Routine Histotechnique And Staining PDF

 Malformation: Defect due to localize error in morphogenesis resulting in an abnormal shape or structure, w...

 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 Developmental Disturbances Of Oral Anomaly: Any deviation from normal. It is same as malformation but there is no interference with function. E.g. peg shaped lateral And Para Oral Structures Anomalad: Malformation and subsequently derived structural changes. E.g. Robin anomalad where hypoplasia of the mandible result in cleft palate and respiratory difficulty. Basic Sciences Wed. Sep. 4. 2024 1 6 Congenital Developmental Anomalies: Acquired Developmental Anomalies: Defects which are present at birth or before birth during Defects develop during intra-uterine life due to some pathological environment condition the intra-uterine life because of either heredity or environmental influences E.g. - Cleft lip & palate Can be Prenatal / neonatal / Postnatal E.g.: 1. Congenital Syphilis - Notched incisors - Mulberry molars Hereditary Developmental Anomalies: 2. Fluorides Defects are genetically transmitted from the parents to the offspring, where definite genetic - Enamel hypoplasia 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 9 Developmental Disturbances of soft tissue Lip pits:Congenital lip pits. Paramedian lip pits: Commissural: common 1-20% As deep as 2 cm ▪ Autosomal D: in some cases ▪ Uni/bilateral blind tracts at angle of lip, up to 4 mm Double lip: usually congenital ▪ Horizontal folds of mucosal tissue Inner aspect of U > L lip 13 14  MACROGLOSSIA Frenal Tag:  It is a condition when patient have an enlarged tongue  True macroglossia and pseudomacroglossia ▪ Autosomal D ▪ U labial frenum  Pseudomacroglossia includes any of the following conditions,which force the tongue to sit in an abnormal position: Habitual posturing of the tongue, Fordyce granules: Enlarged tonsils/adenoids Collection of sebaceous glands  True macroglossia can be congenital or acquired Mostly bilateral on Buccal mucosa CAUSES FOR CONGENITAL MACROGLOSSIA Yellow spots Over development of the musculature Histologically: Down syndrome superficial no hair Beckwith-Wiedemann syndrome Glands (1-5 lobules) that empty into a duct that opens on the mucosal surface. 15 20 Down syndrome (Trisomy 21 syndrome) CLEFT TONGUE/Bifid Tongue Flat face  Complete cleft tongue occurs due to lack of merging of lateral lingual swellings. Large anterior fontanel  Partial cleft tongue occurs due to incomplete merging and failure of groove obliteration by underlying mesenchymal proliferation Open sutures  Partially cleft tongue occurs more common and is manifested as deep groove in Small slanting eyes with epicanthal folds the midline of dorsal surface  Food debris and microorganisms collect in base of cleft and cause irritation Open mouth Cardiac abnormalites Macroglosia High arched palate 21 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 pegs, neutrophilic micro abscesses within the epithelium, and a mixed inflammatory infiltrate in the lamina propria. 27 28  HAIRY TONGUE Histological features: BLACK HAIRY TONGUE, LINGUA NIGRA, LINGUA VILLOSA  characterized by marked accumulation of keratin on filiform papillae of the dorsal Atrophic stratified squamous epithelium surface resulting in a hair like appearance  Occasionally pseudoepitheliomatous hyperplasia, Histologic Features.  Presence of fungal hyphae,  Loss of papillae,elongated rete ridges and lymphocytic infiltration. Consist of elongated filiform papillae, with mild hyperkeratosis and occasional  Median rhomboid glossitis shows a smooth or nodular surface covered by atrophic inflammatory cells. stratified squamous epithelium overlying a moderately fibrosed stroma Debris accumulation among the papillae and candidal pseudohyphae is not unusual  Fungiform and filiform papillae are not seen, although surface nodules may mimic or finding. 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 31 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  Amelogenesis imperfecta 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 Developmental anomalies of Teeth Types And Jaw Part II 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 3. Hypomaturation type- Defective maturation Basic Sciences 4. Hypomaturation-hypoplastic with taurodontism Wed. Sep. 18. 2024 Hypoplastic type : There is defective formation of matrix. Histologic Features : 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 Hypoplastic type Enamel thickness is usually below normal Lack of differentiation of ameloblast cells with little or no matrix formation Quantity is affected, but quality of formed enamel is normal Tooth appears as though prepared for receiving a prosthetic crown Hypocalcification type Abnormal matrix structure & mineral deposition Hypomaturation type Alteration in the enamel rod & rod sheath structures DENTINOGENESIS IMPERFECTA Histologic Features. It is the hereditary developmental disturbance of the dentin in the absence of any systemic Enamel & mantle dentin are normal disorder. Affected teeth are gray to yellowish-brown The dentin, on the other hand, is composed of irregular tubules, with large areas of uncalcified matrix. Also known as “Hereditary opalescent dentin” & “Capdepont’s teeth” Remaining dentin is severely dysplastic & exhibits vast areas of inter-globular dentin Dentinal tubules are short, disoriented, irregular & widely spaced According to Shields it is classified as Dentinogenesis imperfecta I – It occurs with Osteogenesis Imperfecta with opalascent teeth. Scanty odontoblasts line the pulp and they can be seen in the defective dentin Deciduous teeth more severely affected. The DEJ is Smooth 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 MICROGNATHIA Abnormal enamel & dentin Also known as Mandibular hypoplasia It is a condition in which a child has a very small lower jaw. The widening of the pre-dentin layer Bird face appearance The presence of large areas of inter-globular dentin a)True micrognathia b) Pseudo micrognathia 2 types true micrognathia An irregular tubular pattern of dentin. 1) Congenital Characteristically, the reduced enamel epithelium around uneruptcd teeth shows many 2) Acquired irregular calcified bodies. Large pulp chamber with pulp stones Etiology of congenital – unknown But associate with Congenital Heart Disease or Pierre Robin Syndrome Calcification in follicular connective Acquired Post natal in origin Causes Ankylosis of joint as result of trauma/infection CAUSES OF MICROGNATHIA FACIAL HEMIATROPHY Congenital - Pierre Robin syndrome Also known as Parry Romberg Syndrome, Progressive Facial Hemiatrophy, Progressive hemifacial atrophy - Catel Manzke syndrome Parry and Romberg in 1846 - Cerebrocostomandibular syndrome ORAL MANIFESTATIONS Intrauterine acquired conditions – congenital syphillis Dental anomalies: incomplete root formation, delayed eruption and severe facial asymmetry Eruption of teeth on the affected side may be retarded. Chromosomal abnormality - Trisomy 18 - Turners syndrome Atrophy of half of the upper lip and tongue Deviation of jaws while opening the mouth Autosomal dominant conditions - Treacher Collins syndrome - Pallister Hall Syndrome A characteristic loss in the soft tissues of essentially half the face. Coup de sabre’ – Autosomal recessive conditions - Cohen syndrome - Craniomandibular dermatodysostosis FACIAL HEMIHYPERTROPHY Treacher Collins Syndrome(Mandibulo Facial Dysostosis) Also called Friedreich’s Disease Convex facial profile Significant unilateral enlargement of the face Mandibular and midface hypoplasia Represents hyperplasia of tissues rather than hypertrophy Underdeveloped or absence of zygomatic bones Downward inclination of palpebral fissures Syndromes associated: 75% pt: COLOBOMA: notch on outer portion of lower eye lid Neurofibromatosis Occasional facial clefts Beckwith Wiedemann syndrome Palate: high arched with 30% clefts Albright syndrome Retrusive chin Deformed pinna ETIOLOGY Unknown, but due to vascular or lymphatic absence, CNS disturbances, chromosomal absence.