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

Developmental disorders

Mechanical Chemical (arsenic, acid, lye, drugs – aspirin) Scurvy (Scorbut) Hemoblastosis Infections Allergy (ATB, metals) Autoimmunity (Wegener granulomatosis,

Lupus erytematodes….)

Necrosis

atrophy of mucosa and processus alveolares old age diabetes disorders of inervation, Plummer –Vinson‘s sy (atrophic glossitis

+ epithelial dysplasia in pernitious anemia anemia

Atrophy

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

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

stomatitis – the whole oral cavity

cheilitis- lip,

glossitis- tongue

gingivitis- gingiva

Inflammation of the oral cavity

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 a. Infectious – herpetic stomatitis (herpes virus 1,2) – Herpes zoster ( varicella-zoster) – Herpangina, Hand-foot-mouth disease

(Coxsackie A,B)

b. Non-infectious – Pemphigus vulgaris – Pemphigoid – Dermatitis herpetiformis

2. Without preceding vesiculous diseases

a. Infectious – tbc – syphilis – cytomegalovirus b. Non-infectious – trauma – chemical burning – apthous stomatitis – systemic diseases(SLE) – drug reactions – malignant tumors

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)

Vesiculous inflammation

Viral vesiculous inflammations

a. Herpes simplex 1,2

Infection of non-immunized organisms –

Primary gingivostomatitis -childhood, adulthood Fever, systemic symptoms

resembling flu Mucosal edema, erythema, small

ulcers

-

Infection of immunized organisms

(recurrent)

HSV persist in nerve ganglias, in

activation arises herpes labialis-

(lip, gingiva) – painful lesiosn

healed within 7 days

Dentists 2-10 days after contact –

herpetic panaritium(HSV1),

may last even 2 month

sometime axillary lymphadenitids

Dif. dg: Necrotising ulcerative periodontitis

Pemphigus vulgaris

Erythema multiforme

Erozive lichen planus

Herpetic stomatitis

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

Herpes zoster

Herpangina

Small kids

Summer time

Sudden onset

Diffuse pharyngitis

Apthous inflammations

Apthous stomatitis /recurrent aphta/- very common,

10-25% of population. Etiology unknown - genetic - infection - Immunopathologic state (T

lymphocytes) - Hormonal disturbances - Hematologic diseases - Stress - Some food (citrus, cherry) - Folate and B12 def. - Abnormal response to trauma - GIT disease

Typical features: - Minor apthous ulceration

- Duration -10 days - Regular intervals (cyclic) - Free period usually 3 weeks - Healed without scar

- Major apthous ulceration

- 1-2 ulcers - Size 10mm - Duration – may be month - Non- cyclic - Healed with scars - More commom genital

involvement

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

http://en.wikipedia.org/wiki/File:Noma.png

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/

forms: pseudomembranous atrophic hypertpphic Causes: -immature immune system -ATB therapy -HIV -diabetes -anaemias -immunosuppression -

Less frequently: aspergillosis,

Deep mycosis (blastomycosis, cryptomycosis) – opportunistic inf. - tissue necrosis (because of vessels occlusion)

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