This action might not be possible to undo. Are you sure you want to continue?
Dr. Kush Pathak
Introduction Definition Classification Development of oral mucosa Functions Clinical features Components of oral mucosa Oral epithelium/ Epidermis Epithelial proliferation Epithelial maturation Non keratinocytes Ultra Structure of Epithelial cell Lamina Propria/ Dermis
Submucosa Arterial blood supply of oral mucosa Nerve supply of oral mucosa Tongue Junctions in oral mucosa Gingiva Fibers of gingiva Age changes in oral mucous membrane Clinical considerations Conclusion
The skin, oral mucosa and intestinal lining, all consist of two separate tissue components, which are, the covering epithelium and an underlying connective tissue. As these tissues, together perform a common function, the oral mucosa must be considered as an organ. Understanding the complex structure of a tissue or organ often is easier, when it’s function is known. The structure of oral mucosa reflects a variety of functional adaptations. Any change in these functional adaptations, leads to pathology.
term moist membrane is used to describe moist lining of GIT, nasal passages and other body cavities that communicate with exterior. In the oral cavity this lining is called oral mucous membrane.”
( A ) Based on functional criteria : (1) Masticatory mucosa : Gingiva and hard palate
palate, floor of mouth.
(2) Lining / reflecting mucosa : lip, cheek, soft
(3) Specialized mucosa : Dorsum of tongue
( B ) Based on structure of surface layers :
( 1 ) Keratinized mucosa : Hard palate and gingiva
vestibule, floor of mouth etc.
Development of oral mucosa
At about 26 days of gestation - Primitive oral cavity develops by fusion of embryonic stomatodeum with foregut, after rupture of buccopharyngeal membrane and thus gets lined by epithelium derived from ectoderm and endoderm. Tongue, epiglottis and pharynx are covered by epithelium derived from endoderm, whereas epithelium covering the palate, cheeks, and gingiva is derived from ectodermal origin. By 5 to 6 weeks of gestation – single layer of cells lining the primitive oral cavity, has formed 2 cell layers.
Initially ectomesenchyme consists of widely spaced stellate cells in an amorphous matrix, but by 6 to 8 weeks, extra cellular reticular fibers begin to accumulate.
about 7weeks- Circumvallate, fungiform papillae develop on epithelia.
foliate and the lingual
By 8 weeks – Thickening occurs in the region of vestibular dental lamina complex. At about 8 to 11 weeks.- palatal shelves devate and close. By 8 to 12 weeks, capillary buds and collagen fibers can be detected.
By 10 to 12 weeks - future lining of masticatory mucosa show some stratification of epithelium. By 10 to 14 weeks -Cellular degeneration occurs in central region of the thickening of vestibular dental lamina complex. Between 13 to 20 weeks - all oral epithelium thicken and with the appearance of keratohyalin granules, so a distinction between prickle and granular layer can be made. Between 17 to 20 weeks – elastic fibers become prominent only in connective tissue of lining mucosa.
Protection : Separates and protects deeper tissues and organs from mechanical stresses/ forces, and external environment. Sensation : Temperature, touch and pain sensation. Tongue has taste buds. Reflexes like swallowing, gagging, salivating, also are initiated by receptors in oral mucosa. Secretion : Saliva is secreted by salivary glands and contributes to the maintenance of a moist surface. Thermal regulation : In some animals (dog), considerable body heat is dissipated through oral mucosa by panting. For these animals, oral mucosa plays a major role in regulating of body temperature. This function is not active in humans.
Absorption : Certain substances like nitrates are absorbed from sublingual region. Excretion : Excretes metabolites. Aesthetics : Gingiva facial esthetics. and lip mucosa enhance
Clinical features of oral mucosa:
Deeply colored, most obviously at the lips. Contains only minor salivary glands in comparison to skin that contains hair follicles, sebaceous glands and sweat glands. Surface of oral mucosa tends to be smoother and have fewer folds or wrinkles than skin. Healthy gingiva shows fine surface stippling (small indentations on mucosa surface). Slight whitish ridge present on the buccal surface is called linea alba (white line). It is a keratinized region and may represent the effect of abrasion from rough tooth restorations or cheek biting.
Components of oral mucosa
Oral mucosa consists of 2 separate tissue components : (1) Epidermis Stratified squamous epithelium, called oral epithelium. (2) Dermis – Underlying connective tissue , called lamina propria. Upward projections of connective tissue into epithelium, are called connective tissue papilla. Epithelium is formed into ridges that protrude towards lamina propria. These ridges are called epithelial ridges. At their junction there are 2 different structures with very similar names : (1)Basal lamina (2)Basement membrane
(1) Basal lamina : It is evident at the electron microscopic level and is epithelial in origin. It has two parts : lamina lucida and lamina densa. (2) Basement membrane : It is evident at light microscopic level and is found at the interface of epithelial and connective tissue within the connective tissue. - It is 1 to 4 µm wide. - It is cell free. -Stains positively with PAS, indicating that it contains neutral mucopolysaccarides. -In skin it is shown to contain Fibronectin, laminin (glycoproteins), heparin sulfate, proteoglycans, type 4 collagen and some antigens.
Oral epithelium/ Epidermis
It is a Stratified Squamous epithelium consisting of cells tightly attached to each other and arranged in a number of distinct layers or strata. It maintains it’s structural integrity by a process of continuous cell renewal in which, cells produced by mitotic division in the deepest layers, migrate to the surface to replace those that are shed. The cells of the epithelium thus can be considered to consist of two functional populations : (1) Progenitor population : Its function is to divide and provide new cells. (2) Maturing population : The cells which continually undergo a process of maturation to form a protective surface layer.
Progenitor cells are situated in basal layer in thin epithelia (e.g. Floor of mouth) and in lower two or three cell layer in thick epithelia. Dividing cells are present in clusters at the bottom of epithelial ridges. A small population of progenitor cells represent stem cells. Function of these stem cells is to produce basal cells and retain proliferative potential of the tissues. Large portion of the progenitor compartment is composed of amplifying cells. Their function is to increase the no. of cells available for subsequent maturation.
There are two main patterns of maturation : (1) Keratinization (2)Non-Keratinization (1) Keratinization : Keratinized epithelium has following layers : (a) Stratum basale (b) Stratum spinosum (c) Stratum Granulosum (d) Stratum corneum.
Layers of oral mucosa
They are present above the basement membrane. They have cuboidal or columnar cells. Cells of the basal layer shows most mitotic activity. This layer is also called Germinative layer. They are attached to the basement membrane by hemidesmosomal junction.
Present just above the basal layer. Arranged in several rows. Cells are larger elliptical or spherical in shape and are known as Prickle cell layer. Cells are fused together due to the presence of intercellular bridges or desmosomes. In the upper part of this layer, membrane coating granules/ lamellate granules/odland bodies are present. These granules are small, membrane bound structures. They are 250nm in size. They contain glycolipids originating from golgi complex.
Cells of stratum spinosum
Present just above the spinous layer. Cells are large and flattened containing small granules. These granules are Keratohyaline granules and layer is called granular layer. Cells in the superficial part of this layer develop a noticeable thickening on the inner(intracellular) aspect of their membrane, that contributes to the considerable resistance of keratinized layer against chemical solvent. This thickening is due to protein known as involucrin. Membrane coating granules are present and they appear to fuse with superficial cell membrane to discharge their content in the intercellular space. This discharge is associated with formation of lipid rich permeability barrier, that limits the movement of aqueous substance through intercellular spaces.
Stratum granulosum Cells
Consists of squames or flat cells. They do not contain any nuclei. They stain bright pink with eosin as they are eosinophilic. Pattern of maturation of these cells often is termed as ORTHOKERATINISATION. In Parakeratinised epithelium, surface layer stains for keratin, but shrunken (pyknotic) nuclei are retained in many squames/ flat cells.
Ortho kratin izd Strati fied Squa mous epith elium
Parak eratin ized epith elium of gingi va
As the cells of the granular layer reach the junction with the keratin layer, sudden changes in appearance occur, with loss of nuclei, organelles and Keratohyaline granules. Cells get dehydrated and take up hexagonal shape called Squames. Keratinized layer in oral cavity is composed of nearly 20 layers of squames. . Incomplete Keratinization / Parakeratinisation : Outer most squames of keratinized or Parakeratinised layer do not look like rest of the keratin but show a staining similar to that of deeper nuclear cells. This is called Incomplete Keratinization.
(2) Non - Keratinization : Layers of non keratinized epithelium are :
(a) Stratum basale (b) Stratum intermedium (c) Stratum superficial flexible)
This layer is similar to that of keratinized epithelium. Only difference is that the cells of this layer in non keratinized epithelium are slightly larger than that of keratinized epithelium. Intercellular bridges are less conspicuous.
Glycogen is present Rarely keratohyaline granules are also visible at this level, but they are not associated with tonofilaments. Membrane coating granules are present and they appear to be circular in shape with an amorphous core. Granules discharge their content in the intercellular spaces. But the contents have different lipid composition and do not form as effective barrier for aqueous substances as keratinized epithelium. FILLAGRIN is absent. LORICRIN is present and may contribute to internal thickening of cell membrane.
Cells appear slightly more flattened than other layers. They contain dispersed tonofilaments and nuclei and dehydrated cells. This surface is flexible and tolerant to compression and distension.
Cells that contain clear halo around the nuclei are caller clear cells .These cells are glycogen abundant and so they don’t get stained by Hematoxylin and eosin. Thus resulting in a clear cytoplasm. They are collectively known as Non keratinocytes. They are : (a)Melanocytes (b)Merkel cells (c)Langerhan’s cells (d)Inflammatory cells (lymphocytes)
1. v v v v
Melanocytes : Present in basal layers. These cells contain dendrites. No desmosomes and filaments. Premelanosomes and melanosomes are present. Functions : v Synthesizes melanin pigment granules (melanosomes) and transfer to surrounding keratinocytes. Thus, it causes endogenous pigmentation of oral mucosa.
2. Langerhan ’ s cells : v Present predominantly in suprabasal layer v Small rod or flask shaped granules called Birbeck granules present. v Dendrites present. v No desmosomes and tonofilaments. Functions : v Antigen trapping and processing.
3 . Merkel cells : v Present in basal layer. v No dendrites present. v Desmosomes and tonofilaments present. v Characteristic electron dense vesicles and associated nerve axon present. Function : v It is a tactile sensory cell.
4. Lymphocytes ( Inflammatory cell ) : v Present variably. v Contains large circular nucleus. v Cytoplasm is scanty with few organelles. v No desmosomes and tonofilaments present. Function : v Associated with inflammatory response in oral mucosa. v
Ultra structure of Epithelial cell
Along with all cell organelles (nuclei, endoplasmic reticulum, ribosomes, mitochondria, golgi complex) , cells also contain certain structures : Tonofilaments Desmosomes Hemidesmosomes Keratohyalin granules Keratin
v v v v v
are fibrous proteins and are seen as long filaments.
Synthesized by ribosomes. Diameter is approximately 8nm. They belong to a class of intracellular elements called intermediate filaments. They are intimately associated with keratohyalin granules.
Also called macula adherens. Circular or oval areas of adjacent cell membranes, adhering by specialized intracellular thickenings known as attachment plaques. It consists of 2 proteins :- Desmoplakin and Plakoglobin . Bundles of tonofilaments get inserted into these attachment plaques. Proteins naming Cadherins (Desmoglein and Desmocollin ), penetrate the membrane and enter the intercellular region of desmosome.
Adhesion between epithelium and connective tissue is provided by hemidesmosomes. Hemidesmosomes are present on the basement membrane of the epithelium. Tonofilaments get inserted in hemidesmosomes also.
Keratins are classified according to their size (i.e. molecular weight) and charge. Different types of keratin are present in different cells and even in different layers of a single stratified epithelium. When they become aggregated, they form bundles of filaments called tonofibrils. Keratins represent 30 different proteins of differing molecular weights. Those with lowest molecular weight (40 kDa) are found in glandular and simple epithelia.
Those with intermediate molecular weight are found in stratified epithelium. Those with highest molecular weight (67 kDa) are found in keratinized stratified squamous epithelium. All stratified oral epithelium possess keratin 5 and 14. All keratinized stratified oral epithelium contain keratins 1,6,10 and 16. All non keratinized epithelium contain keratins 4, 13 and 19.
Keratohyalin granules appear as basophilic granules under light microscopy and as electron dense structures in electron microscopy. Granules are irregular in shape. Their size is 0.5 to 1nm. They are synthesized by ribosomes. They are associated intimately with Tonofibrils and are thought to facilitate aggregation and formation of cross links between the cytokeratin filament of keratinized layer. For this reason, protein making up bulk of these granules are called FILAGGRIN. Sulfur rich component called LORICRIN also occurs.
Two other type of connections are seen between cells:
v Gap junction or ‘ nexus ’ – Region where membranes of adjacent cells run closely together, separated by only a small gap. Such junctions may allow electrical or chemical communication between cells and are sometimes called ‘Communicating Junctions ’.
v Tight Junction – Ø Also called ‘ Occluding junctions ’. Ø Here adjacent cell membranes are so tightly joined to each other, that there is no intercellular space left. Ø It is very rarely found.
Connective tissue supporting the oral epithelium is termed as Lamina propria. It is divided into 2 layers : v Superficial papillary layer (associated with epithelial ridges) : Here, collagen fibers are thin and loosely arranged. v Deeper reticular layer (lies between papillary layer and underlying structures) : This layer has collagen fibers arranged in thick bundles that tend to lie parallel to the surface plane.
Lamina propria consists of cells, blood vessels, neural elements and fibers embedded
Cells of Connective tissue : 1 . FIBROBLASTS v They are stellate or elongated cells with abundant endoplasmic reticulum. v They secrete fibers and ground substance. v They are disturbed throughout the lamina propria.
v v v
2. v v v v v
HISTIOCYTES – Spindle or stellate shaped cells. They contain dark staining nuclei. Contain abundant Lysosomal vesicles. They are precursors of functional macrophages. They are present throughout the lamina propria.
3. v v v v
MACROPHAGES – They are round with pale staining nucleus. Contain lysosomes and phagocytic vesicles. Helps in phagocytosis. Present in areas of chronic inflammation. MAST CELLS – They are round cells with basophilic granules. They stain metachromatically. Secretes inflammatory mediators. Present throughout the lamina propria.
4. v v v v
5. v v v
PMN CELLS – They are round with lobed nucleus. Helps in phagocytosis. Present in areas of acute inflammation. LYMPHOCYTES – They are round with dark staining nucleus and scanty cytoplasm. They help in humoral and cell mediated immunity. Found in areas of chronic inflammation.
6. v v v
7. v v v v
PLASMA CELL – They have cart wheel pattern with basophilic nucleus. They contain abundant rough endoplasmic reticulum. Helps in synthesis of immunoglobulins. Seen in areas of chronic inflammation.
ENDOTHELIAL CELLS – Present in lining of the blood Vessel.
High concentration of blood vessels and nerves are present. It is a site of the minor salivary glands. In the intestine the submucosa is called the muscularis mucosae There is no such thing in oral mucosa. In cheeks, lips and part of the hard palate – submucosa layer is made of loose areolar or adipose tissue In regions such as gingiva and part of the hard palate, the submucosais not present and the oral mucosa attaches directly to the periosteum of underlying bone. This is called
Arterial blood supply of oral mucosa
Hard palate Ø Major palatine artery. Ø Nasopalatine artery. Ø Sphenopalatine artery.
Soft palate : Ø Minor palatine artery
Floor of mouth : Ø Sublingual artery Ø Branch of lingual artery
Tongue : Ø Deep lingual artery . Ø Dorsal lingual artery.
Nerve supply of oral mucosa
Hard palate: Ø Greater palatine Ø Lesser palatine Ø Sphenopalatine branches of maxillary nerve.
Soft palate : Ø Lesser palatine branch of maxillary nerve Ø Nerve of pterygoid canal Ø Tongue : Ø Lingual branch of mandibular nerve Ø Glossopharyngeal nerve. Ø
Mucosa of dorsal surface of the tongue, although covered by what is functionally a masticatory mucosa, has different types of lingual papillae. Some of these papillae possess mechanical functions, whereas some bare taste buds, therefore having sensory function. Following papillae's are present on the tongue : Fungiform papillae Filiform papillae Foliate papillae Circumvallate papillae
v v v v
Fungiform papillae : v Present on the anterior portion of the tongue along with Filiform papillae. v v Single Fungiform papillae is surrounded by numerous filiform papillaes at the tip of the tongue. v v They are smooth and round structures. v v They appear red, because of their highly vascular connective tissue core. v v Present on the superior surface. v
A : Fungiform papilla B : Filiform papillae D : Heavy Keratinization
Filiform papillae : v Cover entire anterior part v v Consist of cone shaped structures, each covered by a thick keratinized epithelium. v v Together form a tough, abrasive surface that is involved in compressing and breaking the food. v v Dorsal mucosa functions as masticatory mucosa. v
Tiny Proje ction s
Filif orm Papi llae
Histo logic al appe aranc e
Foliate papillae : v leaf like. v v Sometimes present on lateral margins of posterior part of tongue. v v Pink papillae with 4 to 11 parallel ridges with deep grooves in mucosa. v v Few taste buds are present in the epithelium of lateral walls of ridges. v v Seen in mammals, not in human beings.
Histo logic al appe aranc e
Foli ate Papi llae
Elev ation s :foliat e papill ae
Circumvallate papillae : v Present adjacent and anterior to the sulcus terminalis. v v They are 8 to 12 in number. v v Large structures, each surrounded by a deep, circular groove into which ducts of minor salivary glands (glands of von ebner)open. v v Superiorly, connective tissue core of these papillae is covered with keratinized epithelium, whereas on lateral walls, it is covered with non keratinized epithelium. v v Taste buds are present on the lateral walls.
It is composed of two types of cells, supporting (sustentacular) cells.
The neuroepithelial cells communicate with the free surface of the mucosa by the taste canal. Microvilli ("taste hairs") project from the ends of the neuroepithelial cells into the taste canal. The neuroepithelial cells are usually located centrally in the structure, surrounded by their supporting or sustentacular cells.
A :Taste buds
Tast e bud s
B :Micro villi (tast e hairs)
Papillae are mainly concerned with different taste sensations :
v Vallate papillae : Bitter v Fungiform papillae : Sweet and salty v Foliate papillae : Sour
Junctions in oral mucosa
A. v v v v v Mucocutaneous junction : Junction between skin and mucosa. At this junction, few sebaceous glands are present. Epithelium is keratinized but thin. Red in color (vermilion zone) due to close proximity with blood. No salivary gland are there in the vermilion zone and only few sebaceous glands are present, so it tends to dry out and cracked in winters.
B. Mucogingival junction : C. v Junction between gingiva and alveolar mucosa. v v Histologically, a change occurs in this junction, not only in type of epithelium but also in composition of the lamina propria. v v Stippling is seen, and reflects the attachment of the collagen fibers.
C. Dentogingival Junction : D. v Region where oral mucosa meets the surface of the tooth is called dentogingival junction.
The junctional epithelium is that epithelium which lies at, the base of the gingival sulcus. It attaches to the surface of the tooth with hemidesmosomes. It is 1mm in width. Cells in the junctional epithelium tend to have wide intercellular spaces, to allow the transmission of W.B.C’s from blood vessels to bottom of the gingival sulcus, to help prevent the disease. Its irregular in texture.
Tissue which covers the alveolus and encircles the neck of teeth is called gingiva.
Functions : v Surrounds and supports the teeth. v Prevents invasion of bacteria to periodontal ligament. v Parts of Gingiva : v Free gingiva (Marginal or unattached) v Attached gingiva v Interdental papilla
Free gingiva :
v Knife edge part of gingiva. v v In normal healthy individual, width is about 1mm. v v Causes food lodgment, when knife edge is thickened. v Attached gingiva :
v Part which is firmly bound to periosteum is called attached gingiva. v v Superiorly, it is bound to free gingival groove and inferiorly extends up to mucogingival line. v v It is firm and reselient.
v It’s width is maximum in maxillary incisor region :- 3.5 to 4.5 mm v v It’s width is minimum in mandibular 1st premolar region :- 1.8mm v v Increase in width of attached gingiva is due to supra eruption of a tooth with increased cementum deposition. v v Any decrease in width is pathological. v Interdental Papillae :
v Part which extends between two teeth up to the contact point is called interdental papillae. v v It has a ‘facial side’ and a ‘lingual side’ . v v It’s margins are concave. v
v Due to inflammation, interdental papillae looses it’s concavity. v COL : v Connecting facial and lingual side of the interdental papilla (on proximal side) is an epithelial structure called COL. v v It’s concave shape means, gingiva is healthy. v v It becomes dome shaped, in gingival recession and inflammation. v v It is covered by non keratinized stratified squamous mucosa.
Fibers in gingiva :
v Dentogingival fibers : Run from cementum to gingiva. v v Circular fibers : Hugs around the tooth. v v Alveologingival group of fibers : Run from alveolar crest into lamina propria of free and attached gingiva. v v Dentoperiosteal group : Run from cementum to periosteum of alveolar crest.
Functions : v Braces marginal gingiva firmly against the tooth. v v Withstand forces of mastication. v v Unites attached gingiva with cementum to augment, action of junctional epithelium.
Age changes in oral mucosa
Oral mucosa of an elderly patient has a smoother and dryer surface than younger patient, due to dry therapy or any systemic diseases. Epithelium appears thinner histologically. Flattening of epithelial ridges. Reduction in no. of filiform papillae. Glossy and smooth appearance. Langerhan’s cells become fewer with age, leading to decrease in cell mediated immunity.
Nodular varicose veins on the under surface of the tongue(caviar tongue). Decrease in cellularity occurs in lamina propria with increase in collagen. Sebaceous (Fordyce’s spots) glands of lips and cheeks increase with age. Elderly post menopausal women, have symptoms such as dryness of mouth, burning sensations and abnormal taste.
Classification of oral lesions : : Mucosal lesions
v v v v v v v
Leukoedema Oral leukoplakia Proliferative verrucous leukoplakia Epithelial dysplasia Oral hairy leukoplakia Oral lichen planus Candidiasis Oral ulcerative lesions : Acute : Traumatic Bacterial Troponemal
§ v v v
v v v v v v v v
Viral Fungal Drug reactions Erythema Multiforme Lupus Erythematosus Reiter’s syndrome
Chronic : v Vesiculobullous lesions v Malignant diseases
Recurrent : v Recurrent Apthous stomatitis : Major Apthous ulcers Minor Apthous ulcers
v Herpetiform ulcers v Bechet’s syndrome
v v v v
Acute ulcerative : Acute necrotizing ulcerative gingivostomatitis (ANUG) Streptococcal gingivostomatitis Oral Tuberculosis Gonococcal stomatitis
Syphilis : Congenital syphilis Primary syphilis Secondary syphilis Tertiary syphilis Fungal : v Oral Candidiasis v Histoplasmosis
Viral : v Herpes simplex v Recurrent Herpes simplex v Herpes labialis
v Varicella zoster v Coxsackie
Discoid Lupus Erythematosus
Reiter’s syndrome Bechet’s syndrome Drug Reactions : Barbiturates, Salicylates, Phenolphthalein, Quinine, digitalis, Grisefulvin, Dilantin
Chronic ulcerative : v Pemphigus vulgaris v Mucous membrane (cicatricial) pemphigoid v Traumatic Granuloma
Hyperpigmentation of oral mucosa : v Exogenous : qForeign material – Amalgam tattoos, , carbon, seeds, leaves of various plants, tobacco qPharmacologic agents: Minocycline, AZT, antimalarials, amiodarone, OCP, doxorubicin qHeavy metal exposure: bismuth, mercury, silver, lead, tin, copper
v Endogenous : q Systemic : Addison’s disease, Peutz-Jeghers syndrome, hemochromatosis q Neoplasms: nevi, oral and labial melanotic macules, melanoma q Reactive process: post-inflammatory hyperpigmentation q v Others : - Acute Tonsilitis - Carcinoma of Tongue - Angular Chelitis - Torus Palatinus - Torus Mandibularis - Cold Sores - Oro Pharynx Necrosis
- Salivary gland stone - Oral Fibroma - Lingual Cavernous Hemangioma - Lingual Hemangioma - Mass on base of Tongue - Sialocele - Oro Maxillary Fistula - Lichenoid reaction v Pigmentation : Melanoplakia
v White sponge nevus
Keratotic lesions : - Hyperplastic - Atrophic Dyskeratotic lesions – eg. Dyskeratotic leukoplakia
Malignant tumors : - Oral Squamous cell carcinoma - Adenocarcinoma Dermatological lesions : - Stevens-Johnsons syndrome - Lichen Planus - Discoid Lupus Erythematosus
Developmental disturbances of Oral mucosa:
Fordyce’s disease (Fordyce’s granules)
It is a developmental anomaly characterized by heterotrophic Clinical features : collections of sebaceous glands at various sites in oral cavity.
v Small yellow spots. v They form large plaques. v Found frequently in a bilateral symmetrical pattern on the mucosa of cheeks, opposite molars and also on the inner surface of lips. v
FOR DYC E’S GRA NUL Yellow small macular or papular structures on buccal mucosa. They are usually symptomless. ES
v Occasionally they are found on tongue, gingiva, frenum and palate. v Besides oral cavity, they are also found in esophagus, female genitalia, palms and soles, parotid gland, larynx and orbit.
Histological features : but not associated with hair follicles.
v Heterotrophic collections of sebaceous glands are common in skin, v Glands are usually superficial and may consist of only a few or many lobules, grouping around one or more ducts opening on the surface of mucosa. v Ducts may show keratin plugging.
HIST OLO GIC AL IMA Lobules of Sebaceous glands emptying into ductal structures that communicate with the surface of the mucosa. GE
HIST OLO GIC AL IMA Excessive accumulation of larger lobules of Sebaceous glands that often produce a noticeable mucosa swelling. GE
Focal Epithelial Hyperplasia (Heck’s disease)
Clinical features :
v Primarily occurs in children. v It is HPV induced epithelial proliferation and is known to be produced by subtypes of HPV, i.e. HPV -13 and possibly HPV – 32.
HEC K’S DISE Multiple Sessile and papillary lesions of the anterior gingiva and labial mucosa of an adult. ASE
v No gender predilection. v Site – Labial, buccal, lingual mucosa. Some gingival and tonsillar lesions have also been reported. v Fissured appearance of entire mucosal area, due to clustering of the hyper plastic lesions. v Lesion is papillary in nature.
Histological appearance : Focal acanthosis of oral epithelium. Mucosa is 8-10 times thicker than normal. Lesional rete ridges are at same depths as normal rete ridges. Ridges are widened and club shaped. Mitotic figures (mitosoid cell) seen. Sessile in nature.
HIST OLO GIC AL IMA Spinous layer epithelial cells with unusual arrangement of the nuclear material resembling abnormal mitotic figures (mitosoid cells). GE
Lacks central keratin filled core of keratoacanthoma. Lacks sub epithelial foamy or granular histocytes like cells required for diagnosis of Verruciform Xanthoma.
v Common oral mucosa condition of unknown cause. v More common in blacks than in whites.
Clinical Features :
v Diffuse, grayish- white, milky, opalescent appearance of mucosa. v Wrinkles present on the surface of mucosa. v Lesion does not rub off.
v Occurs bilaterally but adjacent mucosa can also be involved. v Occurs mainly on buccal mucosa and extends up to labial mucosa. Sometimes it can also involve floor of the mouth.
Histological appearance :
v Increase in thickness of the epithelium. v Intracellular edema of the spinous layer is seen. v Pyknotic nuclei present in large vacuolated cells. v Epithelial surface is frequently parakeratinized v Rete ridges are broad and elongated.
HIST OLO GIC AL IMA GE
Developmental disturbances of Gingiva :
Fibromatosis gingivae :
Also called Elephantiasis gingivae, hereditary gingival fibromatosis, congenital microgingivae. It is a diffused fibrous overgrowth of gingival tissues. It is considered Hereditary, being transferred from dominant autosomal gene.
Clinical features :
v v It is a dense, diffuse, smooth or nodular overgrowth of gingival tissues usually appearing at the time of eruption of permanent incisors.
Histological appearance :
v Epithelium thickened. v Elongated Rete pegs. v Coarse bundle of collagen fibers with few fibroblasts and blood vessels.
v Small, 2-4 mm slightly elevated nodule on the lingual mucosa of mandibular cuspids. v Soft, well circumscribed, sessile, mucosal nodule, bilateral but can also be unilateral. v Prominent in children.
CLIN ICAL IMA A reddish, slightly-raised sessile small nodule behind or lingual to the lower cuspid tooth. GE
Histological appearance :
v Appears as an elevated mucosal tag often showing mild hyperkeratosis or hyperparakeratosis. v Surfaced of orthokeratinized or parakeratinized squamous epithelium. v Can be with or without acanthosis.
v Underlying connective tissue is highly vascularised. v Large stellate fibroblasts. v Occasional epithelial rests.
Developmental disturbances of Tongue :
v Very rare.
Aglossia and Microglossia syndrome
feet, cleft palate.
v Associated with malformations in extremities, mainly hands and
v Actually, Aglossia syndrome is a microglossia with extreme glossoptosis (Rudimentary or small tongue).
Mandible does not grow in the anterior direction due to lack of muscular stimulus. It’s etiology is unknown, but some say it’s some sort of fetal cell traumatism in first few weeks of gestation.
CLIN ICAL IMA Congenital short lingual frenum of the tongue with microglossia GE
v Also called as tongue hypertrophy, prolapsus of tongue, enlarged tongue, pseudomacroglossia. v It means large tongue. v May occur due to some congenital syndromes. E.g. Down’s syndrome and Beckwith- wiedmann syndrome.
MAC ROG LOS SIA
Ankyloglossia or Tongue tie
v Occurs when inferior frenum attaches to the bottom of the tongue and resists it’s free movement. v Tongue tie may contribute to dental problems as well, causing persistent gap between mandibular incisors v There is difficulty in speech and feeding. v Frenulectomy is recommended.
v A complete cleft or bifid tongue is a rare condition. v Occurs due to lack of merging of lateral lingual swellings. v A partial cleft tongue is more common and is actually a deep groove in the midline of dorsal surface.
v It occurs due to incomplete merging and faliure of groove obliteration by underlying mesenchymal proliferation. v It is a feature of oral- facial- digital syndrome.
v Grooves that vary in depth are present along the dorsal and lateral aspects of tongue. v A polygenic mode of inheritance is suspected. v Seen in Melkersson – Rosenthal syndrome, Down’s syndrome, Geographic tongue (Benign migratory glossitis)
Scrotal tongue/ fissured tongue, lingua plicata
Histological appearance :
v Increase in the thickness of the lamina propria. v Loss of filiform papillae of surface mucosa. v Hyperplasia of rete pegs. v Mixed inflammatory infiltrate in lamina propria.
Median Rhomboid Glossitis
v Post dorsal point of fusion is occasionally defective, leaving a rhomboid shape, smooth and erythematous mucosa. v Lack of papillae/ taste buds. v Occurs in candidiasis and also
known as ‘Chronic Atrophic Candidiasis’.
Clinical features :
v Kissing lesion : Infected cases may also demonstrate a midline soft palate erythema in the area of routine contact with the underlying tongue involvement. This is commonly called kissing lesion. v v
Histological appearance :
v Smooth or nodular surface covered by atrophic stratified squamous epithelium. v Dilated capillaries. v Fungiform and filiform papillae not seen. v Chronic inflammatory cell infiltrate may be seen. v Extreme elongation of rete processes v Dyskeratosis.
Benign migratory glossitis (Geographic tongue)
v Psoriasiform mucositis of the dorsum of tongue. v It’s dominant characteristic is constantly changing pattern of serpiginous white lines surrounding areas of smooth, depapillated mucosa.
Histological appearance :
v Thickened keratin layer with neutorphils. v Inflammatory cells often produce small micro abscesses, called Monroe's abscesses in keratin and spinous layer. v Rete ridges are thin and elongated. v Chronic inflammatory cells seen in variable numbers within stroma.
HIST OLO GIC AL IMA Hyperkeratotic epithelium GE
Hairy as Lingua nigra, lingua villosa, lingua villosa nigra, Also known tongue
black hairy tongue.
v It is a condition of defective desquamation of filiform papillae. v It may appear brown, white, green, pink.
v Etiology :Ø Hypertrophy of filiform papillae on dorsal surface of the tongue. Ø Occurs due to poor oral hygiene. Ø Tobacco use. Ø Coffee and tea drinking.
Histological appearance :
v Elongated filiform papillae. v Mild hyperkeratosis. v Occasional inflammatory cells.
v Varix is a dilated, tortuous vein.
Lingual varices (lingual/ sublingual varicosities)
surface and lateral borders of tongue as well as in floor of mouth.
v Appear as red or purple shot like clusters of vessels on ventral
v Also occur in upper and lower lip, buccal mucosa, buccal commissure.
Lingual thyroid nodule
v It is an anamolous condition in which follicles of thyroid tissue are found in the substance of the tongue.
CLIN ICAL IMA GE
Histological appearance : v Nodules exhibit colloid degeneration or goiter.
HIST OLO GIC AL IMA Lingual thyroid nodule GE
Developmental disturbances of oral lymphoid tissue
v Lingual tonsil, located on the posterior portion of the tongue frequently becomes inflamed and enlarged. v It is bilateral . v Also is called ‘foliate papillitis’ due to foliate papillaes present in this area. v They are firm, nodular, sub mucosal mass. v They are tender.
Reactive lymphoid aggregate (Reactive lymphoid hyperplasia)
CLIN ICAL IMA Reddish smooth-surfaced papules of the posterior lateral border of the tongue in the foliate papilla area. GE
HIST OLO GIC AL IMA Superficial and deep perivascular and periadnexal lymphoid infiltrate. GE
Also called angiofollicular lymph node hyperplasia, angiomatous lymphoid, castleman tumor, follicular reticuloma giant benign lymphoma, hamartoma of lymphatics, giant lymph node hyperplasia)
v Castleman’s disease is a rare disorder characterized by noncancerous benign growth that may develop in the lymph node tissue throughout the body.
v Most often, occurring in chest, stomach and neck. v Abnormal enlargement of lymph nodes occur.
3 types of Castleman's disease : These are non cancerous
a) Hyaline vascular type (90%) : overgrowths.
b) Plasma cell type : Associated with fever, weight loss, skin rash, early destruction of R.B.C. c) Multicentric / Generalized Castleman’s disease : v Abnormal large liver and spleen (hepatospleenomegaly).
v Exact cause of castleman’s disease is not known. v Some researches say it’s because of increase in production of interleukin- 6 (IL-6) v Interleukin – 6 is a substitute produced by structures within lymph nodes.
v Also called Epitheloid hemangioma, histocytoid hemangioma,
Angiolymphoid hyperplasia with eosinophilia
pseudopyogenic granuloma, papular angioplasia, inflammatory angiomatous nodules.
v Uncommon disorder. v Present with isolated or grouped plaques or nodules in skin of head and neck. v Lesion is benign. v
v A distinct entity, ALHE is marked by proliferation of blood vessels with distinctive large endothelial cells. v
Histological appearance :
v Papules around ear may suggest ALHE enlarged endothelial cells with uniform ovoid nuclei and intracytoplasmic vacuoles.
HIST OLO GIC AL IMA Benign cutaneous vascular tumor largely composed of epithelioid vascular cells with focal glomeruloid features. GE
v Develops within a benign lymphoid aggregate or accessory tonsil of the oral or pharyngeal mucosa. v Surface of such aggregates may be indented with tonsillar crypts. v The crypts may become obstructed by keratin or other debris. v Certain cases develop complete disunion of the crypt epithelium from the surface epithelium.
HIST OLO GIC AL IMA GE Yellow lymphoepithelial cyst on the margin of the tongue
Histological appearance :
v Lined by atrophic and often degenerated stratified squamous epithelium. v Lack rete processes. v Minimal granular cell layer.
v Rarely, mucus filled goblet cells may be seen within superficial layers of the epithelium. v Orthokeratin seen sloughing from the epithelial surface into the cystic lumen.
HIST OLO GIC AL IMA Often lined by squamous epithelium GE
HIST OLO GIC AL IMA Lined by non-neoplastic glandular epithelium GE
ORA L LEU KOP LAKI A
ORA L VER RUC OUS LEU KOP LAKI A
EPIT HELI AL DYS PLA Nodular leukoplakia showing severe epithelial dysplasia SIA
ORA L HAIR Y LEU KOP LAKI Leathery white callus on the side of the tongue A
ORA L HAIR Y LEU KOP LAKI It is considered pathognomonic for aids. When a clinician encounters a patient with hairy leukoplakia, he assumes he is dealing with a person with HIV virus and recommends that the patient have serological test for HIV A
ORA L LICH EN PLA NUS
CAN DIDI ASIS
ORA L ULC ERA TIVE LESI ON
Acute Necrotizing Ulcerative Gingvostomatitis
ORA L TUB ERC ULO SIS
SYP HILI S
HIST OPL ASM OSIS
HER PES LABI ALIS
COX SAC KIE VIR US INFE CTIO N
DIS COI D LUP US ERY THE MAT OSU (A.) Extraoral photograph of patient with discoid lupus erythematosus. Note the butterfly shaped rash on the malar area. (B) Intraoral photograph of the same patient showing erosive lesions surrounded by radiating white striae on the left buccal mucosa. S
REIT ER’S SYN DRO Tongue lesion ME
BEC HET’ S SYN DRO ME
PEM PHG US VUL GAR IS
MUC OUS MEM BRA NE PEM PHIG OID
REC URR ENT APT HOU S STO MATI TIS
TOR US PAL ATIN US
TOR US MAN DIB ULA RIS
ANG ULA R CHE LITIS
COL D SOR ES
STE VEN SJOH NSO N SYN DRO Also called erythema multiforme ME
ORA L PHA RYN X NEC ROS IS
Salivary gland stone
ORA L FIBR OMA
LING UAL CAVE RNO US HEM ANGI OMA
MAS S AT BAS E OF THE TON GUE
SIAL OCE LE
ORA L MAX ILLA RY FIST ULA
Tencate’s textbook of dental histology; 7th edition. Orban’s textbook of oral histology; 11th edition. Oral anatomy, histology& embryology ; berkovitz ; 3rd edition. Textbook of periodontology; Carranza ; 10th edition Oral and Maxillofacial Pathology; Neville; 2nd edition. Shafer’s Textbook of Oral Pathology; 6th edition.
Contemporary Oral and Maxillofacial Pathology ; 2nd edition. Handbook Of Oral Disease, diagnosis and management ; Crispian scully ; 1st edition. Francis.V.Howell. Oral mucous membrane lesions.
California Medicine 1964 ; 100(3); 186-91. Francis B. Quinn ,Matthew W. Ryan. Ulcerative Lesions Of The Oral Cavity. UTMB Grand rounds 2002 ;1-11
Brad W. Neville, Terry A. Day. Oral Cancer and Precancerous Lesions. CA Cancer J Clin 2002;52:195-215
This action might not be possible to undo. Are you sure you want to continue?