dental Flashcards
- Dental inclusion and root ankylosis
Dental inclusion
Definition: Tooth eruption is halted before its emergence on the alveolar ridge. The tooth is surrounded by bony tissue and is unable to erupt.
Etiology:
Lack of parallelism between the tooth bud and the eruption axis
Ectopic position of the tooth bud
Gingival fibromatosis, tumors, cysts on the eruption tract
Pathology:
- Position of the included tooth’s axis
Vertical
Oblique (mesio – angular, distal – angular)
Horizontal
Inverted
Complications:
Dental «crowding»
Resorbtion of the roots of neighbouring teeth
Changes in the eruption order and in the position of neighboring teeth
Inflammation in the involved region
Development of a dentigerous cyst
Included teeth with complications and clinical manifestations must be surgically removed!!
Radicular ankylosis
Definition: Tooth eruption is halted after its emergence on the alveolar ridge. Bony union of the radicular surface of a tooth to the surrounding alveolar bone in an area of previous partial root resorption.
It occurs in the first two decades of life
Microscopy:
! Fusion between cementum and the alveolar bone with the disappearance of periodontal structures
Etiology:
Idiopathic
Hereditary
Macroscopy:
The incisal margins and occlusal surfaces of the ankylosed teeth are located below the level of adjacent teeth: sub-occlusion.
Diagnosis Rx:
Disappearance of the alveolar ligament
Complications:
Adjacent teeth lean towards the ankylosed one
The antagonist tooth (from the opposite arcade) develops excessively
Bone fractures in case of extraction – previous diagnosis of ankylosis is required
- Dental transposition and ectopy
Transposition
Growth of a tooth in the place of another one on the same arch, and vice versa.
E.g.: the first molar in the place of the second molar
Ectopy
Development of teeth outside the dental arches.
Examples:
Supranumerary teeth
Included in gingiva, the mental protuberance, soft palate and in the spheno-maxillary fissure
Sometimes normal teeth with abnormal location
- Hypodontia and anodontia
Hypodontia/Partial oligodontia Absence of a few teeth . Less than five for hypodontia and more than 6 for partial oligoodntia. Differiential Diagnosis Frequently hereditary origin Frequently associated with MICRODONTIA
Anodontia/agenesis/total oligodontia
Total absence of teeth.
Rare; since birth.
Frequently a part of HEREDITARY ECTODERMAL DYSPLASIA
- Hyperdontia (mesiodens, paramolar and distomolar)
Hyperodontia
The number of teeth is higher than normal
AD,
Associated with MACRODONTIA
MESIODENS= most common supernumary tooth, located in the maxilla’s midline.
90% of supranumerary teeth
Between the central superior incisors (75%)
PARAMOLARS= Paramolar is a supernumerary molar usually small and rudimentary, most commonly situated buccally or palatally to one of the maxillary molars.
The fourth molar/DISTOMOLAR/distodens= supernumary tooth in a distal position in relation to the third molar
- Hypercementosis
HYPERCEMENTOSIS = Hypercementosisis anidiopathic, non-neoplasticcondition characterized by the excessive buildup of normalcementum(calcified tissue) on the roots of one or more teeth.
Growth lines which are parallel to the root
Increases with age – especially in the apical region in order to compensate for the occlusal damage.
- Dilaceration
DILACERATION = Dilacerationis a developmental disturbance in shape of teeth. It refers to an angulation, or a sharp bend or curve, in the root or crown of a formedtooth.
Increased curvatures or angulations of the roots or of root-crown junctions
Causes :
Traumas during root formation:
- Germination/Fusion
GERMINATION/FUSION
Large teeth with two crowns, more or less separated or fused = tooth with doubled dimensions
GERMINATION = Incomplete division (cleavage) of a tooth bud→ two crowns, common root. The divided (double) tooth is considered as a single one→ the number of teeth is normal.
FUSION = Fusion between the dentin of two adjacent tooth buds→ two fused crowns on one or two roots.
Causes: traumatc crowding, lack of space
- Concrescence
CONCRESCENCE = Reuniting of the roots of two already formed adjacent teeth. Exclusive through cementum, the dentin remaining distinct Etiology: Growth disturbances Trauma Hypercementosis caused by chronic inflammation Deep caries Open root canals Periapical inflammatory lesions
- Dental invagination and taurodontism
DENS INVAGINATUS = «dens in dente» = Invagination of the dental crown in the pulp chamber or the root pulp (radicular dens invaginatus). The outer surface folds inwards.
Fusion of two dental buds
Enamel – towards inside
Dentin – towards outside
DENS IN DENTE
It opens through a very prominent dental cingulum (foramen caecum), with a hypomineralized enamel.
Consequences:
Acummulation of food, microbial plaque at the opening => caries, pulpitis, pulp necrosis – quickly
TAURODONTISM = is a condition found in themolar teethof humans whereby the body of the tooth andpulpchamber is enlarged vertically at the expense of the roots.
Very large pulp chamber
The neck diameter of the tooth is larger than normal
+ The root division is placed lower, close to the apex
Diagnosis Rx
Three types:
Hypotaurodontism
Mesotaurodontism (moderate)
Hypertaurodontism (severe)
- Amelogenesis imperfect: hypoplastic A.I.
HEREDITARY ENAMEL DYSPLASIAS!! = AMELOGENESIS IMPERFECTA (A. I.)
Ectodermal anomaly – dysfunction of the adamantine organ (of the ameloblasts)
It doesn’t involve the dentin (mesodermal origin)
Genetically inherited: AD (most frequent), AR, X-linked
Involves the enamel of all the teeth
HYPOPLASTICA.I. – two forms:
ENAMEL APLASIA:
The teeth which remain included are often resorbed
If the teeth erupt:
No enamel deposits (Rx)
Covered with dentin
Yellow-brown colour
Rough surface
ENAMEL HYPOPLASIA:
Reduced production of protein matrix
Normal degree of mineralization
- Secondary enamel dysplasia: Turner hypoplasia (local infection), dental trauma, fluorosis, congenital syphilis
TURNER HYPOPLASIA !!!
Definition: Hypoplastic enamel on the crown of a permanent tooth due to the periapical inflammation of the subjacent temporary tooth!!!
TRAUMAS:
= Enamel hypoplasia in a permanent tooth, when the subjacent temporary tooth is traumatized
FLUOROSIS: developmental disturbance of dental enamel caused by excessive exposure to high concentrations offluorideduringtooth development.
Excess of fluorine → Enamel hypomaturation → increased porosity
CONGENITAL SYPHILIS
Spirochetes enter the fetal circulation after the 16th week of intrauterine life – after formation of tooth buds
Involves only the permanent dentition
- Dentinogenesis imperfecta
DENTINOGENESIS IMPERFECTA = Dentinogenesis imperfecta(DI) is agenetic disorder (AD)oftooth development. This condition is a type of dentin dysplasia that causesteethto be discolored (most often a blue-gray or yellow-brown color) and translucent giving teeth an opalescent sheen.[1]Teeth are also weaker than normal, making them prone to rapid wear, breakage, and loss.
- Enamel caries: white plaque, cavitary lesion
Enamel 95% of hydroapatite – very hard tissue. Due to the action of proteolytic enzymes and cariogenic acids > succession of demineralization and remineralization phases. The enamel caries start below the bacterial plaque. Plaque… strep lactob…
Cavitary lesion due to a slow dissolution of the enamel, along the prisms and the interprismatic areas.
- Dentin caries
DENTIN CARIES:
Secondary to enamel caries (coronal caries) or cementum caries (cervical caries)
Evolves more rapidly
Large amount of organic substances in the dentin -30%
Dentin is injured
Initially by the bacterial cariogenic acids
Different bacterial species than the ones for enamel:
Role of anaerobes (lactobacilli) is more important
Later, bacteria penetrate the dentinal tubules
As a result, the organic component is demineralized and then liquefied
Dentin caries are cone shaped, with the tip pointing towards the pulp chamber
LAYERS:
NECROTIC (surface)
INFECTED / AFFECTED
SCLEROTIC (DEEP)
- Internal and external resorbtion
RESORBTION= Loss of dental tough subtance on the surfaces which are not exposed to the outside.
In contact with the pulp region (crown, roots)
In contact with the periodontal ligament (roots)
INTERNAL RESORBTION: Rare Causes: Pulp traumas Pulpitis secondary to caries Pulpotomy Starts in the pulp and evolves towards the surface of the cementum or the crown => until it produces a communication between the pulp and the periodontal space or the external surface of the crown
EXTERNAL RESORBTION:
Much more frequent
Starts at the surface of the tooth, in contact with the periodontal ligament
- Acute reversible and irreversible pulpitis
REVERSIBLE PULPITIS (PULP HYPEREMIA): Reversible pulpitis is generally characterized by sharp sensitivity to cold, sometimes to sweets and sometimes to biting.
The initial stage of pulp inflammation
Closed
Partial – the tissue zone is expanded only a little
Aseptic
Acute
Causes:
Deep, but closed caries
Large, incorrect metallic obturations
Evolution:
Healing after the disappearance of irritant factors
Towards a total acute pulpitis if the agression persists
ACUTE IRREVERSIBLE PULPITIS: Irreversible pulpitis is generally characterized by prolonged sensitivity to cold and/or heat, and sometimes to sweets. Swelling may be present.
Etiopathogenesis:
Exacerbation of a reversible pulpitis by opening the pulp chamber
- Chronic pulpitis and the pulp polyp
CHRONIC PULPITIS:
Can appear directly, spontaneously
After an acute pulpitis, when the pus is drained through the carious orifice
CHRONIC HYPERPLASTIC PULPITIS (PULP POLYP): Apulp polyp, also called as Chronic Hyperplastic Pulpitis, is found in an opencarious lesion, fracturedtoothor when adental restorationis missing. Due to lack of intrapulpal pressure in an open lesionpulpnecrosisdoes not take place as would have occurred in a closed caries case.
- Periapical granuloma
PERIAPICAL GRANULOMA
(CHRONIC APICAL PERIODONTITIS) = Aperiapical granulomais a mass of chronically inflamedgranulation tissuethat forms at the apex of the rootof anonvital(dead) tooth. However, a periapical granuloma does not containgranulomatous inflammation, and therefore is not a truegranuloma.
Etiology:
Apical defense reaction to the presence of bacteria and their toxins in the root canal
- Apical periodontal (radicular) cyst
APICAL PERIODONTAL CYST = APICAL RADICULAR CYST = Theperiapical cyst(also termedradicular cyst, and to a lesser extentdental cyst) is the most commonodontogeniccyst. It is caused bypulpalnecrosissecondary todental cariesortrauma. The cyst lining is derived from thecell rests of Malassez. Usually, the periapical cyst is asymptomatic, but a secondaryinfectioncan causepain.
- Periapical abscess
PERIAPICAL ABSCESS (ACUTE PERIAPICAL PERIODONTITIS) = collection of pus usually caused by an infection that has spread from a tooth to the surrounding tissues.
Well delimited purulent inflammation located at the apex of a tooth
EVOLUTION:
DRAINAGE OF PUS TOWARDS THE GINGIVA:
FISTULIZATION→ the symptoms disappear
- Acute gingivitis, acute ulcero-necrotic gingivitis
ACUTE GINGIVITIS = Initial form of a periodontopathy The acute nature is established by the intensity of the local irritation: Sulcular plaque The patient’s immune resistance
ACUTE ULCERATIVE NECROTIC GINGIVITIS (AUNG)= Acute necrotizing ulcerative gingivitis is a common, non-contagious infection of the gums with sudden onset. The main features are painful, bleeding gums, and ulceration of inter-dental papillae. In the early stages some patients may complain of a feeling of tightness around the teeth. Three signs/symptoms must be present to diagnose this condition: Severe gingival pain, Profuse gingival bleeding that requires little or no provocation, Interdental papillae areulceratedwithnecroticslough
- Chronic gingivitis
HRONIC GINGIVITIS = gingivitis is a non destructive periodontal disease.
An inflammatory process of reduced intensity, without symptoms
Elderly people
Causes:
A. From the start
Defective hygiene – chronic accumulation of bacterial plaque
Mechanical and chemical irritation
B. Evolution of an acute gingivitis
C. Down syndrome, diabetes mellitus, increased progesterone levels (pregnancy)
- Drug induced gingival hyperplasia and gingival fibromatosis
DRUG RELATED GINGIVAL HYPERPLASIA = Drug-related gingival hyperplasiais a cutaneous condition characterized by enlargement of the gums noted during the first year of drug treatment.[1]There are three drug classes that are associated with this condition namely, anticonvulsants (such as phenyotoin and phenobartibal), calcium channel blocker( such as amlopidine, nifedipine and verapamil) and cyclosporine, an immunosuppressant.
Hereditary gingival fibromatosis (HGF), also known as idiopathic gingival hyperplasia, is a rare condition of gingival overgrowth.[1] HGF is characterized as a benign, slowly progressive, nonhemorrhagic, fibrous enlargement of keratinized gingiva. It can cover teeth in various degrees, and can lead to aesthetic disfigurement.[2] Fibrous enlargement is most common in areas of maxillary and mandibular tissues of both arches in the mouth.
- Adult chronic periodontitis
ADULT CHRONIC PERIODONTITIS = Chronic periodontitisis a commondiseaseof theoral cavityconsisting ofchronicinflammationof theperiodontal tissuesthat is caused by accumulation of profuse amounts ofdental plaque. Redness + bleeding, gum swelling, halitosis, gingival recession, deep periodontal pockets, loose teeth.
The most frequent cause of dental loss
- Lateral periodontal abscess and acute pericoronitis
LATERAL PERIODONTAL ABSCESS = is a localized collection ofpus(i.e. anabscess) within the tissues of theperiodontium. It is a type ofdental abscess.
Complication of a chronic periodontitis
Cause:
Closure of the periodontal pocket in the superior gingival region
Inside the closed pocket:
Foreign bodies can be found
Fish bones, food
Bacteria multiply, sometimes even change their composition
Pus is formed = lateral abscess of the root
ACUTE PERICORONITIS
Inflammation located around the crown of a partially erupted tooth
The third permanent molar, especially the mandibular one
The pain:
Appears during swallowing
Radiates in the neck, ear and floor of the mouth
Prevents the opening and closure of the mouth
General signs: fever, altered general status, leukocytosis, enlarged lymph nodes
- Clefts of the upper lip and the palate
PPER LIP AND PALATE CLEFTS
Deff:
UPPER LIP CLEFT (ULC)= Lack of joning of the intermaxillary and median nasal buds with the lateral nasal and maxillary buds
Location of the cleft – laterally
It also involves the alveolar bone and sometimes the nostril
PALATE CLEFT (PC)= Lack of joining in the palatal processes of the maxillary buds It also involves the palate in a secondary fashion
UPPER LIP MEDIAN CLEFT:
Rare
Caused by the total lack of the philtrum
From the intermaxillary bud
- Malformations of the tongue
MALFORMATIONS OF THE TONGUE
AGLOSSIA = missing tongue or underdeveloped
Exceptionally rare
The lingual papillae are on the mouth’s floor
Sometimes – incompatible with life
MICROGLOSSIA = abnormal smallness of the tongue
Rare
Small, rudimentary tongue
MACROGLOSSIA = unusually large tongue. The most frequent causes HEMANGIOMA Lingual LYMPHANGIOMA A lot of dilated vascular channels scattered over the surface FACIAL HEMIHYPERTROPHY TYPE I NEUROFIBROMATOSIS CONGENITAL HYPOTHYROIDISM (myxedema) DOWN SYNDROME SECONDARY MACROGLOSSIA: Amyloidosis Myxedema Acromegaly Angioedema Tumors In the newborn: Noisy breath, difficult suckling In childhood: Difficulties in pronouncing lingual consonants
ANKYLOGLOSSIA :
Rare (2-3/10.000)
The lingual frenulum is short, thick and is inserted until the tip of the tongue
When it interferes with speech, surgical removal is necessary
BIFID TONGUE (LINGUAL CLEFT)=
Anomaly of the first branchial arch - mandibular bud
Lack of median joining of the lingual buds
Anatomical and clinical forms
Two tongues
A deep fossette on the dorsal surface
Inside the fossette food rests accumulate → inflammation (glossitis)
Intermediate situations
- Benign migratory glossitis
BENIGN MIGRATORY GLOSSITIS (GEOGRAPHIC TONGUE) = is an inflammatory condition of the mucous membraneof thetongue, usually on thedorsalsurface. It is a common condition, affecting approximately 1–3% of the general population.It is characterized by areas of smooth, red depapillation (loss oflingual papillae), which migrate over time. The name comes from the map-like appearance of the tongue,with the patches resembling the islands of an archipelago
- Herpes stomatitis (HSV-1 infection)
Gingivostomatitis(also known as primary herpetic gingivostomatitis or orolabial herpes) is a combination ofgingivitisand stomatitis, or an inflammation of theoral mucosaandgingiva.Herpetic gingivostomatitis is often the initial presentation during the first (“primary”)herpes simplexinfection. It is of greater severity thanherpes labialis(cold sores), which is often the subsequent presentation. Primary herpetic gingivostomatitis is the most common viral infection of the mouth.
HSV-1:
The most frequent viral infection of the oral mucosa
Involves the oral cavity, lips, pharynx, eyes, the skin of the upper body
- Ulcero-necrotic stomatitis
ULCERATIVE NECROTIC STOMATITIS (gangrenous, noma)=
Very severe
SPECIAL MICROBIAL FLORA:
Anaerobic bacteria (Fusobacterium nucleatum, Borelia vincenti, Prevotella intermedia)
Staphylococcus aureus
Streptococcus
PATHOLOGY:
Oral ulcerative necrotic lesions, which are extensive, deep and mutilating
Can expand around the mouth, nose, orbit
- Oral candidosis
PSEUDOMEMBRANOUS CANDIDOSIS = Acute pseudomembranous candidiasis is a classic form of oral candidiasis,[6]commonly referred to as thrush. It is characterized by a coating or individual patches of pseudomembranous white slough that can be easily wiped away to reveal erythematous, and sometimes minimally bleeding mucosa beneath.[7]These areas of pseudomembrane are sometimes described as “curdled milk”,[4]or “cottage cheese”.[7]The white material is made up of debris,fibrin, anddesquamatedepithelium that has been invaded by yeast cells and hyphae that invade to the depth of the stratum spinosum.[4]
APPEARS in: Newborns, Malnourished infants
Adults: HIV infection, antibiotics, chemotherapy, radiotherapy, leukemia
Debilitated older people
LOCATION: jugal mucosa, dorsum of the tongue, palate, oropharynx
ANATOMIC - CLINICAL:
MACRO:
White, soft, creamy aspect (like coagulated milk)
They are adherent, but can be easily removed by friction or scraping
The underlying mucosa is normal or erythematous
Rarely with hemorrhage (in anticancer treatment)
EVOLUTION:
Acute
After antibiotic treatment
Chronic
Depressed immunity
ERYTHEMATOUS CANDIDOSIS = Erythematous (atrophic) candidiasis is where the condition appears as a red, raw-looking lesion.
ACUTE ATROPHIC CANDIDOSIS:
After antibiotic treatment (tetracycline, topical treat.)
Rare today (because of the addition of antifungal drugs to antibiotic treatment)
Burns (like the ones which appear after a hot drink)
Macroscopy:
Diffuse loss of filiform papillae on the dorsal surface of the tongue → red depapillated tongue
GENERALIZED CANDIDOSIC ERYTHEMA :
In xerostomia (Sjögren syndrome)
FOCAL CANDIDOSIC ERYTHEMA :
In HIV seropositive patients
Red spots on the dorsum of the tongue, soft and hard palate
CENTRAL PAPILLARY ATROPHY : (median rhomboid glossitis)
Initially considered a malformation
Chronic evolution, without symptoms
Macroscopy
On the median line of the dorsum of the tongue, posterior region
A red, swollen, rhomboid, well delineated area
The surface is smooth or lobulated
Loss of filiform papillae
PROSTHESIS CANDIDOSIS:
On the palate – in case of a total prosthesis or a dental plate with prolonged usage (rarely removed for cleaning)
Under the plate: reaction to Candida or other microorganisms
Macroscopy:
Erythema, edema and petechiae on the palate – well delineated at the edge of the prosthesis
Minimal clinical signs
If it is resistant to treatment – associated iron deficiency anemia
CHRONIC HYPERPLASTIC CANDIDOSIS (candidal leukoplakia) = The most common appearance of hyperplastic candidiasis is a persistent white plaque that does not rub off.
Controversial
Leukoplakia + secondary Candida infection
Leukoplakia produced by Candida
Disappears after antifungal treatment
Macroscopy
White plaque which cannot be removed by scraping, of variable thickness and irregular aspect
Dorsum of the tongue, on the retro commissural region in the oral mucosa
Floor of the mouth, ventral tongue
ANGULAR STOMATITIS (CHEILITIS) = isinflammationof one, or more commonly both,[7]of the corners of the mouth. It is a type ofcheilitis(inflammation of the lips). Angular cheilitis often represents an opportunistic infection of fungi and/or bacteria, with multiple local and systemic predisposing factors being involved in the initiation and persistence of the lesion.[4][8]Such factors include nutritional deficiencies,[1]overclosure of the mouth,[9]dry mouth,[1]a lip-licking habit,[9]drooling,[7]immunosuppression,[10]and others, such as the wearing of poor fitteddenturesorsyphilis
20% Candida albicans / 60% Candida albicans+ Staphylococcus aureus / 20% Staphylococcus aureus Etiopathogenesis: accumulation of saliva infected with Candida Associated with : Pseudomembranous Candidosis Rhomboid median glossitis Prosthesis stomatitis Chronic hyperplastic Candidosis Macro (clinical): Erythema Fissures Squames
- Complications of oral and dental inflammatory lesions
OMPLICATIONS OF ORO-DENTAL INFLAMMATORY PROCESSES
DISSEMINATION OF MICROORGANISMS IN SOFT TISSUES :
CELLULITIS:
Definition: acute, edematous, non suppurative expansion of an oro-dental inflammatory process in soft tissues
ANATOMY and CLINICAL:
The region is swollen, with red and warm skin
EVOLUTION :
Healing
Suppuration
Abscess
LUDWIG’S ANGINA:
Def.: suppurative evolution of a cellulitis in the submandibular space
Fast laterocervical and mediastinal expansion
Direct pathway from the mouth’s floor to the mediastinum through the anatomical laterocervical regions of the neck
BONE DISSEMINATION:
OSTEOMYELITIS
SINUS DISSEMINATION
PURULENT SINUSITIS
BLOOD DISSEMINATION OF THE MICROORGANISMS :
SEPTICEMIA:
Septic endocarditis, meningitis, encephalitis
CAVERNOUS SINUS (DURA MATER) THROMBOPHLEBITIS :
Infections of maxillary teeth – dissemination through the pterygoid venous plexus
Infections of the upper lip and the face – dissemination through the angular, facial and ophthalmic veins
- Minor and major aphts
PYOGENIC GRANULOMA = is a vascular lesion that occurs on both mucosa and skin, and appears as anovergrowthof tissue due toirritation,physical traumaorhormonal factors.
DEF.:
A pseudotumor produced due to irritation and trauma in the presence of a special oral microbial flora
More frequent
In children, adolescents and pregnant women
Appears in the first semester of pregnancy, grows until birth and then decreases in size = PREGNANCY TUMOR
GIANT CELL PERIPHERAL GRANULOMA (EPULIS WITH MYELOPLAXES) DEF.: Gingival pseudotumor due to a deep gingival irritation PREDISPOSING FACTORS: Dental extraction, dental fracture Periodontal treatments Irritation given by prostheses Chronic infections EVOLUTION: Slowly, towards fibrosis
- Leukoplakia and erythroplakia
LEUKOPLAKIA = normally refers to a condition where areas ofkeratosisappear as firmly attached white patches on themucous membranesof theoral cavity. Leukoplakia in the mouth (oral leukoplakia), is defined as "a predominantly white lesion of theoral mucosathat cannot be characterized as any other definable lesion". MACROSCOPICAL FORMS : THIN (MINIMAL) LEUKOPLAKIA: GRANULAR (NODULAR) LEUKOPLAKIA: VERRUCOUS LEUKOPLAKIA: VERRUCOUS PROLIFERATIVE LEUKOPLAKIA :
ERYTHROPLAKIA (de Queyrat)= is a clinical term to describe anyerythematous(red) area on amucous membrane,[2]that cannot be attributed to any otherpathology
MICRO: 90% of cases: Invasive carcinoma, in situ carcinoma, severe dysplasia (superficial multifocal carcinoma) 10% of cases: Minimal dysplasia Red color :
- Anatomo-clinical forms of oral cancer
CARCINOMA OF THE LIP: The most frequent Ulceration >1cm, 12-16 months old Location: Lower lip, M Upper lip, F
CARCINOMA OF THE TONGUE:
40% of all oral cancers (without the lips)
Nodule or painless ulceration
Location:
2/3 on the posterior margin
20% on the anterior-lateral and ventral surfaces of the tongue
4% on the dorsal surface of the base of the tongue (on syphilitic lesions)
The ones at the tongue base – the most malignant
MOUTH FLOOR CARCINOMA: 35% of oral cancers Growing frequency in women Predisposing factors : Leukoplakia, erythroplakia Secondary neoplasm
CARCINOMA OF THE CHEEK MUCOSA:
15% of oral cancers
At or under the occlusion line from the molar region
Rapidly metastasizing
GINGIVAL, ALVEOLAR CARCINOMA: 10% of oral cancers Location: posterior mandible On an area of keratosis In the beginning : Can mimic a dental inflammation
PALATE OR OROPHARYNX CARCINOMA:
Tonsillar region, posterior palate, base of tongue
- Spreading of oral cancer
SPREADING OF ORAL CANCER
INVASION OF ADJACENT TISSUES :
Invasion !!!
Under the tongue mucosa between muscle bundles, with a posterior orientation (difficult to detect during surgery)
In the mylohyoid and hyoglossus muscles (of the mouth floor): much more rare
In the submandibular space or behind the mylohyoid muscles –posterior tumors (of the glossotonsillar sulcus)
PERINEURAL INVASION :
Rare in the case of squamous carcinoma
Usually along the mandibular nerve
Invasion and expansion takes place along the nerve tract in both directions (cranial and distal)
Most frequent → intracranial expansion of the tumor
VASCULAR INVASION:
Invasion of lymph vessels - correlates with lymph node metastases
Invasion of the internal jugular vein – is not correlated with hematogenous metastases
Arteries – are rarely invaded, because of their elastic tissue
BONE INVASION : Facilitated by : Inferior dental canal Incisive foramen, palatine foramen More frequent in the mandible
LYMPH NODE METASTASES :
Difficult to appreciate clinically :
A large lymph node is not necessarily involved by metastases and a normal sized lymph node may contain metastases !!
Location:
Cancer of the tongue, mouth floor, alveolar ridge : metastases on the same side in submandibular, jugulodigastric and middle deep cervical lymph nodes
Cancer of the retromolar trigone : submandibular, jugulodigastric, middle and superior deep cervical and parapharyngeal lymph nodes
Cancer of the lips and tip of the tongue : submental and submandibular lymph nodes
Cancer of the median line (lips, mouth floor, tongue): bilateral cervical lymph nodes
- Xerostomia
XEROSTOMIA DEFINITION: Decreased or absent secretion of saliva → dry mouth syndrome CAUSES: Salivary gland aplasia Atresia/Obstruction of salivary ducts Aging Excessive smoking Oral breathing Radiation Sjögren syndrome (autoimmune) HIV infection Dehydration FAVORS: Oral candidosis Ascending infections of salivary glands (sialadenitis) Frequent and rapidly evolving caries, periodontitis, dental loss in both dentitions
- Mucocele
MUCOCELE:
CYSTIC LESION OF OBSTRUCTIVE ORIGIN:
Characteristic for minor salivary glands, rarely in major ones
MUCOCELE DUE TO EXTRAVASATION:
Def: retention of saliva in the surrounding connective tissue due to a traumatic rupture of the excretory canal of a salivary gland, which is:
Minor
Or major – in the case of ranula
- Sialolithiasis
SIALOLITHIASIS
At all ages, more frequent in adults
Formation of small «stones», called calculi or sialoliths, inside the salivary ducts
70-90% - submandibular glands
Rare – parotid, sublingual or minor glands
Deposits of Ca
COMPLICATIONS:
Obstruction → retention of saliva → favors ascending infection and CHRONIC SCLEROSING
- Necrotizing sialometaplasia
NECROTIZING SIALOMETAPLASIA
Benign destructive lesion which favors macroscopical and microscopical confusion with a squamous carcinoma
In minor salivary glands
75% in the posterior hard palate, 2/3 of the lesions are unilateral
Rarely – in lips, retromolar area of the tongue, parotid (8%), nose, maxillary sinus, larynx
PATHOGENESIS:
Local ischemia by trauma, injections in the dental region, maladapted prostheses, neighboring cysts and tumors, surgical procedures, allergy
- Inflammation of salivary glands
INFLAMMATION OF SALIVARY GLANDS
NOMENCLATURE: sialadenitis (inflam. of the gland), sialoangiitis (infl. of the ducts)
ACUTE POSTOPERATIVE PAROTIDITIS
Rare, in adults, unilateral/bilateral (20-25%)
At 2-20 days after surgery, with fever, trismus
After prolonged open mouth surgery – e.g. dental extraction
EVOLUTION:
Can fistulize to the skin
Can spread around the pharynx towards the mediastinum
Can cause thrombosis of the superior longitudinal sinus in the dura mater
CHRONIC SCLEROSING SIALADENITIS:
CAUSES: sialolithiasis
In adults, more frequent in males
MACROSCOPY/CLINICAL
Swelling and recurrent pain in a gland
Usually the submandibular gland, which has an increased volume and is tough – called KÜTNER’S TUMOR
MICROSCOPY:
In easy/medium cases:
Periductal and intralobular inflammation, with a moderate acinar atrophy
In severe cases:
Acinar destruction with fibrous replacement + ductal ectasia
- Glandular cheilitis
is characterized by progressive enlargement and eversion of the lower labial mucosa that results in obliteration of the mucosal-vermilion interface. With externalization and chronic exposure, the delicate lower labial mucous membrane is secondarily altered by environmental influences, leading to erosion, ulceration, crusting, and, occasionally, infection.
- Pleiomorphic adenoma
PLEIOMORPHIC ADENOMA (mixed tumor of the salivary glands) = is a common benign salivary gland neoplasm characterised by neoplastic proliferation of parenchymatous glandular cells along with myoepithelial components, having a malignant potentiality. It is the most common type ofsalivary gland tumorand the most common tumor of theparotid gland.
- Warthin’s tumor
WARTHIN’S TUMOR = is abenigncystictumorof thesalivary glandscontaining abundantlymphocytesandgerminal centers. Itsetiologyis unknown, but there is a strong association with cigarettesmoking. Smokers are at 8 times greater risk of developing Warthin’s tumor than the general population
4-11% of salivary gland tumors
Exclusively in the parotid, the second most frequent tumor of the parotid
EVOLUTION:
Benign
Sometimes the lymphoid component can become malignant → lymphoma
A carcinoma may develop on this tumor
- Mucoepidermoid carcinoma
MUCOEPIDERMOID CARCINOMA = Mucoepidermoid carcinomais the most common type ofsalivary glandmalignancy in adults. Mucoepidermoid carcinoma can also be found in other organs, as bronchi, lacrimal sac[1]and thyroid. Presents as painless, slow-growing mass that is firm or hard. Most appear clinically as mixed tumors. This tumor is not encapsulated and is characterized by squamous cells, mucus-secreting cells, and intermediate cells.
- Adenoid cystic carcinoma
ADENOID CYSTIC CARCINOMA (formerly called cylindroma) = Adenoid cystic carcinoma(AdCC) is a rare type ofcancerthat can exist in many different body sites. It most often occurs in the areas of the head and neck, in particular thesalivary glands. This tumor is generally well-differentiated and slow growing.
3-10% of salivary gland tumors 70% in minor glands 30% in major glands (especially the submandibular, where it is the most frequent malignant tumor) MACRO: Painful nodule First mobile, then fixed EVOLUTION: Metastasis: rare and late
- Coronoid hyperplasia, torus palatinus and torus mandibularis
CORONOID HYPERPLASIA = Coronoid hyperplasia is a rare condition which is macroscopically characterized by an increase in the dimensions of the coronoid process resulting from an abnormal bony elongation of histologically normal bone. Unilateral cases are more frequent than bilateral ones and can recognize a number of etiological factors, such as exostoses, osteochondroma, traumatic events, inflammatory reactions, neoplasia.
CLINICAL: the hyperplastic coronoid process presses on the zygomatic bone and prevents the opening of the mandible, which deviates towards the lesion
Progressive limitation in opening of the mouth
TORUS PALATINUS= is abonyprotrusion on thepalate. Palatal tori are usually present on the midline of the hard palate.[1]Most palatal tori are less than 2cm in diameter, but their size can change throughout life.
TORUS MANDIBULARIS= is abonygrowthin themandiblealong the surface nearest to thetongue. Mandibular tori are usually present near thepremolarsAND above the location of themylohyoid muscle’s attachment to the mandible.
- Osteoradionecrosis
OSTEORADIONECROSIS = is a condition of nonvital bone in a site of radiation injury. ORN can be spontaneous, but it most commonly results from tissue injury. The absence of reserve reparative capacity is a result of the prior radiation injury.
5-13% of the people with head and neck radiation therapy
Dose: 4000-8000 R
Latency: months → years
Yellowish, with sequestrums (fragments of necrotic bone inside the bone marrow), hemorrhage ± osteomyelitis (infection of bone and its marrow)
- Rickets
RICKETS= Ricketsis defective mineralization of bones beforeepiphyseal closurein immature mammals due to deficiency or impaired metabolism ofvitaminD,phosphorusorcalcium,potentially leading to fractures and deformity. Rickets is among the most frequentchildhood diseasesin many developing countries.
Maxillary prognathism, ogival hard palate
Mandible like a boxer
Teeth:
Temporary incisors and canines : microdontia
Both dentitions: late eruption, in an abnormal order
Permanent teeth developed in the first two years of life: enamel and dentin hypoplasia
- Cherubism
CHERUBISM= Cherubismis a rare genetic disorder that causes prominence in the lower portion of the face.
AD, starts in infants
Involves
Mandibular angle, in a symmetrical manner: chubby aspect
In severe cases, also the upper jaw - symmetrical
- Acute suppurative and chronic osteomyelitis
CUTE SUPPURATIVE OSTEOMYELITIS = Osteomyelitis is an inflammatory reaction of bone to infection which originates from either a tooth, fracture site, soft tissue wound or surgery site. The dental infection may be from a root canal, a periodontal ligament or an extraction site. Suppurative osteomyelitis can involve all three components of bone: periosteum, cortex, and marrow. Acute osteomyelitis is similar to an acute primary abscess in that the onset and course may be so rapid that bone resorption does not occur.
MACROSCOPY/CLINICAL:
Pain, trismus, fever, altered general condition
Redness and swelling of soft tissues
EVOLUTION: if it’s not quickly and radically resorbed – it becomes chronic
CHRONIC SUPPURATIVE OSTEOMYELITIS :
Follows an acute osteomyelitis
Sometimes directly
On and off evolution (remissions and recurrences with sequestrum discharge): 20-25 years
- Dentigerous cyst and eruption cyst
DENTIGEROUS (FOLICULAR) CYST = Adentigerous cystorfollicular cystis anodontogeniccyst- thought to be of developmental origin - associated with the crown of an unerupted (or partially erupted) tooth. The cyst cavity is lined byepithelial cellsderived from the reducedenamelepithelium of the tooth forming organ. Histologically a normal dental follicle is lined by enamel epithelium, whereas a dentigerous cyst is lined by non-keratinized stratified squamous epithelium.
ERUPTION CYST= aneruption cyst, oreruption hematoma, is a bluishswellingthat occurs on the soft tissue over an eruptingtooth. It is usually found in children.
- Nasopalatine and nasolabial duct cyst
NASOPALATINE DUCT CYST = Thenasopalatine duct cyst(abbreviatedNPDC) occurs in the median of the palate, usually anterior to first molars. It often appears between the roots of the maxillary central incisors. It is usually asymptomatic, but may sometimes produce an elevation in the anterior portion of the palate.
Rare Age: 40-60 , M>F On the median line of the anterior maxilla Variants: Nasopalatine cyst Incisive canal cyst Median palatine cyst Palatine papilla cyst Median alveolar cyst No symptoms
NASOLABIAL DUCT CYST = Thisnasolabial cyst, also known as anasoalveolar cyst, is located superficially in the soft tissues of the upper lip. Unlike most of the otherdevelopmental cysts, the nasolabial cyst is an example of an extraosseous cyst, one that occurs outside of bone.
Rare
In soft tissues: rests of nasolacrimal canal
- Ameloblastoma
AMELOBLASTOMA = is a rare,benign tumorofodontogenicepithelium much more commonly appearing in thelower jawthan theupper jaw. While thesetumorsare rarelymalignantormetastatic, and progress slowly, the resultinglesionscan cause severe abnormalities of thefaceandjaw.
The most frequent odontogenic tumor (equal to all the others combined)
- Odontoma
ODONTOMA = Anodontomais abenign tumour[1]ofodontogenicorigin (i.e. linked totooth development).[2]Specifically, it is a dentalhamartoma, meaning that it is composed of normaldental tissuethat has grown in an irregular way.
Dental tissue hamartomas (malformations)
Contain denticles with a normal proportion between enamel, dentin and pulp
10-20 years old
More frequent in the maxilla (anterior) than in the mandible (posterior)
COMPOUND ODONTOMA = Acompoundodontoma still has the three separate dental tissues (enamel, dentin and cementum), but may present a lobulated appearance where there is no definitive demarcation of separate tissues between the individual “toothlets” (or denticles). It usually appears in the anteriormaxilla.
COMPLEX ODONTOMA = Thecomplexodontoma is unrecognizable as dental tissues, usually presenting as a radioopaque area with varying densities. It usually appears in the posterior maxilla or in themandible. Osteosarcoma is the most commonhistologicalform of primarybonecancer.It is most prevalent in children and young adults.
- Osteosarcoma
STEOSARCOMA = Osteosarcomais a cancerousbonetumor.Specifically, it is an aggressivemalignantneoplasm—arising from primitive transformed cells ofmesenchymalorigin (and thus asarcoma)–that exhibitsosteoblasticdifferentiation and produces malignantosteoid. Osteosarcoma is the most commonhistologicalform of primarybonecancer.It is most prevalent in children and young adults.
- Malformations of the temporomandibular joint
MANDIBULAR CONDYLE APLASIA = Rare Uni/bilateral Unilateral Facial asymmetry Malocclusion When the mouth opens, the mandible deviates towards the involved side
HYPOPLASIA OF THE MANDIBULAR CONDYLE : CONGENITAL: Mandibulofacial dysostosis Oculoauriculovertebral syndrome Hemifacial microstomia SECONDARY: Trauma Irradiation Arthritis Uni/Bilateral Less prominent signs than in the case of aplasia
HYPERPLASIA OF THE MANDIBULAR CONDYLE : ETIOLOGY: Respiratory, endocrine disturbances Trauma Proliferative osteomyelitis Macro: Prognathism Deviation towards the healthy side Facial asymmetry Malocclusion Sometimes: compensatory enlargement of the maxilla
- Traumatic lesions of the TMJ
LUXATION:
Dislocation of the TMJ
The condyle’s head is displaced forward, above the articular eminence
Blocks movements of the mandible
Cannot be reduced voluntarily (in case you succeed, you actually get a subluxation)
Causes: Sudden and very wide opening of the mouth:
FRACTURES OF THE MANDIBULAR CONDYLE:
Traumatic
Limitation of mandibular movement, pain, swelling
At the condyle’s head or neck
The head is in the cavity or anterior and median to it (infra-temporal)
Neglected fractures –> facial deformities
LESIONS OF THE ARTICULAR MENISCUS :
Produced by a malocclusion
Starts suddenly after a trauma (ex. wide opening of the mouth)
Pain in the TMJ, ears, teeth and paresthesia in the tongue
A slight coarse sound
Blockage with the mouth closed
ANKYLOSIS: permanent blockage of the joint
- Rheumatoid arthritis of the TMJ
RHEUMATOID ARTHRITIS = Rheumatoid arthritis(RA) is a chronic,systemicinflammatory disorderthat primarily affectsjoints.[1]It may result in deformed andpainfuljoints, which can lead to loss of function.
Chronic synovitis which leads to ankylosis
- Pyogenic granuloma, giant cell peripheral granuloma
PYOGENIC GRANULOMA = is a vascular lesion that occurs on both mucosa and skin, and appears as anovergrowthof tissue due toirritation,physical traumaorhormonal factors.
DEF.:
A pseudotumor produced due to irritation and trauma in the presence of a special oral microbial flora
More frequent
In children, adolescents and pregnant women
Appears in the first semester of pregnancy, grows until birth and then decreases in size = PREGNANCY TUMOR
GIANT CELL PERIPHERAL GRANULOMA (EPULIS WITH MYELOPLAXES) DEF.: Gingival pseudotumor due to a deep gingival irritation PREDISPOSING FACTORS: Dental extraction, dental fracture Periodontal treatments Irritation given by prostheses Chronic infections EVOLUTION: Slowly, towards fibrosis
