of the lamina propria with epithelial atrophy leading to stiffness of oral mucosa causing trismus and inability to eat. Histological features Juxtaepithelial hyalinization. Atrophic epithelium without of retepegs. Dense bundles of collagen fibres in connective tissue I Focal collection of inflammatory cells 20  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology LICHEN PLANUS Derived from greek lichen means tree moss and planus means flat. Lichen planus is a common, chronic inflammatory disease of the skin and mucous membrane Erasmus Wilson, 1869 Six Ps : it characterize the lesion Lichen planus P : Planar P: Polygonal P: Purple P: Pruritic P: Papules P: Plaques A network of fine grayish white lines which covered the papules – WICKHAM’S STRIAE Fresh lesions may appear on scratch marks Linear lesions may appear at sites of trauma – KOEBNER’S PHENOMENON 21  PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology HISTOPATHOLOGY Basal cell damage in the form of multiple scattered Civatte bodies. Hyperkeratosis Saw tooth appearance of rete ridges “LIQUEFACTIVE DEGENERATION” in the u basal cell layer Absence of epithelial dysplasia 22 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Lichenoid reaction It is same as with lichen planus but this occur due to any drug or after drug discontinued. Hisopatholgy: Lichenoid drug reaction may show deep as well as superficial dermal. Lymphocyte infiltrate. Lesion shows parakeratinized, atrophic epithelium, liquefaction degeneration of the basal cell layer. 23 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Discoid lupus erythematosus Follicles resembling CARPET TACKS extension. Oral manifestation : Most common on buccal mucossa, tongue, palate HISTOPATHOLOGY ñ Hyperorthokeratosis or hyperparakeratosis Hydropic degeneration of basal cell layer 24 PREMALIGNANT LESIONS AND CONDITIONS/Oral Pathology Work-up and the Early Detection of Oral Cancer Oral examination Supravital staining Oral cytology Chemiluminescent light Tissue autofluorescence 25 Tile Histopathology of Dental Caries Basic Sciences Department Wed. Oct. 30. 2024 1  Classification Dental caries Based on morphological Based on Based on Morphology of anatomy severity Chronology Anatomical site Rampant Occlusal Caries Pit & Fissure Caries Incipient caries Infancy Caries Smooth Surface Carie Cervical caries Acute & chronic Adolescent Root Caries Arrested caries Caries Linear Enamel Caries Recurrent Caries 7  Histopathology of Dental Caries / Oral Patholgy Pit & Fissure Caries Site : Occlusal surface of premolars & Molars Smooth Surface Caries Def; Caries that develop on the proximal surfaces of the teeth or the gingival third of the buccal & lingual surfaces Site: proximal surfaces Cervical caries Site:Buccal, lingual or labial surfaces They are crescent shaped cavities & is almost always a open cavity Root Caries Carious lesion which initiates at the dentin root portion of a tooth Found in old age & teeth with gingival recession & exposed root surfaces 8  Histopathology of Dental Caries / Oral Patholgy Recurrent Caries So recurrent caries occur beneath a restoration if all carious dentin is not removed before inserting the filling. Rampant Caries It is also defined as sudden rapid & almost uncontrollable destruction of the teeth. Also known as baby-bottle tooth decay, nursing-bottle caries and milk-bottle syndrome. It is the only severe dental disease common in children under 3 years of age. Keyes suggested that micro-organisms (plaque), a substrate (sugar), and a susceptible tooth surface were required for caries to initiate. This is the "Keyes Triad". 10 Histopathology of Dental Caries / Oral Patholgy Saliva The role of saliva is critical in controlling caries. 0.5-1.0 litres per day of saliva is produced by major and minor salivary glands. The Composition and Buffering capacity of Saliva is affected by flow rate varies between person to person. Chemical factors Lysozymes:Prevents the mouth from colonization of extraneous microorganism Lactoperoxidase:Active against microorganisms which do not produce catalase ( Strepto & lacto) Lactoferrin:Baceriocidal effect 11 Histopathology of Dental Caries / Oral Patholgy Histopathology of enamel caries Loss of inter rod substance Mucopolysaccharide , Transverse striation on enamel Accentuation of incremental lines of Retzius EARLY LESION – SMOOTH SURFACE Earliest visible changes are seen as a chalky white spot on the tooth just adjacent to contact point. 12  Zones of enamel caries Before complete disintegration of enamel several zones can be Traslucent zone distinguished Dark zone Body As caries progresses, the lesion of Straie of retzius smooth surface caries has a distinctive conical shape with its base towards Intact surface zpne enamel surface and apex towards DEJ. Sclerotic dentine This conical lesion when observed in a Intact surface light microscope reveals four different zones as seen from deepest advancing Fissure Straie of retzius zone first Body 1. Translucent zone 2. Dark zone Dark zone Translucent zone 3. Body of lesion 4. Surface zone 13 Histopathology of Dental Caries / Oral Patholgy Zone 1: Translucent zone Occurs due to formation of submicroscopic pores at enamel rod boundaries. Lies at advancing front of teeth Seen in ground sections Polarized light Structureless & well demarcated from adjacent normal enamel transparent light Prisms, cross striations & striae of Retzius are visible This zone is slightly more porous than sound enamel having a pore volume of 1% compared to 0.1% of sound enamel. 14 Histopathology of Dental Caries / Oral Patholgy Zone 2: Dark Zone Superficial to body of lesion & just superficial to body of lesion Appears dark in mounting media Seen 90-95% of cases Pore volume of 2-4% Positive zone Pores are smaller in size Increased porosity in this zone is due to greater degree of demineralization in this zone. 15 Histopathology of Dental Caries / Oral Patholgy Zone 3 Body of the lesion Largest zone Lies between unaffected surface layer & dark zone Pore volume 5-25% Striae of retzius appears intact 16 Histopathology of Dental Caries / Oral Patholgy Zone 4: Surface Zone Partial demineralization 1-10% Loss of mineralization5% Sharply demarcated from underlying radiolucent zone Surface has greater resistance Enamel lamellae 17 Histopathology of Dental Caries / Oral Patholgy Caries of dentin Starts at DEJ Microorganism travels at a variable speed, depending on number of factors When lateral spread occurs at the DEJ with involvement of underlying dentin slightly clinically evident changes is seen in the overlying enamel. Two types Early Advanced Early dentinal caries Transparent dentin Dentinal sclerosis 18 Histopathology of Dental Caries / Oral Patholgy The first change to occur in the caries process within dentin is fatty degeneration of the tome’s fibers, with deposition of lipid globules within these fibers. This is then followed by dentinal sclerosis, which is minimal in rapidly advancing acute caries and maximum in slow, chronic caries.This is considered as a protective measure by dentinal tubules to seal off the invading bacteria. In spite of all these attempts to prevent spread of caries process, dentin is continually destroyed. Thus behind the zone of dentinal sclerosis a narrow zone of decalcification is seen, just ahead of bacterial invasion of dentinal tubules. At this stage, only a few tubules are invaded even before clinical evidence of caries. These bacteria are called “Pioneer bacteria.” 20 Histopathology of Dental Caries / Oral Patholgy Coalescence and breakdown of adjacent dentinal tubules leads to formation of Liquefaction foci described by Miller It is an ovoid area of destruction of tubules parallel to the course of tubules and is packed with necrotic debris derived from destruction of tubules. 22 Histopathology of Dental Caries / Oral Patholgy ZONES OF DENTINAL CARIES Observing from the pulpal side at the advancing edge of carious lesion following different zones can be seen ZONE 1 – Zone of fatty degeneration of Tomes’ fibers ZONE 2 – Zone of dentinal sclerosis ZONE 3 – Zone of decalcification ZONE 4 – Zone of bacterial invasion ZONE 5 – Zone of decomposed dentin 23 Tile HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES Basic Sciences Department Wed. Nov. 06. 2024 1  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology 2. Stress 3. Substance abuse 4. Poor nutrition Ascorbate (vitamin C) deficiency HISTOPATHOLOGIC FEATURES Incipient gingivitis demonstrates a light inflammatory infiltrate consisting of polymorphonuclear leukocytes that accumulate in the connective tissue adjacent to the sulcular epithelium. With progression, the infiltrate becomes more intense and demonstrates a mixture of lymphocytes, plasma cells, and l acute inflammatory cells. Areas of fibrosis, hyperemia, edema, and hemorrhage may be present. 9  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology GINGIVAL DISEASES Plaque induced gingival disease is the most common form of gingival disease. Histologic Features. The gingiva in chronic gingivitis reveals infiltration of the connective tissue by varying numbers of lymphocytes, monocytes, and plasma cells. Polymorphnuclear leukocytes are occasionally noted, particularly beneath the crevicular epithelium. The junction of the epithelial attachment to the tooth represents a weak point in the epithelial barrier to the oral environment, and at this point a collection of Polymorphonuclear leukocytes and lymphocytes are always found 10  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology NECRONECROTIZING ULCERATIVE GINGIVITIS (VINCENT’S INFECTION; TRENCH MOUTH) TIZING ULCERATIVE GINGIVITIS Histologic Features. The surface epithelium is ulcerated and replaced by a thick fibrinous exudate,containing many polymorphonuclear leukocytes and microorganisms. The connective tissue is infiltrated by dense numbers of polymorphonuclear leukocytes and shows an intense hyperemia. 11  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology PLASMA CELL GINGIVITIS (ATYPICAL GINGIVOSTOMATITIS) A distinctive pattern of gingival inflammation, plasma cell gingivitis. Patients with plasma cell gingivitis experience a rapid onset of sore mouth, which often is intensified by dentifrices and hot or spicy foods. Histologic Features. The cases of classic plasma cell gingivitis of the 1970s demonstrated psoriasiform hyperplasia and spongiosis of the surface epithelium, with intense exocytosis and neutrophilic micro abscesses. The underlying lamina propria contains numerous dilated vascular channels and an extremely dense chronic inflammatory infiltrate that is composed predominantly of plasma cells. 12  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology GRANULOMATOUS GINGIVITIS The affected areas appear as red or red-and-white macules, which most frequently involve the interdental papillae but also may occur along the marginal gingiva. HISTOPATHOLOGIC FEATURES Focal collection of histiocytes, lymphocytes, and multinucleated giant cells within the superficial lamina propria of the gingiva. Well-formed histiocytic granulomas with multinucleated giant cells are seen. 13 HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology Drug-induced Gingival Enlargement Refers to an abnormal growth of the gingival tissues secondary to use of a systemic medication. The term is a misnomer because neither the epithelium nor the cells within the connective tissue exhibit either hyperplasia or hypertrophy. Diphenylhydantoin (dilantin sodium) was the first reported anticonvulsant to produce gingival enlargement Dilantin sodium induces gingival enlargements in 3–84.5% of the patients receiving the drug. L Cyclosporine, a potent immunosuppressive agent, has also been reported to produce gingival enlargement. Calcium channel blockers such as nifedipine, nitrendipine, and verapamil also induce gingival enlagement. 14  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology HISTOPATHOLOGIC FEATURES The overlying surface epithelium may demonstrate elongation of the rete ridges, with long extensions into the underlying lamina propria. E In patients with secondary inflammation, there is increased vascularity and a chronic inflammatory cellular infiltrate that most frequently consists of lymphocytes and plasma cells. In patients with pyogenic granuloma-like overgrowths, the proliferations often demonstrate an increased vascularity and significant subacute inflammation. 15  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology ENLARGEMENT ASSOCIATED WITH SYSTEMIC FACTORS There are three types of conditioned enlargements: hormonal, nutritional, and allergic Hormonal Enlargement Inflammatory gingival enlargement often occurs at puberty, both in men and women. The so-called pregnancy gingivitis, more properly spoken of as ‘gingivitis in pregnancy’, is often associated with isolated gingival proliferation, sometimes so severe that it is referred to as a ‘pregnancy tumor,’ which is basically a pyogenic granuloma Microscopic studies of these gingival lesions reveal increased vascularity, multiplication of fibroblasts, edema, and infiltration of leukocytes into the gingiva. 16  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology ENLARGEMENT DUE TO SYSTEMIC DISEASES Leukemia Gingival enlargement is often an early finding in acute monocytic, lymphocytic or myelocytic leukemia Histologic Features: This type of gingival enlargement shows that the gingival tissues are packed with immature leukocytes. Granulomatous Diseases Common diseases in which gingiva is involved are Crohn’s disease,sarcoidosis,Wegner’s granulomatosis. 17  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology GINGGINGIVAL FIBROMATOSIS (FIBROMATOSIS GINGIVAE;ELEPHANTIASIS GINGIVAE) Gingival fibromatosis is a slowly progressive gingival enlargement caused by a collagenous overgrowth of the gingival fibrous connective tissue. Hypertrichosis (increased body hair of the back and buttocks) in association with gingival fibromatosis. HISTOPATHOLOGIC FEATURES The enlargements of gingival fibromatosis consist of dense hypocellular, hypovascular collagenous tissue, which forms numerous interlacing bundles that appear to run in all directions. Surface stratified squamous epithelium exhibiting long, thin rete ridges and underlying dense, fibrous connective tissue. 18  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology Gingival Abscess Gingival abscess is an acute, localized, and painful lesion of sudden onset. Histologic Features. Connective tissue shows edema and formation of abscess cavity surrounded by a diffused collection of polymorphonuclear leukocytes. The overlying epithelium exhibits secondary changes in the form of intra- and inter-cellular edema, micro abscess formation,and sometimes ulceration. 19  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology Pericoronitis It is an inflammatory lesion occurring around the impacted or partially erupted tooth. Histologic Features. The epithelium of the pericoronal flap shows hyperplasia, intercellular edema, and leukocytic infiltration. The underlying connective tissue exhibits increased vascularity, dense diffused infiltration with lymphocytes. 20  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology Nutritional Enlargement Vitamin C Deficiency. The spongy, bleeding gums of scurvy, vitamin C deficiency have long been recognized as a specific entity. Allergic Enlargement Plasma Cell Gingivitis (Atypical gingivitis, plasma cell gingivostomatitis). Histologic Features. The surface epithelium is hyperplastic, shows intracellular edema, and micro abscesses. The underlying connective tissue is densely infiltrated with chronic inflammatory cells There is marked vascular dilatation with severe thinning of epithelium over the connective tissue pegs. 21 HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology Regional Enteritis(Crohn’s Disease) It is a slowly progressive disease of unknown etiology. Most commonly involved areas are the buccal mucosa. Lips which appear diffusely swollen and indurated Palate where multiple ulcers occur. Microscopically It consists of fibrosis and a focal dense collection of lymphocytes and plasma cells. Lymph vessels appear dilated. 22 HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology Idiopathic Gingival Enlargement If the enlargement is present before tooth eruption, the dense fibrous tissue may even interfere with or prevent eruption Other names for this condition are ‘fibromatosis’ ‘fibromatosis gingivae,‘elephantiasis gingivae, and‘congenital macrogingiva’. Histologic sections Show hyperplastic epithelium with elongation of rete ridges and mild hyperkeratosis. The underlying stroma is made up almost entirely of dense bundles of mature fibrous tissue with few young fibroblasts present. 23  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology PERIODONTITIS Gingiva becomes more inflamed and swollen. Histologic Features The apical border of the inflamed area approaches the crest of the alveolar bone and the crestal fibers of the periodontal ligament. The crevicular epithelium shows various degrees of proliferation, and often, tiny ulcerations. They soon appear to lie in the littlebays of bone resorption known as Howship’s lacunae 24  HISTOLOGICAL FEATURES OF PERIODONTAL DISEASES/Oral Pathology PAPILLON-LEFÈVRE SYNDROME 1924, Papillon and Lefevre initially described the syndrome that bears their names. HISTOPATHOLOGIC FEATURES Hyperplastic crevicular epithelium with exocytosis. The underlying connective tissue exhibits increased vascularity and a mixed inflammatory cellular infiltrate consisting predominantly of polymorphonuclear leukocytes, lymphocytes, histiocytes, and plasma cells. 25 Tile Allergic and Immunologic Diseases of the Oral Cavity Basic Sciences Department Wed. Nov. 13. 2024 1  Allergic and Immunologic Diseases of the Oral Cavity/Oral Pathology TRANSIENT LINGUAL PAPILLITIS Transient lingual papillitis (lie bumps, tongue torches). The pathogenesis currently is unknown, but the lesions most likely arise from a variety of influences. Suggested causes include local irritation, stress, gastrointestinal disease, hormonal fluctuation, upper respiratory tract. Transient lingual papillitis. Multiple painful Transient lingual papillitis. Clusters of Transient lingual papillitis: Tender, yellow- asymptomatic, elevated, yellow papules on the white papules on the lateral dorsum and tip of pink papule on the dorsum of the tongue. dorsolateral surface of the tongue tongue. 6 Allergic and Immunologic Diseases of the Oral Cavity/Oral Pathology HISTOPATHOLOGIC FEATURES On histopathologic examination of the first two variants, affected papillae demonstrate normal surface epithelium that may reveal focal areas of exocytosis or ulceration. The underlying lamina propria exhibits a proliferation of numerous small vascular channels and a mixed inflammatory cellular infiltrate. The papulokeratotic variant demonstrates marked hyperparakeratosis in which the surface is ragged and reveals bacterial colonization. A chronic lymphocytic infiltrate is noted in the superficial lamina propria with extension into the basilar portion of the adjacent epithelium. 7  Allergic and Immunologic Diseases of the Oral Cavity/Oral Pathology Recurrent Aphthous Stomatitis (Aphthous ulcers, aphthae, canker sores) It is characterized by the development of painful recurring solitary or multiple ulcerations of the oral mucosa. CLASSIFICATION  Recurrent aphthous minor, which is the most common form of the disease and the one referred to by the lay public as the ‘canker’ sore. Recurrent aphthous major, which is now believed to be simply a more severe form of recurrent aphthous minor Recurrent herpetiform ulcerations, which consist of clusters of ulcers resembling herpetic lesions but lacking evidence of the presence of viruses in patients with a low incidence of antibody to oral mucosa. Recurrent ulcers associated with Behçet’s syndrome, will be considered separately. 8  Allergic and Immunologic Diseases of the Oral Cavity/Oral Pathology Recurrent Minor apthous ulcer The ulcers arise almost exclusively on nonkeratinized mucosa and may be preceded by an erythematous macule in association with prodromal symptoms of burning, itching, or stinging. The ulceration demonstrates a yellow-white, removable fibrinopurulent membrane that is encircled by an erythematous halo. Classically, the ulcerations measure between 3 and 10 mm in diameter and heal without scarring in 7 to 14 days 9  Allergic and Immunologic Diseases of the Oral Cavity/Oral Pathology Recurrent Major apthous ulcer Suttons disease/ Periadenitis mucosa necrotica recurrens Uncommon, 10% of RAU Severe, irregular, deep ulcers Site: free movable mucosa, tongue, palate, lip 1-3 cm in size Painful  Number: single or maximum 3 10 Allergic and Immunologic Diseases of the Oral Cavity/Oral Pathology Recurrent Herpet