Developmental disorders Facial cleft – disorder in the migration of neural crest cells failure of the fusion process and failure of inwards growth of the mesoderm genetics play a part in the development of facial clefts Lateral cleft –the commonest -cheiloschisis (harelip) -incomplete cleft–coloboma labii -cleft extending to the nose cavity - labium leporinum -cleft palate, soft palate - uranoschisis, jaw - gnatoschisis and uvula- staphyloschisis Medial, transverse,oblique cleft, Developmental disorders Vestibular defect Accesory mouth Macrostomy Microstomy Aglossia Microglossia Macroglossia Ankyloglossia Lingua plicata (scrotal tongue) Mikrognatia, progenia, prognatia Fordyce´s spots Dermoid cyst Heterotopic gastric and intestinal mucoses Heterotopic nerve tissue White nevus(white sponge n, AD inheritance intracellular edema Necrosis Mechanical Chemical (arsenic, acid, lye, drugs – aspirin) Scurvy (Scorbut) Hemoblastosis Infections Allergy (ATB, metals) Autoimmunity (Wegener granulomatosis, Lupus erytematodes….) Atrophy atrophy of mucosa and processus alveolares old age diabetes disorders of inervation, Plummer –Vinson‘s sy (atrophic glossitis + epithelial dysplasia in pernitious anemia anemia Pigmentation of the oral cavity melanin: physiological in darked races Hormonal: Graphite spots in Addison‘s disease melanin spots in Peutz-Jeghers syndrome Reactive: pigmentation in lichen planus actinic keratosis Therapy associated: Oral contraceptives Antimalarials Phenothiazines Methyldopa Pigmentation of the oral cavity hemosiderin after trauma rarely in hemochromatosis exogenic pigmentation – chronic poisoning by heavy metals-- lead, mercury,zinc, amalgam Addison´s disease Inflammation of the oral cavity stomatitis – the whole oral cavity cheilitis- lip, glossitis- tongue gingivitis- gingiva Non-specific inflammation Inflammation with exsudate predominance: serous catharral purulent Inflammation with alteration predominance (tissue damage) pseudomembranous ulcerative gangrenous Serous inflammation – stomatitis acuta simplex Inflammatory erythema The mildest form May be local or accompany systemic diseases All known causative agents Transient, without consequences Catharral inflammation Catharrals – serous exsudate + mucus overproduction Etiology: similar as in serous i. Purulent inflammation – stomatitis purulenta Mosty odontogenic etiology flegmonous inflammation may spread to sublingual, submandibular, parapharyngeal areas - angina Ludovici (Ludwig´s angina= angina maligna=morbus strangularis) -cheilitis phlegmonosa – orinates from furuncle, serious complication – spread through vessels to cranial cavity with brain sinuses tromboflebitis splavů, leptomeningitis glossitis abscedens- foreign body actinomycosis- anaerobic mikrobes actinomyces- abscending and granulomatous reacton with scarring Periodontal inflammation and osteomyelitis. - Ludwig´s angina Actinomycosis Pseudomembranous inflammation Pseudomembrane : necrotic tissue infiltrated by fibrin and PMN Causes: -bacterial (diptheria, scarlet fever) scarlet fever– beta hemolytic streptococcus group A, rapsberry tongue , lymphadenopathy, (peritonsil abscessus, otitis, meningitis…) -viral: inf. mononucleosis, influenza - immunosuppression -chemicals- acid, lye burns, Ulcerative inflammation 1. Preceding vesiculous diseases 2. Without preceding vesiculous diseases a. Infectious a. Infectious – herpetic stomatitis (herpes virus 1,2) – tbc – Herpes zoster ( varicella-zoster) – syphilis – Herpangina, Hand-foot-mouth disease – cytomegalovirus (Coxsackie A,B) b. Non-infectious b. Non-infectious – trauma – Pemphigus vulgaris – chemical burning – Pemphigoid – apthous stomatitis – Dermatitis herpetiformis – systemic diseases(SLE) – drug reactions – malignant tumors Vesiculous inflammation Characterised by blisters formation (vesicula, bulla with rapid maceration and ulceration Mechanisms 1. Spongiosis 2. Cytolysis and baloon degeneration 3. Akantolysis = dissolution of intercellular adhesions 4. Epidermolysis (separation of the epidermis in the basement membrane) Viral vesiculous inflammations a. Herpes simplex 1,2 Infection of immunized organisms Infection of non-immunized organisms – (recurrent) Primary gingivostomatitis HSV persist in nerve ganglias, in -childhood, adulthood Fever, systemic symptoms activation arises herpes labialis- resembling flu (lip, gingiva) – painful lesiosn Mucosal edema, erythema, small ulcers healed within 7 days - Dif. dg: Necrotising ulcerative periodontitis Pemphigus vulgaris Erythema multiforme Erozive lichen planus Dentists 2-10 days after contact – herpetic panaritium(HSV1), may last even 2 month sometime axillary lymphadenitids Herpetic stomatitis Herpes zoster Virus varicela zoster Elderly people Immunosuppression, often in lymphomas ( Hodgkin´s and T lymphomas), leukemias Efflorescence spread from one or more ganglia along nerves of an affected segment and infect the corresponding dermatome (an area of skin supplied by one spinal nerve) How the virus remains latent in the body, and subsequently re-activates is not understood. Strong painful rash Often n. trigeminus+ n facialis (paresis) Postherpetic neuralgia Herpangina Small kids Summer time Sudden onset Diffuse pharyngitis Apthous inflammations Apthous stomatitis /recurrent Typical features: aphta/- very common, 10-25% of population. - Minor apthous ulceration - Duration -10 days Etiology unknown - Regular intervals (cyclic) - Free period usually 3 weeks - genetic - Healed without scar - infection - Immunopathologic state (T lymphocytes) - Major apthous ulceration - 1-2 ulcers - Hormonal disturbances - Size 10mm - Hematologic diseases - Duration – may be month - Stress - Non- cyclic - Healed with scars - Some food (citrus, cherry) - More commom genital - Folate and B12 def. involvement - Abnormal response to trauma - GIT disease Apthous inflammations Minor apthous ulceration. Major apthous ulceration Autoimmune vesiculous diseases Pemphigus vulgaris It is an autoimmune disease caused by antibodies directed against both desmoglein 1 and desmoglein 3 resulting in the loss of cohesion between keratinocytes in the epidermis, classified as a type II hypersensitivity reaction. It is characterized by extensive flaccid blisters and mucocutaneous erosions. Potentially fatal 50% of cases begins in mouth Paraneoplastic pemphigus (usually fatal) Pemphigoid Autoimmune disease with subepithelial bullae – epidermolysis Female preponderance Elderly people Pemhigus vulgaris Necrotizing and gangrenous inflammation Noma Noma is a rapidly progressive, polymicrobial, opportunistic infection that occurs during periods of compromised immune function.Fusobacterium necrophorumand Prevotella intermedia are thought to be key players in the process and interact with one or more other bacterial organisms (such as Borrelia vincentii , Staphylococcus aureus and nonhemolytic Streptococcus The reported predisposing factors: Malnutrition or dehydration Poor oral hygiene Poor sanitation Unsafe drinking water Recent illness Malignancy An immunodeficiency disorders, including AIDS Necrotizing and gangrenous inflammation Acute ulcerative gingivitis Vincent´s angina (Vincent´s organisms Borrelia vincentii and Fusiformis) Interdental papillae Healthy individuals Immunocompromised Mycotic infections Candidiasis /disease of the diseased/ Less frequently: aspergillosis, forms: pseudomembranous Deep mycosis atrophic (blastomycosis, hypertpphic cryptomycosis) – Causes: opportunistic inf. - -immature immune system tissue necrosis -ATB therapy -HIV (because of vessels -diabetes occlusion) -anaemias -immunosuppression - Chronic inflammation chronic gingivitis - insufficient oral hygiene, tartar, diabetes, avitaminosis, May be comined with resorption of alveolar processes chronic hyperplastic gingivitis - in pregnant, antiepileptic drugs Granuloma fissuratum Stomatitis nicotinica (palate, mucosal hyperplasia sliznice with hyperkeratosis) Atrophic glossitis (Hunter‘s) - pernitious anaemis Anguli infectiosi (stomatitis angularis, angulae cheilitis) salivary maceration, Fe, vitamin B deficiencies, malabsorption Chronic inflammation granulomatous cheilitis cheilitis granulomatosa - unknown etiology, macrocheilia, perivascular granullomas Melkersson-Rosenthal‘s syndrome (paresis of facial nerve+ lingua plicata) Specific inflammation Syphilis TBC – rare, as complication of pulmonary TBC Acquired syphilis -Treponema pallidum 1. stage: chancre (tongue, lips) Healed spontaneously within 3 month Acquired syphilis 2. stage: condylomata lata Flat placques or ulcerations Acquired syphilis 3. stage: (30% of patients) gumma (very often as intersticial glossitis) Congenital syphilis – Hutchinson´s teeth (peg shaped) Imperfect formation of enamel Hutchinsonova trias: + labyrintitis Keratitis Others: Gothic palate, saddle nose Progressive changes Macroglosia Gingival hyperplasia Leukoplakia Granullomas Epulis Epulides Epulis (Galén) Epulis is a soft tissue swelling of the gingival margins Hyperplastic inflammatory lesions arising from periodontal tissues Epulis granulomatosa Epulis fibromatosa Epulis gravidarum Epulis gigantocelularis (giant cell) Epulis fibromatoza Giant cell epulis Giant cell epulis Progressive changes of the tongue Makroglossia congenital (lymphangioma, Down´s syndrom) acquired (acromegaly, AL amyloidosis) Lingua villosa nigra Elongation of filliforme papillae+propagation of chromogenic bacterias, bad hygiene, smoking, drugs, Fuligo lingue Granulomatous disease Foreign body granuloma Pyogenic granuloma (teleangiectaticum) – dark red, (5mm), similar to capillary hemangioma + neutrophils Oro-facial granulomatosi (swollen lip) Crohn´s disease Sarcoidosis Melkersson-Rosenthal‘s syndroms Wegener´s granulomatosis Histiocytoses Central giant cell granuloma local reactive intraosseal neoplasia, dif.dg – osteoklastoma Pyogenic granuloma Precanceroses Leukoplakia - white patch acanthosis, hypekeratosis zvláštním typem je chronická hyperplastická kandidioza Hairy leukoplakia - tongue margins, in HIV Plummer-Vinson‘s syndrome- atrophic glossitis+ dysplasia erythroplasia- bright red patches with dysplasia .