Developmental Anomalies of Oral and Para Oral Structures PDF

no  INTRODUCTION Malformation or defects resulting from disturbance of growth & development are known...

no  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. Developmental Disturbances Of Oral And Para Oral Structures 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. Basic Sciences Wed. Sep. 4. 2024 1 5 Malformation: Defect due to localize error in morphogenesis resulting in an abnormal Congenital Developmental Anomalies: shape or structure, with interference in function. E.g. cleft palate Defects which are present at birth or before birth during the intra-uterine life because of either heredity or environmental Deformation: An alteration in shape or structure of a previously normally formed part. influences E.g. - Cleft lip & palate E.g. torticollis Anomaly: Any deviation from normal. It is same as malformation but there is no Hereditary Developmental Anomalies: interference with function. E.g. peg shaped lateral Defects are genetically transmitted from the parents to the offspring, where definite genetic location is identified E.g. Downs syndrome –Trisomy 21 Anomalad: Malformation and subsequently derived structural changes. E.g. Robin anomalad where hypoplasia of the mandible result in cleft palate and respiratory difficulty. Familial Developmental Anomalies: Defects are transmitted from the parents to the offspring, where definite genetic location is not identified E.g. – Diabetes 6 8 Developmental Disturbances of soft tissue Acquired Developmental Anomalies: Lip pits:Congenital lip pits. Defects develop during intra-uterine life due to some pathological environment condition Commissural: common 1-20% Can be Prenatal / neonatal / Postnatal E.g.: 1. Congenital Syphilis ▪ Autosomal D: in some cases - Notched incisors ▪ Uni/bilateral blind tracts at angle of lip, up to 4 mm - Mulberry molars 2. Fluorides - Enamel hypoplasia r 9 13 Paramedian lip pits: Frenal Tag: As deep as 2 cm ▪ Autosomal D ▪ U labial frenum Fordyce granules: Collection of sebaceous glands Double lip: usually congenital ▪ Horizontal folds of mucosal tissue Mostly bilateral on Buccal mucosa Inner aspect of U > L lip Yellow spots Histologically: superficial no hair Glands (1-5 lobules) that empty into a duct that opens on the mucosal surface. 14 15  MICROGLOSSIA Retrocuspid Papilla  It is a rare congenital anomaly manifested by the presence of Rudimentary or small tongue ▪Slightly raised area, about 2-4 mm, often bilaterally  The condition when tongue being completely absent is known as Aglossia ▪Commonly located lingual to the cuspids  Patient finds difficulties in eating and swallowing ▪Attached gingiva CLASSIFICATION True microglossia Relative microglossia ▪incisive papilla ▪Histologically: ▪A focus of fibrovascular tissue ▪With an orthokeratinized no /parakeratinized surface ▪Covers the osseous foramen of a nutrient blood vessel 17 19 MACROGLOSSIA Down syndrome (Trisomy 21 syndrome)  It is a condition when patient have an enlarged tongue Flat face  True macroglossia and pseudomacroglossia Large anterior fontanel  Pseudomacroglossia includes any of the following conditions,which force the tongue to sit in an abnormal position: Open sutures Habitual posturing of the tongue, Small slanting eyes with epicanthal folds Enlarged tonsils/adenoids Open mouth  True macroglossia can be congenital or acquired Cardiac abnormalites CAUSES FOR CONGENITAL MACROGLOSSIA Over development of the musculature Macroglosia Down syndrome b High arched palate Beckwith-Wiedemann syndrome 20 21 ANKYLOGLOSSIA (tongue-tie) CLEFT TONGUE/Bifid Tongue  It can be defined as a developmental condition characterized by fixation of tongue to  Complete cleft tongue occurs due to lack of merging of lateral lingual swellings. the floor of the mouth, causing restricted movement  Partial cleft tongue occurs due to incomplete merging and failure of groove  It can be either complete ankyloglossia or partial ankyloglossia (tongue tie) obliteration by underlying mesenchymal proliferation  Partially cleft tongue occurs more common and is manifested as deep groove in  Complete ankyloglossia occurs as a result of fusion between the tongue and the the midline of dorsal surface floor of the mouth  Food debris and microorganisms collect in base of cleft and cause irritation  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 26 FISSURED TONGUE/ SCROTAL TONGUE MEDIAN RHOMBOID GLOSSITIS ▪ Deep fissures may be seen in children or adults but ↑ with age Central papillary atrophy of the tongue / posterior lingual papillary atrophy ▪ Down syndrome & Melkersson-Rosenthal Syndrome  It is an asymptomatic elongated erythematous patch of atrophic mucosa on the mid Histologic Features dorsal surface of the tongue. 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 28  BENIGN MIGRATORY GLOSSITIS Histological features: Geographic tongue, erythema migrans, wandering rash of tongue Atrophic stratified squamous epithelium Filiform papillae mm  Occasionally pseudoepitheliomatous hyperplasia, Migrate & periods of remission  Presence of fungal hyphae, Asymptomatic but acidic & spicy food  Loss of papillae,elongated rete ridges and lymphocytic infiltration. Histological features:  Median rhomboid glossitis shows a smooth or nodular surface covered by atrophic Hyperparakeratosis, spongiosis, acanthosis, elongated rete ridges stratified squamous epithelium overlying a moderately fibrosed stroma Red areas-keratin desquamated, neutrophils and lymphocytes in epithelium  Fungiform and filiform papillae are not seen, although surface nodules may mimic or A thickened layer of keratin is infiltrated with neutrophils, perhaps represent anlage of these structures. as are lower portions of the epithelium to a lesser extent  A mild to moderately intense chronic inflammatory cell infiltrate may be seen within subepithelial and deeper fibrovascular tissues. 29 30 HAIRY TONGUE LINGUAL VARICES BLACK HAIRY TONGUE, LINGUA NIGRA, LINGUA VILLOSA  It is a dilated, tortuous vein which is often subjected to increased hydrostatic pressure but is poorly supported by surrounding tissue  characterized by marked accumulation of keratin on filiform papillae of the dorsal  Involved veins appear red or purple shotlike clusters of vessels on the ventral surface resulting in a hair like appearance surface and lateral borders of tongue as well as in the floor of the mouth 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 r 31 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 4 i r in  r I v  r r r Developmental anomalies of Teeth And Jaw Part II Basic Sciences Wed. Sep. 18. 2024 Amelogenesis imperfecta I I Also known as Hereditary enamel dysplasia/Hereditary brown enamel/Hereditary brown Hypoplastic type : opalescent tooth 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 Group of conditions caused by defects in the genes encoding enamel matrix proteins areas Enamel thickness is usually below normal Affects both dentition deciduous and permanent Quantity is affected, but quality of formed enamel is normal Tooth appears as though prepared for receiving a prosthetic crown 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 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)  Environmental enamel hypoplasia Histologic Features : Focal enamel hypoplasia Also known as Turner’s hypoplasia Hypoplastic type Lack of differentiation of ameloblast cells with little or no matrix formation Most common form of enamel hypoplasia Hypocalcification type Occurs due to trauma or infection to deciduous teeth affecting the developing permanent tooth Abnormal matrix structure & mineral G deposition Hypomaturation type Usually affects single tooth & is called as Turners tooth Alteration in the enamel rod & rod sheath structures 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. Dentin Dysplasia (Rootless teeth) Enamel & mantle dentin are normal A hereditary defect characterized by defective dentin formation & abnormal pulpal The dentin, on the other hand, is composed of irregular tubules, with large areas of morphology uncalcified matrix. Remaining dentin is severely dysplastic & exhibits vast areas of inter-globular dentin Type I Radicular dentin dysplasia I Dentinal tubules are short, disoriented, irregular & widely spaced Also known as “Rootless teeth” Scanty odontoblasts line the pulp and they can be seen in the defective dentin Type II (Coronal dentin dysplasia) The DEJ is Smooth Type I is more common. Conditions associated with dentin dysplasia Rheumatoid arthritis Sclerotic bone and skeletal anomalies Histologic Features: REGIONAL ODONTODYSPLASIA Type I (radicular). Also known as GHOST TEETH/ Odontodysplasia/ odontogenic dysplasia/ odontogenesis imperfecta A portion of the coronal dentin is usually normal. n Its a dental abnormality that involves the hard tissues that are derived from both epithelial r Apical to this may be areas of tubular dentin, but most of that which obliterates the pulp (enamel) and mesenchymal (dentin and cementum) components of tooth forming apparatus. is calcified tubular dentin, osteodentin, and fused denticles. The teeth exhibit short roots, open apical foramina, and enlarged pulp chambers. Type II (coronal) Thickness and defective mineralization quality of enamel and dentin layers have given rise to the term Ghost teeth. The deciduous teeth exhibit amorphous and atubular dentin in the radicular portion, while coronal dentin is relatively normal. The permanent teeth are affected more than primary. The permanent teeth also show relatively normal coronal dentin, but the pulp has Maxillary anterior are affected more than other teeth multiple pulp stones or denticles.  Histologic Features Agnathia Abnormal enamel & dentin Also known as Otocephaly, Holoprosencephaly agnathia The widening of the pre-dentin layer Characterized by is absence of a portion or the entirety of one or both jaws. It is a very rare condition. The presence of large areas of inter-globular dentin Etiology: An irregular tubular pattern of dentin. Failure of migration of neural crest mesenchyme i into the maxillary prominence at the Characteristically, the reduced enamel epithelium around uneruptcd teeth shows many fourth to fifth week of gestation irregular calcified bodies. Incidence: less than 10% Large pulp chamber with pulp stones Calcification in follicular connective MICROGNATHIA CAUSES OF MICROGNATHIA Also known as Mandibular hypoplasia Congenital - Pierre Robin syndrome It is a condition in which a child has a very small lower jaw. - Catel Manzke syndrome Bird face appearance - Cerebrocostomandibular syndrome a)True micrognathia b) Pseudo micrognathia 2 types true micrognathia Intrauterine acquired conditions – congenital syphillis 1) Congenital 2) Acquired Chromosomal abnormality - Trisomy 18 - Turners syndrome Etiology of congenital – unknown But associate with Congenital Heart Disease or Pierre Robin Syndrome Autosomal dominant conditions - Treacher Collins syndrome - Pallister Hall Syndrome Acquired Post natal in origin Causes Ankylosis of joint as result of trauma/infection Autosomal recessive conditions - Cohen syndrome - Craniomandibular dermatodysostosis Pierre Robin syndrome MACROGNATHIA Also know as Robin sequence, Pierre Robin Anomalad, Robin complexes, Pierre Robin Increase in both jaws Malformation Cleft palate c Macrognathia can be associated with pituitary gigantism, tumors, and other disorders. Micrognathia and glossoptosis Hypoplasia of mandible ‘Bird facies’ This condition could be secondary to other diseases, as in Paget’s disease (overgrowth of cranium & max/mandible) & in Acromegally (mand). Respiratory difficulty Congenital heart defects Occular lesions Factors favoring mandibular prognathism Mental retardation Long rami Increased mandibular body length/ decreased maxillary length Excess condylar growth Prominent chin button Varying soft tissue contours FACIAL HEMIATROPHY FACIAL HEMIHYPERTROPHY Also known as Parry Romberg Syndrome, Progressive Facial Hemiatrophy, Progressive Also called Friedreich’s Disease hemifacial atrophy Significant unilateral enlargement of the face Parry and Romberg in 1846 Represents hyperplasia of tissues rather than hypertrophy ORAL MANIFESTATIONS Syndromes associated: Dental anomalies: incomplete root formation, delayed eruption and Neurofibromatosis severe facial asymmetry Beckwith Wiedemann syndrome Eruption of teeth on the affected side may be retarded. Albright syndrome Atrophy of half of the upper lip and tongue ETIOLOGY Deviation of jaws while opening the mouth Unknown, but due to vascular or lymphatic absence, CNS disturbances, chromosomal absence. A characteristic loss in the soft tissues of essentially half the face. Coup de sabre’ –  Treacher Collins Syndrome(Mandibulo Facial Dysostosis) ORAL MANIFESTATION Convex facial profile Dentition is abnormal in three respects – Crown size and root may be large Mandibular and midface hypoplasia Underdeveloped or absence of zygomatic bones Involve any tooth but most frequently in cuspid, premolar and first molar Downward inclination of palpebral fissures 75% pt: COLOBOMA: notch on outer portion of lower eye lid Occasional facial clefts Bone of maxilla and mandible also enlarged Palate: high arched with 30% clefts Retrusive chin Tongue: commonly involved, shows bizzare pattern of enlargement of papillae Deformed pinna Buccal mucosa freq appears velvety and may hang in soft pendulous folds on affected side 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 Tile Trapezoid shaped appearance of lips Pulp and Periapical Pathology Basic Sciences Department Wed. Sep. 25. 2024 1 Reversible Pulpitis (Pulp Hyperemia) Acute irreversible pulpitis Etiology Definition — reversible pulpitis is a mild to moderate condition of the pulp caused by stimuli Acute dental caries in which pulp is capable of returning to the uninflamed state following the removal of stimuli. Pulp exposure HISTOLOGICAL FEATURES: Histopathological features Inflammation involves the whole dental pulp Pulp hyperemia (dilation of blood vessels) Edema fluid collection due to damage of vessel wall & allowing extravasations of RBC or diapedesis of WBC Vascular dilatation and edema Chronic inflammatory cellular infiltrate Reparative secondary dentin may be noted Inflammatory (granular cells) infiltration Exudation Inflammatory cell infiltration (neutrophils) Odontoblasts near to the cause are destroyed Reactions usually remain localized adjacent to the cause Formation of a minute pulp abscess 9 In a few days pulp undergoes liquefaction and necrosis 11 Pulp and Periapical pathology / Oral Pathology Pulp and Periapical pathology / Oral Pathology ACUTE PULPITIS CHRONIC PULPITIS A common condition affecting a tooth accompanied by dull, bearable pain. A common condition affecting a tooth accompanied by severe, relentless pain HISTOLOGIC FEATURES: HISTOLOGIC FEATURES: Infiltration of mononuclear cells, lymphocytes & plasma cells, with vigorous connective Edema in pulp with vasodilation. tissue reaction. Infiltration of polymorphonuclear leukocytes along vascular channels & migrate Capillaries are prominent; fibroblastic activity & collagen fibers in bundles. through endothelium lined structures. When granulation tissue formation occurs in wide open exposed pulp surface – ulcerative Destruction of odontoblasts at pulp dentin border. pulpitis. (with bacterial stains & micro-org. in carious lesion) 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 The dental pulp exhibits an area of fibrosis and chronic inflammation peripheral to the zone of abscess formation. 12 14  Pulp and Periapical pathology / Oral Pathology Chronic Hyperplastic Pulpitis (pulp polyp) The polyp surface is covered with stratified squamous epithelium. Overgrowth of pulp tissue outside the boundary of pulp chamber as protruding mass. Epithelium may be derived from gingiva or from freshly desqumated epithelial cell of mucosa or tongue. Histological features The polyp consists of granulation tissues Hyperplastic tissue is basically granulation tissue, consisting delicate CT fibers & young blood capillaries. It contains delicate connective tissue, fibers and blood vessels EInflammatory cell infilterate,plasma cells, lymphocytes. Mononuclear inflammatory cell infiltration Fibroblast and endothelial cell proliferation prominent. Stratified squamous type epithelial lining resembles oral mucosa with well formed rete pegs. 15 16 Pulp and Periapical pathology / Oral Pathology Pulp and Periapical pathology / Oral Pathology Internal Resorption: True Pulp stone: Odontoclastoma, Pink Tooth of Mummery They rare and contains dentin with distint dentinal tubules lined by odontoblasts. It arises as a result of epithelial mesenchymal interaction. Histological Features False Pulp stone: Resorption is of irregular lacunar variety showing occasional osteoclast or odontoclast It contains a concentric layers of mineralized tissue formed by surface accretion around hence the term “Odontoclastoma” blood thrombi, dying or dead cells or collagen fibers. It arise from degenerating cells of the pulp that eventually get mineralized. Pulp tissue exhibits chronic inflammatory reaction 17 19 Pulp and Periapical pathology / Oral Pathology Pulp and Periapical pathology / Oral Pathology Apical Periodontitis: Chronic Apical Periodontitis : A growth of granulomatous tissue continuous with the Periodontal ligament resulting from the It’s a painful inflammation of periodontium as a result of trauma, irritation or infection through death of the pulp. the root canal, regardless whether pulp is vital or not. HISTOLOGIC FEATURES: Histopathology Hyperemia and edema of the PDL ligament with infiltration of chronic inflammatory cells. An inflammatory reaction occurs in Apical PDL-vascular dilation infiltration of PMNs PMNs (Polymorphonuclear neutrophils) Inflammatory and locally increased vascularity of the tissue are associated with resorption Accumulation of serous exudates distends the PDL and extrudes the tooth slightly of the surrounding bone adjacent to this area. PDL shows signs of inflammation to Inflammation is transient, if caused by acute trauma. Granulation tissue mass consists proliferating fibroblasts, endothelial cells & numerous If irritant not removed, progress into surrounding bone resorption. immature blood capillaries with bone resorption. Abscess formation may occur if it is associated with bacterial infection Acute periapical abscess / Alveolar abscess. Capillaries lined with swollen endothelial cells. 21 22 Pulp and Periapical pathology / Oral Pathology Pulp and Periapical pathology / Oral Pathology Periapical Abscess (Dentoalveolar Abcess, Alveolar Abscess, Root end Abscess ) Acute Exacerbation of Chronic Periapical Abscess (Phoenix Abscess) It is an acute or chronic suppurative process of the dental periapical region Definition -Its an acute inflammatory reaction superimposed on an existing chronic lesion Histological Features such as cyst or granuloma Area of suppuration composed of PMN leukocytes, lymphocytes, cellular debris, necrotic materials & bacterial colonies. Histopathology Dilatation of PDL and adjacent marrow spaces of the bone Areas of liquefaction necrosis with disintegration of PMNs and cellular debris Marrow spaces show chronic inflammatory cell infiltrate Tissue around area show suppuration containing serous exudate. 0 This area is surrounded by infiltration of macrophages, lymphocytes and plasma cells Sheet of polymorphonuclear leukocytes intermixed with scattered histiocytes 23 24  Pulp and Periapical pathology / Oral Pathology Pulp and Periapical pathology / Oral Pathology Periapical Granuloma OSTEOMYELITIS: The word “osteomyelitis” originates from the ancient Greek words It is one of the most common of all sequel of pulpitis osteon (bone) and muelinos (marrow) Acute Suppurative osteomyelitis: Serious sequela of periapical infection that often results Histological Features in diffuse spread of infection throughout the medullary spaces, with subsequent necrosis of Granulation tissue mass consists proliferating fibroblasts, endothelial cells & numerous variable amount of bone. immature blood capillaries with bone resorption Histological Features Bone tissue at the periphery is lined by osteoclast cells with areas of bone resorption Necrotic bone- loss of osteocytes from their lacunae, peripheral resorption and bacterial colonization. o Lesion is usually sterile in nature and microrgs not seen unless secondarily infected Medullary space→ filled with inflammatory exudates Capillaries lined with swollen endothelial cells. Osteoblasts bordering the bony trabeculae are destroyed It is relatively homogenous lesion composed of macrophages, lymphocytes & plasma cells. Trabeculae may lose their viability and begin to undergo slow Plasma cells containing Russels body are found extracellularly. resorption 25 28 Pulp and Periapical pathology / Oral Pathology Pulp and Periapical pathology / Oral Pathology CHRONIC FOCAL SCLEROSING OSTEOMYELITIS ( CONDENSING OSTEITIS) CHRONIC DIFFUSE SCLEROSING OSTEOMYELITIS : is the clinical entity characterized Unusual reaction of bone to infection by a nonsuppurative, inflammatory process associated with recurrent swelling, trismus and pain HISTOLOGIC FEATURES HISTOLOGIC FEATURES Dense bony trabeculae with little interstitial marrow tissue Dense, irregular trabeculae of bone bordered by active layer of Osteoblasts; focal Osteoclastic area may be present. Many reversal and resting lines giving pagetoid appearance Mosaic pattern appearance If interstitial soft tissue is present, it is generally fibrotic and infiltrated with small amount of lymphocytes Trabecular bone with the presence of reparative and reactive new bone formation. There was a marked Osteocystic Lacunae appears empty abundant osteoid and osteoblastic rim. Interstitial soft tissue is fibrotic Proliferating fibroblasts and occasional small capillaries as well as small focal collection of 31 lymphocytes and plasma cells 32 Pulp and Periapical pathology / Oral Pathology Pulp and Periapical pathology / Oral Pathology CHRONIC OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS: (Garre’s chronic nonsuppurative sclerosing osteitis ,periostitis ossificans) CELLULITIS/ PHLEGMON Cellulitis is a diffuse inflammation of soft tissues which is not circumscribed or confined HISTOLOGIC FEATURES to one area, but which, in contrary to the abscess, tends to spread through tissue spaces and Subperiosteal mass is composed of much reactive new bone and osteoid tissue, with along fascial spaces. Osteoblasts bordering many of trabeculae HISTOLOGICAL FEATURE Trabeculae is perpendicular to cortex and parallel to each other A microscopic section through an area of cellulitis shows a diffuse exudation of polymorphoneuclear leukocyte and lymphocyte. Connective tissue is fibrous and shows sprinkling of lymphocytes and plasma cells Considerable serous fluid and fibrins causing separation of connective tissue and muscle fibres. 33 35 Bacterial Infection / Oral Pathology SCARLET FEVER (Scarlatina) Caused by beta hemolytic streptococci. Oral Manifestation: Reffered as Stomatitis Scarlatina Tile Small, red macules may appear in the hard and soft palate and uvula which are called BACTERIAL INFECTIONS Forchheimer spots. Basic sciences Department Wed. Oct. 02. 2024 1 7  Bacterial Infection / Oral Pathology Bacterial Infection / Oral Pathology In early course of the disease, tongue exhibits a white coating and the fungiform Histological features: pappila are edematous and hyperemic. This phenomenon has been described clinically as ‘strawberry tongue’. Neutrophilic infiltrate with spongiosis C Parakeratosis in the epidermis. Necrotic conective tissue. Later, the tongue coating is lost and appears red and glistening and smooth except the pappliae this is called as ‘raspberry tongue’. 8 9 Bacterial Infection / Oral Pathology Bacterial Infection / Oral Pathology TUBERCULOSIS DIPTHERIA Caused by gram +ve bacillus, Corynebacterium diptheriae. Causative Micro organism:- Mycobacterium Tuberculosis Also called Klebs Loeffler bacillus Ulcer is commonly tongue followed by palate, lips, gingiva, buccalmuccosa Oral Manifestations Formation of ‘Diptheric Membrane’. Histological features: In oral cavity, appears as nonspecific ulcers. 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. Histopathology: Marked proliferation of fibroblasts and dense collagen fibers are laid down all around the tubercle. 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. 10 11 Bacterial Infection / Oral Pathology Bacterial Infection / Oral Pathology ACTINOMYCOSIS SYPHILIS (Lues) Also known as LUMPY JAW. 3 Caused by Treponema palladium It shows typical ‘sulfur granules’. Acquired Syphilis HISTOLOGICAL FEATURE Typical lesion is granulomatous with central abscess formation showing colonies of microorganisms within it. Primary Syphilis:- lesion known as CHANCRE. Lip, tongue, palate, gingiva and tonsil. Colonies appear to be floating in the sea of PMNS. Peculiar appearance of colonies, with peripheral radiating filaments, termed as RAY FUNGUS. APPEARANCE:- It is an elevated, ulcerated nodule showing local induration and producing regional lymphadenitis. Lesion on lip may have brownish crustered appearance. 12 13 Bacterial Infection / Oral Pathology Bacterial Infection / Oral Pathology SECONDARY OR METASTATIC STAGE Oral Manifestation: Short maxilla Commences 6 weeks after primary lesion. o High palatal arch n o Saddle Nose APPEARANCE:- u oHuthinson’s triad: hypoplasia of incisors, molar teeth,8th nerve deafness and intestinal keratitis. Oral Lesions called ’mucous patches’ are usually multiple, painless, grayish white plaques overlying an ulcerated surface. TERTIARY SYPHILIS Snail track ulcer Classical lesion of tertiary syphillis is ‘GUMMA’. Intraorlly: tongue and palate. SITES AFFECTED:- Tongue, gingiva , buccal mucosa 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 14 15 Bacterial Infection / Oral Pathology Bacterial Infection / Oral Pathology Secondary syphilis shows a psoriasiform hyperplasia with superficial neutrophils 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. Tertiary syphilis shows necrotising granulomatous inflammation. Histological features: Extensive necrosis and destruction of soft tissues and bones. 16 17 Bacterial Infection / Oral Pathology Bacterial Infection / Oral Pathology ACUTE NECROTISING ULCERATIVE GINGIVITIS (Trench Mouth, Vincent’s Infection) Leprosy (Hansen’s disease) Chronic granulomatous infection caused by Mycobacterium leprae. Teeth seem to be slightly extruded, sensitive to pressure, or to have a “woody sensation”, slightly mobile with Leprosy manifests in two polar forms, namely, tuberculoid type and lepromatous type. difficulty in eating. Typical lesion is, Punched out, necrotic, crater like ulceration seen over the interdental papillae Oral Manifestations: Ulceration may develop on the cheeks, lips and the tongue, palate & pharyngeal area. Oral lesions consist of small tumor like masses called lepromas, which develop on the tongue, lips, or hard palate. Histological features: These nodules show a tendency to break down and ulcerate. Most superficial is a bacterial area of fibrous mesh composed of epithelial cells, leukocytes, and a variety of Gingival hyperplasia with loosening of the teeth bacterial cells, including rods, fusiform bacteria, and spirochetes. Histologic Features: Deep to that layer exists a neutrophil-rich zone composed of a higher number of leukocytes, spirochetes, and bacterial cells. Typical granulomatous nodule shows collections of epithelioid histiocytes and lymphocytes in a fibrous stroma. Next lies a necrotic zone containing disintegrated cells, spirochetes, and fusiform bacteria. Langhans type giant cells are variably present. The deepest layer contains spirochete infiltration. Sheets of lymphocytes with vacuolated macrophages called lepra cells are scattered throughout the lesions. 18 19 Bacterial Infection / Oral Pathology Bacterial Infection / Oral Pathology BOTRYOMYCOSIS (Bacterial actinophytosis, actinobacillosis) GRANULOMA INGUINALE (Granuloma venereum, donovanosis) Disease is a progressive, chronic, infectious, granulomatous disease Chronic granulomatous infection Oral Manifestations: Oral Manifestations: Papules or nodules, which ulcerate to form clean, granular lesions with rolled margins and which show a tendency for peripheral enlargement. Human botryomycosis is usually a localized granulomatous infection of the skin or mucosa. Histologic Features. Histologic Features. Various forms of granuloma inguinale is one of granulation tissue with infiltration of polymorphonuclear Chronic granulomatous nodules are characterized by the presence of suppurative foci which contain grains or leukocytes and plasma cells. granules Pathognomonic of the disease is the presence of large mononuclear phagocytes, each containing intra cytoplasmic The eosinophilic,peripheral clubs formation typical of actinomycetes is usually not identifiable in this disease. 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. 20 21 Bacterial Infection / Oral Pathology Bacterial Infection / Oral Pathology PYOSTOMATITIS VEGETANS CELLULITIS Uncommon inflammatory disease of the oral cavity It is a diffuse inflammation of soft tissues which is not circumscribed or confined Oral Manifestations: Oral lesions consist of large numbers of broad based papillary projections, tiny abscesses or vegetations It is also known as Phlegmon. developing in areas of intense erythema. Small projections are red or pink in color. HISTOLOGIC FEATURES:- Collection of fibrin & serum fluid in the tissue; thus causing separation of CT and muscle Histologic Features: fibres. Papillary projections generally show hyperplastic stratified squamous epithelium with an underlying loose Acute inflammatory cell infiltration / diffuse exudation by PMN leukocytes & lymphocytes. 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 23  Fungal And Viral infections/ Oral Pathology Pseudomembranous candidiasis The best recognized form of candidal infection is pseudomembranous candidiasis. Also known as thrush. Tile Pseudomembranous candidiasis is characterized by the presence of adherent white plaques that resemble cottage cheese or curdled milk on the oral mucosa. Fungal And Viral infections Scraping them with a tongue blade or rubbing them with a dry gauze sponge can remove these plaques. Basic Sciences Department Wed. Oct. 09. 2024 1 8 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology It may be initiated by exposure of the patient to broad-spectrum antibiotics or by impairment Histological features- of the patient’s immune system. 1) PAS positive candidal hyphae invading Site: buccal mucosa, mucobuccal folds, dorsal tongue 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. 9 10 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Erythematous Candidiasis Central papillary atrophy (median rhomboid glossitis) Other forms of erythematous candidiasis are usually asymptomatic and chronic. This category is Site -tongue, gingiva,palate the condition known as central papillary atrophy of the tongue, or median rhomboid glossitis. Tongue shows depapillation & dekeratinization n Clinically, central papillary atrophy appears as a well-demarcated erythematous zone that affects the midline, posterior dorsal tongue and often is asymptomatic. 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 12 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Some patients with central papillary atrophy may also exhibit signs of oral mucosal candidal Angular cheilitis infection at other sites. This presentation of erythematous candidiasis has been termed chronic It is characterized by erythema, fissuring, and scaling Saliva tends to pool in these areas, keeping multifocal candidiasis. them moist and thus, favoring a yeast infection. The palatal lesion appears as an erythematous area that, when the tongue is at rest, contacts the The candidal infection more extensively involves the perioral skin, usually secondary to actions dorsal tongue lesion, resulting in what is called a “kissing lesion” because of the intimate that keep the skin moist (e.g chronic lip licking, thumb sucking), creating a clinical pattern proximity of the involved areas. known as cheilocandidiasis (exfoliative lesions of the vermilion zone and perioral skin are due to superficial candidal infection) Angular cheilitis. Cheilocandidiasis. 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 14  Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Denture stomatitis Chronic inflammatory changes of the denture bearing mucosa 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 Newton's classification prosthesis. Type I – Pinpoint erythema Type II- Diffuse areas of erythema and edema of palatal mucosa The palatal mucosa and tissue-contacting surface of the denture are swabbed and separately Type III- Nodular hyperplastic areas of mucosa interspersed with normal streaked onto a Sabouraud’s agar slant. 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 Sabouraud’s agar slanthas been streaked with swabs 15 16 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Hyperplastic Candidiasis (Candidal leukoplakia) Site -buccal mucosa , palate 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. 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 17 3)Lesions may have an increased frequency of epithelial dysplasia 18 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Histoplasmosis Histological features- Histoplasmosis showing a diffuse infiltrate macrophages more commonly, collections of Granulomatous fungal disease caused by Histoplasma capsulatum. macrophages organized into granulomas with cytoplasmic microorganisms Histoplasmosis, the most common systemic fungal infection. Site -gingiva, tongue and palate I r Multinucleated giant cells are usually seen in association with the granulomatous inflammation. 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 This medium-power photomicrograph shows scattered epithelioid macrophages admixed with be indistinguishable clinically from a malignancy. 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.) 19 20 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Blastomycosis Histological features- Caused by dimorphic fungus known as Blastomyces dermatidis Large yeasts of Blastomyces dermatitidis (arrow) and pronounced host inflammatory response Blastomycosis is a relatively uncommon disease. to the organism. These lesions may have an irregular, erythematous or white intact surface, or they may appear as Lesional tissue typically shows a mixture of acute inflammation and granulomatous ulcerations with irregular rolled borders and varying degrees of pain. inflammation surrounding variable numbers of yeasts. Clinically, because the lesions resemble squamous cell carcinoma, biopsy and histopathologic They are characterized by a doubly refractile cell wall and a broad examination are required. 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. 21 22  Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology CRYPTOCOCCOSIS Histological features- Relatively uncommon fungal disease caused by the yeast Cryptococcus neoformans. Lesion generally show a granulomatous inflammatory response to the organism. Oral lesions are relatively rare, they have been described either as craterlike, nonhealing ulcers The yeast appears as a round-to-ovoid structure, by a clear halo that represents the capsule. that are tender on palpation or as friable papillary erythematous plaques. Staining with the PAS or Grocott- Gomori methenamine silver method readily identifies the fungus; moreover, a mucicarmine stain uniquely demonstrates its mucopolysaccharide capsule. 23 24 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology ZYGOMYCOSIS (MUCORMYCOSIS; PHYCOMYCOSIS) Histological features- It involve any one of several areas of the body, but the rhinocerebral form is most relevant to the oral health care provider. Lesional tissue shows extensive necrosis with numerous large (6 to 30 um in diameter), branching, nonseptate hyphae at the periphery. Patients may experience nasal obstruction, bloody nasal discharge, facial pain or headache, facial swelling or cellulitis, and visual disturbances with concurrent proptosis. The hyphae tend to branch at 90-degree angles. Symptoms related to cranial nerve involvement (e.g., facial paralysis) are often present. The extensive tissue destruction and necrosis associated with this disease are undoubtedly attributable to the preference of If the condition remains untreated, palatal ulceration may evolve, with the surface of the ulcer the fungi for invasion of small blood vessels. typically appearing black and necrotic. This disrupts normal blood flow to the tissue, resulting in infarction and necrosis. r A neutrophilic infiltrate usually predominates in the viable tissue. 25 26 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology ASPERGILLOSIS TOXOPLASMOSIS Relatively common disease caused by the obligate intracellular protozoal organism Toxoplasma Fungal disease that is characterized by noninvasive and invasive forms. gondii. Histological features- Histological features- Histopathologic examination of a lymph node obtained from a patient with active toxoplasmosis Tissue sections of invasive Aspergillus lesions show varying numbers shows characteristic reactive germinal centers exhibiting an accumulation of eosinophilic of branching, septate hyphae, 3 to 4 μm in diameter. macrophages. The macrophages encroach on the germinal centers and accumulate within the subcapsular and These hyphae show a tendency to branch at an acute angle and to invade adjacent small blood sinusoidal regions of the node. vessels. 27 28 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Herpes Simplex Infection Primary Herpetic Stomatitis Herpes simplex virus (HSV) includes HSV 1 and HSV 2. More severe primary infection can become latent when HSV remains dormant in neural Herpetic stomatitis is a common oral disease transmitted by droplet spread or contact with the ganglia. lesions. It affects children and young adults. Recurrent event has a shorter duration and milder clinical findings than the primary infection The most common site of recurrence for HSV-1 is the vermilion border and adjacent skin of the HSV-1 lips. This is known as herpes labialis (“cold sore” or “fever blister”). Gingivostomatitis is primary HSV Infection occurs most often in young children but may be seen in older children and adults. Multiple small, erythematous papules develop and form clusters of fluid filled vesicles Onset usually consists of fever, malaise, drooling, and oral and perioral lesions 33 34  Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Histologic Features. Chronic herpetic infection Herpetic vesicle is an intraepithelial blister filled with fluid. Numerous mucosal erosions, each of which is surrounded by a slightly raised,yellow-white border, in a patient with acute myelogenous leukemia. The virus exerts its main effects on the epithelial cells. Herpes simplex. Altered epithelial cells exhibiting ballooning degeneration, margination of Infected epithelial cells exhibit acantholysis, nuclear clearing, and nuclear enlargement, which chromatin, and multinucleation. 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 36 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology Varicella The vermilion border of the lips and the palate are the most common sites of involvement, These may cause localized or systemic manifestations that varies from erythematous lesions followed by the buccal mucosa. vesiculation, ulceration, scarring or severe constitutional symptoms. Occasionally, gingival lesions resemble those noted in primary HSV infections. The varicella-zoster virus (VZV, HHV-3) is ensues, herpes simplex virus (HSV) in many respects. The lesions begin as 3- to 4-mm, white, opaque vesicles that rupture to form 1- to 3-mm ulcerations Chickenpox represents the primary infection with the VZ; latency ensues and recurrence is possible as herpes zoster, often after many decades. 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. 37 38 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology HERPES ZOSTER (SHINGLES) The lesions often extend to the midline and frequently are present in conjunction with After the initial infection with VZV (chickenpox), the virus is transported up the sensory nerves involvement of the skin overlying the affected quadrant. and presumably establishes latency in the dorsal spinal ganglia. Facial paralysis has been seen in association with herpes zoster of the face or external auditory Clinically evident herpes zoster occurs after reactivation of the virus, with the involvement of canal. the distribution of the affected sensory nerve. Ramsay Hunt syndrome is the combination of cutaneous lesions of the external auditory canal Oral lesions occur with trigeminal nerve involvement and may be present on the movable or and involvement of the ipsilateral facial and auditory nerves. bound mucosa. r 39 40 Fungal And Viral infections/ Oral Pathology Fungal And Viral infections/ Oral Pathology INFECTIOUS MONONUCLEOSIS (MONO; GLANDULAR FEVER; “KISSING Ramsay-Hunts syndrome