sign in sign up
<<
Home , Epulis, Noma (disease)

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 , soft palate - uranoschisis, jaw - gnatoschisis and uvula- staphyloschisis

 Medial, transverse,oblique cleft,

Developmental disorders

 Vestibular defect  Accesory mouth  Macrostomy  Microstomy  Aglossia  Microglossia   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 + epithelial dysplasia in pernitious anemia anemia

Pigmentation of the oral cavity

 melanin:

 physiological in darked races

 Hormonal:

 Graphite spots in Addison‘s

 melanin spots in Peutz-Jeghers syndrome

 Reactive: pigmentation in 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 – the whole oral cavity - , glossitis- tongue - 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  The mildest form  May be local or accompany systemic  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

- 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 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) – – , Hand-foot-mouth disease – cytomegalovirus (Coxsackie A,B) b. Non-infectious b. Non-infectious – trauma – vulgaris – chemical burning – – 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. 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 - resembling flu (lip, gingiva) – painful lesiosn Mucosal edema, erythema, small ulcers healed within 7 days

-

Dif. dg: Necrotising ulcerative periodontitis Pemphigus vulgaris 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 ( 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  is a rapidly progressive, polymicrobial, opportunistic infection that occurs during periods of compromised immune function.Fusobacterium necrophorumand are thought to be key players in the process and interact with one or more other bacterial organisms (such as vincentii , 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

fissuratum

 Stomatitis nicotinica (palate, mucosal 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, , perivascular granullomas Melkersson-Rosenthal‘s syndrome (paresis of facial nerve+ lingua plicata)

Specific inflammation

 Syphilis  TBC – rare, as complication of pulmonary TBC Acquired syphilis

- pallidum 1. stage: chancre (tongue, ) 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   Granullomas  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  (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

- tongue margins, in HIV

 Plummer-Vinson‘s syndrome- atrophic glossitis+ dysplasia

 erythroplasia- bright red patches with dysplasia