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INTRODUCTION TO ORAL AND DENTAL DISEASES
DR.Rami ALJUAIDI
ORAL MUCOSA
The oral mucoua is the mucous membrane that covers
all oral structures except the clinical crowns of the teeth.
It is composed of two layers: (1) the stratified squamous
epithelium and (2) supporting connective tissue, called
the lamina propria. The epithelium may be keratinized,
parakeratinized, or nonkeratinized dependingupon its location .
The lamina propria varies in thickness The oral mucosa may be
divided into three majorfunctional types: (1) masticatory
mucosa, (2) lining orreflective mucosa, and (3)
specialized mucosa.
The masticatory mucosa is composed of the free and attached gingiva and the mucosa
of the hard palate. The epithelium of these tissues
is keratinized, and the lamina propria is a dense, thick,
firm connective tissue containing collagenous fibers.
The dense lamina propria ofthe attached gingiva is connected to the
cementumand the periosteum of the bony alveolar process
The lining or reflective mucosa covers the inside of thelips, cheek, vestibule, lateral surfaces of the alveolarprocess (except the mucosa of the hard palate), floor ofthe mouth, soft palate, and inferior surface of thetongue. Lining mucosa is a thin, movable tissue with arelatively thick, nonkeratinized epithelium and a thinlamina propria. The submucosa is composed mostly ofthin, loose connective tissue with muscle and collagenousand elastic fibers, with different areas varyingfrom one another in their structure. The junction of liningmucosa with masticatory mucosa is the mucogingivaljunction, located at the apical border of the attached gingivafacially and lingually in the mandibular arch andfacially in the maxillary arch ..
the specialized mucosa covers the dorsum of the tongue and the taste
buds. The epithelium is nonkeratinized
except for the covering of the dermal filiform
papillae
The bar in the image shows you the thickness of the stratified squamous epithelium. The layers underneath it are composed mainly
of connective tissue and muscle .
The cells of the outermost layers of
the stratified squamous epithelium are not all squamous (flat). some of
the cells seem to be separating from the surface of the tissue. This is called sloughing and is a normal
process in epithelial tissues that form coverings and linings,
especially the stratified tissues .
Keratine covers the dry areas of the skin whilest the moist areas of the
skin are not keratinized
The epidermis is the outermost layer of the skin,[1] composed of
terminally differentiated stratified squamous epithelium,[2] acting as the body's major barrier against an
inhospitable environment.[3] It is the thinnest on the eyelids at .05 mm and the thickest on the palms and
soles at 1.5 mm
Cellular componentsThe epidermis is [avascular], nourished by
[diffusion] from the [dermis], and composed of four types of cells,i.e: keratinocytes,
melanocytes, Langerhans cells, and the Merkel cells.[1] Keratinocytes are the major
constituent, constituting 95% of the epidermis.[2] . The melanocyte produces
pigment (melanin), the Langerhans' cell is the frontline defense of the immune system
in the skin, and the Merkel's cell's function is not clearly known .
LayersThe epidermis is composed of 4-5
layers depending on the region of skin being considered. Those layers in
descending order are the stratum corneum, stratum lucidum,
stratum granulosum, stratum spinosum, and stratum basale
.[3] The term Malpighian layer refers to both the basal and spinosum layers
Cellular kineticsThe stratified squamous epithelium is maintained
by cell division within the basal layer. Differentiating cells slowly displace outwards through the stratum spinosum to the stratum
corneum, where anucleate corneal cells are continually shed from the surface
(desquamation). In normal skin the rate of production equals the rate of loss,[2] taking about two weeks for a cell to migrate from the basal cell
layer to the top of the granular cell layer, and an additional two weeks to cross the stratum
corneum
keratinisation - organic process by which keratin is deposited in cells
parakeratosis
the persistence of nuclei in the
stratum corneum keratin layer of stratified squamous epithelium .
Precancerous LesionsWhat is a precancerous lesion?
A precancerous lesion is a change in some areas of your skin that carries the risk of turning into skin cancer. It is
a preliminary stage of cancer. These precancerous lesions can have several causes; UV radiation, genetics,
exposure to such cancer-causing substances (carcinogens) as arsenic, tar or x-ray radiation.
Because precancerous lesions can turn into skin cancer and since skin cancer can possibly lead to death it is
very important to catch skin cancer at an early stage. If you discover any suspicious lesion take it
seriously and seek the advice of a dermatologist.
Oral and MaxillofacialPathology
.GENERALOral mucosa has the same susceptibility to
pathological change as does other covering tissue. Common abnormalities of the skin
and the gastrointestinal tract may evidence themselves on oral mucosa. Local, focal oral
mucosal lesions, generalized mucosal involvement, or intraoral lesions associated with a systemic problem may be caused by bacterial, fungal, or viral organisms. Benign
or malignant lesions must always be considered when examining a patient's
mouth.
Elementary lesions of the oral mucosaDiseases that manifest themselves on the oral mucosa generally
produce tissue morphological alterations as clinical signs that are so characteristic, that they have been classified as primitive elementary lesions. Many of these lesions do not retain their
original appearance due to causes such as: traumatism, mastication, maceration, movement of the tissues, and time
itself; the lesions thus derived from these primitive or primary ones are known as secondary lesions. This labelling is important
in terms of order of appearance but not clinical importance, since in many cases these lesions are as useful as the primary ones to
help establish a diagnosis.The primitive lesions that occur most frequently, both on skin
and mucosa are: spots, papules, nodules, vesicles, blisters, pustules, keratosis, warts, tubercules, hives and tumors.
The most common secondary lesions of the oral cavity are: erosions, fissueas or cracks, ulcers, ulcerations, scabs, scars y
desquamations."Elementary lesions are like the letters of the alphabet.
Without a knowledge of them you cannot learn the language of stomatology". David Grinspan
VESICLEA vesicle is a circumscribed,
superficial elevation on the skin or mucous membrane containing fluid
(serum, plasma, or blood). If the vesicle opens, it becomes an ulcer
(an inflammatory loesin
ULCER (Figure 1- 7)An ulcer is an open sore of a superficial nature extending
below the covering epithelial surface. The base of an ulcer is composed of granulation tissue resulting from initial
healing. A secondary infection may develop in an ulcer, resulting in delay of the healing and repair process. A
common cause of oral ulceration is trauma, which might even be a result of toothbrush injury. Irritation from a rough
or broken tooth surface can also result in ulceration. Some ulcers start with vesicle formation. This painful ulceration
on the lateral border of the tongue represents a nonspecific response to tissue injury. The cause of an ulcer must be determined and appropriate treatment initiated. Normal
healing will often result without use of medication
SpotsA spot is just a change of coloration of the
oral mucosa, which is not elevated. They occur very frequently. They are primarily
constituted by variations of hematologic or melanocitic pigments, but also by the organism’s own pigments or external ones. Structural changes of the soft
tissues also produce changes in coloration.
White spots due to:Lichen Leukoplakia on the oral mucosa
Brown spots due to:Pigmentation in AIDS Racial pigmentationFixed pigmented erythema
Red spots due to:PúrpuraFlat hemangioma on skin and
oral mucosa
Spots due to foreign pigments:Due to ballpoint pen
Vesicles, bullae (blisters) and pustulesVesicles, bullae and pustules are superficial lesions with a
liquid content. The two first ones can only secondarily become pustulent by overlaying infections. The pustule initially contains pus and is very rare in th oral mucosa.
These lesions are rarely found intact when occuring inside the mouth, since masticatory trauma ruptures them rather
easily.Vesicles are primarily formed by spongiosis of an eczema or
by a ballooning and reticular degeneration during viral infections.
The mechanism by which a blister is formed is fundamental to confirm the diagnosis of the underlying disease. Blisters
may be intraepithelial, by acantholysis of the spiny cells, as occurs in the different types of pemphigus, or subepidermal
separating the connective tissue from the epithelium as occurs in the pemphigoidal lesions: Duhring’s disease,
erythema multiforme, and bullous pemphigoid.
Vesicles due to:Labial herpesCoalescence of vesicles during labial
herpesHerpes zoster
Vesiculopustular lesions due to:Varicella
Bullae (blisters) due to:Pemphigus on skinPemphigus blistered “roof”Pemphigus on the gingiva
Pustules due to:Impétigo
Pigmented oral lesions Most red oral lesions are
inflammatory in nature, but some are potentially
malignant, especially erythroplasia .
Causes of red lesions
Widespread redness Localised red patches
Candidiasis Candidiasis Iron deficiency Erythroplasia
Avitaminosis B Purpura Irradiation mucositis Telangiectases
Lichen planus Angiomas Mucosal atrophy Kaposi's sarcoma
Polycythaemia Burns Lichen planus
Lupus erythematosus Avitaminosis
Erythroplasia (erythroplakia) Erythroplasia is a rare, isolated, red, velvety lesion that
affects patients mainly in their 60s and 70s. It usually involves the floor of the mouth, the ventrum of the tongue,
or the soft palate. This is one of the most important oral lesions because 75-90% of lesions prove to be carcinoma or
carcinoma in situ or are severely dysplastic. The incidence of malignant change is 17 times higher in erythroplasia
than in leucoplakia. Erythroplasia should be excised and sent for histological examination
Erythroplasia is an isolated red lesion that typically occurs in elderly people
It is usually dysplastic or malignant and is bestremoved
Erythematous candidiasis
Erythematous candidiasis may complicate treatment with corticosteroids or antimicrobials and cause widespread erythema and
soreness of the oral mucosa, sometimes with thrush. It may also occasionally be seen in HIV infection, xerostomia, diabetes, and in
people who smoke .Red persistent lesions are especially noticeable on the palate and
tongue. Median rhomboid glossitis (central papillary atrophy) is a red depapillated rhomboidal area in the centre of the tongue dorsum, now
believed to be associated with candidiasis. Biopsy may show pseudoepitheliomatous hyperplasia, but the condition is not potentially
malignant .ManagementErythematous candidiasis may respond to stopping
smoking and antifungal agents (usually fluconazole) .
Denture induced stomatitis (denture sore mouth)
This is a common form of mild chronic erythematous candidiasis, usually seen after middle age as erythema limited to the area beneath an upper denture. The fitting surface of the denture is infested
mainly with Candida albicans. Despite its name, this condition is rarely sore,
though angular stomatitis may be associated. Patients are usually
otherwise healthy.
Factors that predispose to denture induced stomatitis include wearing dentures (especially
through the night), poor oral and denture hygiene, xerostomia, and carbohydrate-rich diets. It is not caused by allergy to the denture material .
Management includes
Denture stomatitis occurs mainly when Candida proliferate beneath and infest the
dentureIt may be asymptomatic but may be
associated with angular stomatitisDenture wearing should be minimised and
the infection eradicated
Eradicating infection by soaking dentures overnight in chlorhexidine or 1% (v/v) hypochlorite solution then using miconazole denture lacquer.
Metal dentures should not be soaked in hypochlorite as they may discolour
Using miconazole gel (5 ml), nystatin pastilles (100 000 units), or amphotericin lozenges (10 mg) in the mouth four times daily for up to
one month Using systemic fluconazole 50 mg daily for resistant cases Adjustment of the dentures .Other red lesions
Petechiae are usually caused by trauma or suction but may also be seen in thrombocytopenia, amyloidosis, localised oral purpura, or
scurvy. Telangiectasia may be a feature of hereditary haemorrhagic telangiectasia or systemic sclerosis .
Non keratotic white lesions
Habitual cheek bitingBurnsUremic stomatitisRadiation mucositisKoplik.s spots
Cheek Chewing
White lesions of the oral tissues may result from chronic irritation
due to repeated sucking, nibbling, or chewing.These insults result in the traumatized area becoming
thickened,scarred, and paler than the surrounding tissues. Cheekchewing is most commonly seen in people who are understress or in psychological situations in which cheek and lipbiting become habitual.Most patients with this condition aresomewhat aware of their habit but do not associate it withtheir lesions .
The white lesions of cheek chewing may sometimes
be confused with other dermatologic disorders involving
the oral mucosa, which can lead to misdiagnosis .
Prevalence rates ranging from 0.12 to 0.5% have been reported
TYPICAL FEATURES
The lesions are most frequently found bilaterally on the posteriorbuccal mucosa along the plane of occlusion. They maybe seen in combination with traumatic lesions on the lips ortongue. Patients often complain of roughness or small tags oftissue that they actually tear free from the surface. This producesa distinctive clinical presentationThe lesions are poorly outlined whitish patches that may beintermixed with areas of erythema or ulceration. The occurrenceis twice as prevalent in females and three times morecommon after the age of 35 years.The histopathologic picture is distinctive and includeshyperparakeratosis and acanthosis. The keratin surface is usuallyshaggy and ragged with numerous projections of keratinthat demonstrate adherent bacterial colonies.When the lesionis seen on the lateral tongue, the clinical and histomorphologicfeatures mimic those of oral hairy leukoplakia.
TREATMENT AND PROGNOSISSince the lesions result from an unconscious and/or
nervoushabit, no treatment is indicated. However, for those
desiringtreatment and unable to stop the chewing habit, a plasticocclusal night guard may be fabricated. Isolated tongueinvolvement requires further investigation to rule out oralhairy leukoplakia especially when appropriate risk factors
forinfection with human immunodeficiency virus (HIV) are
present.Differential diagnosis also includes chemical burns,and candidiasis.
Morsicatio buccarum represented by a frayed macerated irregular leukoplakic
area in the cheek.
burnsChemical Injuries of the Oral MucosaTransient nonkeratotic white lesions of the oral mucosa areoften a result of chemical injuries caused by a variety of
agentsthat are caustic when retained in the mouth for long
periodsof time, such as aspirin, silver nitrate, formocresol, sodiumhypochlorite, paraformaldehyde, dental cavity varnishes,
acidetchingmaterials, and hydrogen peroxide. The whitelesions are attributable to the formation of a superficialpseudomembrane composed of a necrotic surface tissue
andan inflammatory exudate.
burns
Aspirin burn, creating a pseudomembranous
necroticwhite area.
Diffuse slough of marginal gingivae due to misuse of commercial mouthwash
TYPICAL FEATURES
The lesions are usually located on the mucobuccal fold areaand gingiva. The injured area is irregular in shape, white,
coveredwith a pseudomembrane, and very painful. The area ofinvolvement may be extensive.When contact with the tissue isbrief, a superficial white and wrinkled appearance withoutresultant necrosis is usually seen. Long-term contact (usuallywith aspirin, sodium hypochlorite, phenol, paraformaldehyde,etc) can cause severer damage and sloughing of the necroticmucosa. The unattached nonkeratinized tissue is more
commonlyaffected than the attached mucosa.
TREATMENT AND PROGNOSIS
The best treatment of chemical burns of the oral cavity is prevention.
Children especially should be supervised while takingaspirin tablets, to prevent prolonged retention of the agent inthe oral cavity. The proper use of a rubber dam duringendodontic procedures reduces the risk of iatrogenic chemicalburns. Most superficial burns heal within 1 or 2 weeks. Aprotective emollient agent such as a film of methyl cellulosemay provide relief. However, deep-tissue burns and necrosismay require careful débridement of the surface, followed byantibiotic coverage. In case of ingestion of caustic chemicals oraccidental exposure to severely corrosive agents, extensive
scarringthat may require surgery and/or prosthetic rehabilitationmay occur
Uremic stomatitisIt is a rarely reported oral mucosal
disorder possibly associated with longstanding uremia Four of 300 patients
with uremia were observed to have probable uremic stomatitis, The clinical features of uremic stomatitis are poorly
defined and are rarely detailed in relevant textbooks
Radiation mucositisOral tissue damage and mucositis pain
can be a significant problem for patients undergoing cancer therapy. The frequency and severity of these problems can vary significantly with
the type of therapy and from patient to patient. While oral complications
primarily are associated with discomfort and interference with oral
function, in patients who are also immunocompromised or debilitated, these complications can become life
threatening
Koplik's spotsand when found in(mucosa are found on the,
combination with rash, cough, are diagnostic for measles.[1]
They are small, irregular red spots, each with a minute bluish white speck in the center, seen on the lingual and buccal
mucosa (the inside ofthe cheek and tongue) and are pathognomonicof early stages of
measles.They often appear a few days before the
rash arrives and can be a useful sign to look for children known to be exposed to the in
measles virus.