Oral Pathology/Medicine revision Flashcards

1
Q
A

Pseudo- membranous Candidiasis:

The best recognized form of candidal infection is pseudo- membranous candidiasis. Also known as thrush.

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2
Q

Pseudo- membranous Candidiasis:

Characteristics:

A

Is characterized by the presence of adherent white plaques that resemble cottage cheese** or **curdled milk on the oral mucosa

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3
Q

Pseudo- membranous Candidiasis:

White plaques:

A

The white plaques are composed of tangled masses of hyphae, yeasts, desquamated epithelial cells, and debris. Scraping them with a tongue blade or rubbing them with a dry gauze sponge can remove these plaques. The underlying mucosa may appear normal or erythematous.

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4
Q

Pseudo- membranous Candidiasis:

Initiated by:

A
  • May be initiated by exposure of the patient to broad-spectrum antibiotics (thus eliminating competing bacteria) or by impairment of the patient’s immune system (leukemic patients or those infected with HIV).
  • Infants may also be affected, ostensibly because of their underdeveloped immune systems
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5
Q

Pseudo- membranous Candidiasis:

Symptoms:

A

Symptoms, if present at all, are usually relatively mild, consisting of a burning sensation of the oral mucosa or an unpleasant taste in the mouth, variably described as salty or bitter

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6
Q
A

Acute atrophic candidiasis:

  • Acute atrophic candidiasis, or “antibiotic sore mouth,” typically follows a course of broad- spectrum antibiotic therapy.
  • Patients often complain that the mouth feels as if a hot beverage had scalded it. This burning sensation is usually accompanied by a diffuse loss of the filiform papillae of the dorsal tongue, resulting in a reddened, “bald” appearance of the tongue. Burning mouth syndrome frequently manifests with a scalded sensation of the tongue; however, the tongue appears normal in that condition.
  • Patients who suffer from xerostomia for any reason (e.g., pharmacologic, postradiation therapy, or Sjögren syndrome) have an increased prevalence of erythematous candidiasis that is commonly symptomatic as well
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7
Q

Other forms of erythematous candidiasis:

A

Other forms of erythematous candidiasis are usually asymptomatic and chronic. Included in this category is the condition known as central papillary atrophy of the tongue, or median rhomboid glossitis. In the past, this was thought to be a developmental defect of the tongue, occurring in 0.01% to 1.00% of adults.

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8
Q

Central papillary atrophy:

A
  • appears as a well- demarcated erythematous zone that affects the midline, posterior dorsal tongue and often is asymptomatic.
  • The erythema is due to the loss of the filiform papillae in this area.
  • The lesion is usually symmetrical, and its surface may range from smooth to lobulated.
  • Often the mucosal alteration resolves with antifungal therapy, although occasionally only partial resolution can be achieved.
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9
Q

chronic multifocal candidiasis:

A

Some patients with central papillary atrophy may also exhibit signs of oral mucosal candidal infection at other sites. This presentation of erythematous candidiasis has been termed chronic multifocal candidiasis. In addition to the dorsal tongue, the sites that show involvement include the junction of the hard and soft palate and the angles of the mouth. The palatal lesion appears as an erythematous area that, when the tongue is at rest, contacts the dorsal tongue lesion, resulting in what is called a “kissing lesion” because of the intimate proximity of the involved areas.

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10
Q
A

chronic multifocal candidiasis

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11
Q

Denture Stomatitis:

Definition:

A

Is as a form of erythematous candidiasis (chronic atrophic candidiasis)

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12
Q

Denture Stomatitis:

Characteristics:

A

Is characterized by varying degrees of erythema, sometimes accompanied by petechial hemorrhage, localized to the denture- bearing areas of a maxillary removable dental prosthesis

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13
Q

Denture Stomatitis:

The process:

A

The process is rarely symptomatic. Usually the patient admits to wearing the denture continuously, removing it only periodically to clean it. Whether this represents actual infection by C. albicans or is simply a tissue response by the host to the various microorganisms living beneath the denture remains controversial

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14
Q

Denture Stomatitis:

Clinician’s approach:

A

The clinician should also rule out the possibility that this reaction could be caused by improper design of the denture (which could cause unusual pressure on the mucosa), allergy to the denture base, or inadequate curing of the denture acrylic

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15
Q
A

Denture Stomatitis

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16
Q

Denture stomatitis:

Medications:

A
  • Nystatin
  • fluconazole
  • itraconazole
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17
Q

Histoplasmosis:

Type of infection:

A
  • Histoplasmosis, the most common systemic fungal infection
  • Humid areas with soil enriched by bird or bat excrement are especially suited to the growth of this organism.
  • Most individuals who become exposed to the organism are relatively healthy
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18
Q

Acute histoplasmosis:

A
  • is a self-limited pulmonary infection that probably develops in only about 1% of people who are exposed to a low number of spores. With a high concentration of spores, as many as 50% to 100% of individuals may experience acute symptoms.
  • These symptoms (e.g., fever, headache, myalgia, nonproductive cough, and anorexia) result in a clinical picture similar to that of influenza
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19
Q

Chronic histoplasmosis:

A
  • also primarily affects the lungs, although it is much less common than acute histoplasmosis.
  • Affects older, emphysematous, white men or immunosuppressed patients.
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20
Q

Disseminated histoplasmosis:

A
  • is even less common. Is characterized by the progressive spread of the infection to extra- pulmonary sites.
  • It usually occurs in either older, debilitated, or immunosuppressed patients.
  • Tissues that may be affected include the spleen, adrenal glands, liver, lymph nodes, gastrointestinal tract, central nervous system (CNS), kidneys, and oral mucosa
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21
Q

Disseminated histoplasmosis:

Affected sites:

A

Most oral lesions occur with the disseminated form of the disease. The most commonly affected sites are the tongue, palate, and buccal mucosa. The condition usually appears as a solitary, variably painful ulceration of several weeks’ duration; however, some lesions may appear erythematous or white with an irregular surface. The ulcerated lesions have firm, rolled margins, and they may be indistinguishable clinically from a malignancy

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22
Q

histoplasmosis:

Diagnosis:

A

The diagnosis of histoplasmosis can be made by histopathologic identification of the organism in tissue sections or by culture

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23
Q

histoplasmosis:

Histopathologic Features:

A

Microscopic examination of lesional tissue shows either a diffuse infiltrate of macrophages or, more commonly, collections of macrophages organized into granulomas. Multinucleated giant cells are usually seen in association with the granulomatous inflammation

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24
Q

Histoplasmosis:

Treatment:

A
  • Disseminated histoplasmosis occurring in an immunesuppressed individual is a very serious condition that results in death in 80% to 90% of patients if they remain untreated
  • Amphotericin B is indicated for such patients; once the life- threatening phase of the disease is under control, daily itraconazole is necessary for 6 to 18 months
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25
Q

Aspergillosis:

Forms:

A

Is characterized by noninvasive and invasive forms.

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26
Q

Noninvasive aspergillosis:

A

usually affects a normal host, appearing either allergic reaction or a cluster of fungal hyphae.

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27
Q

Localized invasive infection:

A

Localized invasive infection of damaged tissue may be seen in a normal host, but a more extensive invasive infection is often evident in the immunocompromised patient.

The clinical manifestations of aspergillosis vary, depending on the host immune status and the presence or absence of tissue damage

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28
Q

Aspergillosis:

Symptoms:

A
  • It maybe encountered after tooth extraction or endodontic treatment, especially in the maxillary posterior segments.
  • Tissue damage predisposes the sinus to infection, resulting in symptoms of localized pain and tenderness accompanied by nasal discharge.
  • Immunocompromised patients are particularly susceptible to oral aspergillosis, and some investigators have suggested that the portal of entry may be the marginal gingiva and gingival sulcus.

*

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29
Q

Aspergillosis:

Treatment:

A
  • Treatment depends on the clinical presentation
  • For immunocompetent patients with a noninvasive aspergilloma, surgical débridement may be all that is necessary
  • For localized invasive aspergillosis in the immunocompetent host, débridement followed by antifungal medication is indicated
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30
Q
A

Aspergillosis

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31
Q

Syphilis:

Causative agent:

A
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32
Q

Syphilis:

Hosts:

A

Humans are the only proven natural host for syphilis

Syphilis itself can cause a series of conditions affecting various systems of the body, some of which can be fatal. Moreover, it can increase individual’s susceptibility to HIV infection. Therefore, prevention and treatment of syphilis are still in urgent need

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33
Q

Syphilis:

Oral lesions:

A

Oral lesions are mostly seen at the stage of secondary syphilis, although they may be present in all stages

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34
Q

Primary syphilis:

Characteristics:

A

Is characterized by the chancre

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35
Q

Primary syphilis:

Chancre:

A
  • begins as papular lesion that develop a central ulceration
  • painless ulcer with smooth surface, raised borders, indurated margins
  • develops at the site of inoculation
  • becoming clinically evident 3 to 90 days after the initial exposure
  • 85% arise in the genital areas, 10% are anal, 4% are oral, and the remaining 1% is discovered in other extragenital locations
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36
Q

Primary syphilis:

Chancre:

If untreated:

A

If untreated, then the initial lesion heals within 3 to 8 weeks

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37
Q

Primary syphilis:

Oral lesions:

A

Oral lesions are seen most commonly on the lip, but other sites include the buccal mucosa, tongue, palate, gingiva, and tonsils

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38
Q

Mouth-site of primary syphilis:

A
  • The mouth, is rarely the site of primary syphilis, and because of its transient nature, the oral ulceration of primary syphilis often goes unnoticed by the patient or by any unsuspicious clinician.
  • Moreover the lesions of primary disease may be confused with traumatic ulceration, squamous cell carcinoma, and non-Hodgkin’s lymphoma
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39
Q
A

Chancre

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40
Q

Secondary Syphilis:

Discovered:

A

Is discovered 4 to 10 weeks after the initial infection

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41
Q

Secondary Syphilis:

Causative agent-features:

A

The features of secondary syphilis reflect the hematogenous spread of T. pallidum

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42
Q

Secondary Syphilis:

Resolution:

A
  • Multiple lesions are typical of secondary syphilis.
  • Spontaneous resolution usually occurs within 3 to 12 weeks; however, relapses may occur during the next year
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43
Q

Secondary Syphilis:

Rash:

A
  • painless, maculopapular cutaneous, which is widespread and can even affect the palmar and plantar areas.
  • May result in areas of scarring and hyperpigmentation or hypopigmentation, it heals without scarring
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44
Q
A
  • Secondary Syphilis
  • Rash
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45
Q

Oral lesions associated with secondary syphilis:

A
  • could be diverse and nonspecific, often clinically and histologically mimicking other oral diseases, such as multiple oral nodules, leukoplakia and pemphigus vulgaris
  • The rash also may involve the oral cavity and appear as red, maculopapular areas
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46
Q

secondary syphilis:

mucous patches:

A
  • In addition, roughly 30% of patients have focal areas of intense exocytosis and spongiosis of the oral mucosa, leading to zones of sensitive whitish mucosa known as mucous patches
  • Mucous patches manifest as oval-to-crescenteric erosions or shallow ulcers of about 1 cm diameter, covered by a grey mucoid exudate and with an erythematous border. The patches usually arise bilaterally on the mobile surfaces of the mouth, although the pharynx, gingivae, tonsils, and very rarely the hard palate can be affected. At the commissures, the mucous patches may appear as split papules, while on the distal and lateral aspects of the tongue, they tend to ulcerate or manifest as irregular fissures. The mucous patches may coalesce to give rise to, or arise de novo as, serpiginous lesions, sometimes termed snail track ulcers
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47
Q
A

secondary syphilis:

mucous patches

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48
Q
A

condylomata lata:

Occasionally, papillary lesions that may resemble viral papillomas arise during this time and are known as condylomata lata

syphilis

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49
Q

“gumma”:

A
  • The characteristic skin lesion of tertiary syphilis is the “gumma”
  • Gumma appears as : an indurated, nodular, or ulcerated painless brownish-red lump of granulomatous inflammation which usually infiltrates the surrounding tissue and may produce extensive tissue destruction. Ulceration and necrosis may occur in the center of the gumma, leading to scar formation after healing
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50
Q
A

“gumma”-tertiary syphilis

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51
Q

Tertiary syphilis:

interstitial glossitis:

A

The tongue may be involved difusely with gummata and appear large, lobulated, and irregularly shaped. This lobulated pattern is termed interstitial glossitis and is thought to be the result of contracture of the lingual musculature after healing of gummas.

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52
Q

tertiary syphilis:

luetic glossitis:

A

Diffuse atrophy and loss of the dorsal tongue papillae produce a condition called luetic glossitis.

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53
Q

tertiary syphilis:

syphilitic leukoplakia:

A
  • A less common oral manifestation of tertiary syphilis is syphilitic leukoplakia
  • It usually affects the dorsal surface of the tongue and carries a high risk of malignant transformation
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54
Q

Neurosyphilis:

A

can cause unilateral or bilateral trigeminal neuropathy and facial nerve paralysis

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55
Q

Chancre:

A

Chancre is characterized by inflammatory infiltration of lymphocytes and macrophages, with large amount of T. pallidum.

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56
Q

Gumma:

A

Gumma is a granulomatous lesion, with necrosis in the center, accompanied by endovasculitis and perivasculitis. T. pallidum is rarely detected.

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57
Q

Tuberculosis:

Causatuve agent:

A

Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis

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58
Q

Tuberculosis:

Affected sites:

A

Lung is the most common involvement site but extrapulmonary involvement may occur at any organ

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59
Q

Extrapulmonary TB:

A
  • is seen and represents an increasing proportion of the currently diagnosed cases. In patients with AIDS, more than 50% will have extrapulmonary lesions.
  • Any organ system may be involved, including the lymphatic system, skin, skeletal system, CNS, kidneys, and gastrointestinal tract.
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60
Q

Extrapulmonary TB:

lupus vulgaris:

A

Involvement of the skin may develop and has been called lupus vulgaris

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61
Q

Tuberculosis:

most common extrapulmonary sites in the head and neck:

A

Head and neck involvement may occur. The most common extrapulmonary sites in the head and neck are the cervical lymph nodes followed by the larynx and middle ear. Much less common sites include the nasal cavity, nasopharynx, oral cavity, parotid gland, esophagus, and spine

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62
Q

Tuberculosis:

Oral clinical features:

A

Oral TB lesions may be either primary or secondary in occurrence

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63
Q

Tuberculosis:

Primary lesions:

A

are uncommon, seen in younger patients, and present as single painless ulcer with regional lymph node enlargement

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64
Q

Tuberculosis:

secondary lesions:

A

The secondary lesions are common, often associated with pulmonary disease, usually present as single, indurated, irregular, painful ulcer covered by inflammatory exudates in patients of any age group but relatively more common in middle-aged and elderly patients

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65
Q

Tuberculosis:

most common presentation for oral involvement:

A

The most common presentations for oral involvement are chronic ulcerations or swellings. Less frequent findings include non- healing extraction sockets, areas of mucosal granularity, or diffuse zones of inflammation

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66
Q

Tuberculosis:

Chronic tongue ulcerations:

A
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67
Q

Tuberculosis:

Most favorable site:

A

Dorsum of the tongue is most favourable site with these lesions appearing as a stellate ulcer. It can also present on the tongue as macroglossia

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68
Q

Actinomyces:

Causative agent:

A
  • Although the term actinomycosis seems to imply a fungal infection, it is an infection of filamentous, branching, gram- positive anaerobic bacteria
  • Actinomyces israelii is the causative organism in the majority of cases
  • The organism penetrate mucosal barriers and enters tissue through an area of prior trauma
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69
Q

Actinomyces:

Type of infection:

A
  • Actinomycetes are normal saprophytic components of the oral flora.
  • Therefore is not an exogenous infection
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70
Q

Actinomyces:

Sites of colonization in healthy patients:

A
  • Documented sites of colonization in healthy patients include the tonsillar crypts, dental plaque and calculus, carious dentin, bone sequestra, salivary calculi, gingival sulci, and periodontal pockets
  • The colonies within the tonsillar crypts may form concretions and become large enough for the patient to feel the firm plugs within the crypts
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71
Q
A

Actinomyces

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72
Q

Actinomyces:

Progression:

A

Actinomycosis may be either an acute, rapidly progressing infection or a chronic, slowly spreading lesion that is associated with fibrosis

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73
Q

Actinomyces:

Affected sites:

A
  • Approximately 55% of cases of actinomycosis are diagnosed in the cervicofacial region, with 25% occurring in the abdominal and pelvic region and 15% in the pulmonary system
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74
Q

Actinomyces:

Oral and cervicofacial disease- association:

A

Oral and cervicofacial disease are associated with dental procedures, trauma, oral surgery, soft tissue injury, periodontal pocket, nonvital tooth, extraction socket, or infected tonsil

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75
Q

Actinomyces:

“wooden” indurated area of fibrosis description::

A

The classic description is of a “wooden” indurated area of fibrosis, which ultimately forms a central, softer area of abscess. The infection may extend to the surface, forming a sinus tract. Pain often is minimal. The soft tissues of the submandibular, submental, and cheek areas are common areas of involvement, with the area overlying the angle of the mandible being the most frequently affected site

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76
Q

Actinomyces:

Affected oral sites:

A
  • The tongue is the most frequently mentioned site, but any oral mucosal location is possible. Involvement of the tonsillar crypts may produce infectious symptoms; in most cases, however, the primary change is one of variable hyperplasia
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77
Q

Leishmaniasis:

Causative agent:

A

The term leishmaniasis comprises of a group of diseases caused by different species of a protozoan called Leishmania

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78
Q

Leishmaniasis:

Transmission:

A

The parasite resides intracellularly and is transmitted between hosts by the bite of the female sand fly (genus Phlebotomus in the Old World localities of Europe, Africa, and Asia, and Lutzomyia in the New World, the Americas, and Oceania)

79
Q

Leishmaniasis:

Primary hosts:

A

The primary hosts are vertebrates such as humans, domestic dogs and cats, opossums, the crab-eating fox, and the common black rat

80
Q

Leishmaniasis:

main clinical forms:

A
  • visceral leishmaniasis,
  • cutaneous leishmaniasis, and
  • mucocutaneous leishmaniasis.
81
Q

Mucocutaneous leismaniasis (MCL)/ML:

A

can occur with a latency of months, even years, after exposure in endemic areas and because of this huge latency, the diagnosis is often seriously delayed

82
Q

Leishmaniasis:

How does it start?

A

All the clinical forms of leishmaniasis can start with primary mucosal lesions in the head– neck region, sometimes affecting the oral cavity, or certain significant symptoms detectable by the dental practitioner. Such symptoms include swallowing difficulties, dysphonia, and dyspnea. Therefore, dentists play an important role in the early diagnosis of oral leishmaniasis, to avoid the systemic spread of the disease

83
Q
A

Leishmaniasis

84
Q

Noma:

Treatment and prognosis:

A

In addition to using appropriate antibiotics and antiseptics to treat noma, the clinician must direct therapeutic attention not only to local wound care but also toward correcting the inadequate nutrition, hydration, and electrolyte imbalances

  • Penicillin** and **metronidazole are the first-line therapeutic antibiotics for necrotizing stomatitis
  • Conservative débridement of gross necrotic areas is recommended, but aggressive removal is contraindicated because it does not stop the extension of the process and compounds the reconstruction problems
  • Without therapy, only 10% to 20% of affected patients survive. With appropriate intervention, the survival is greater than 90%
  • Facial reconstruction often is extremely challenging and should be delayed until healing is complete
85
Q

Dentigerous cyst:

Originates by:

A

the separation of the follicle from around the crown of an unerupted tooth

86
Q

Dentigerous cyst:

Where?

A

Encloses the crown of an unerupted tooth and is attached to the tooth at the cementoenamel junction

87
Q

Dentigerous cyst:

Affected sites:

A
  • Most often they involve mandibular third molars, accounting for approximately 65% of all cases
88
Q

Dentigerous cyst:

Age:

A

All ages - most frequently between 10 and 30 years of age

89
Q

Dentigerous cyst:

Radiographic findings:

A

Radiographically, typically shows a unilocular radiolucent area that is associated with the crown of an unerupted tooth

A large dentigerous cyst may give the impression of a multilocular process because of the persistence of bone trabeculae within the radiolucency.

90
Q

Dentigerous cyst:

Histopathologic Features:

A

Vary, depending on whether the cyst is inflamed or not inflamed

91
Q

Noninflamed dentigerous cyst:

A
  • fibrous connective tissue wall is loosely arranged
  • contains considerable glycosaminoglycan ground substance
  • small islands or cords of inactive-appearing odontogenic epithelial rests
  • may be present in the fibrous wall.
  • epithelial lining consists of two to four layers of flattened
  • nonkeratinizing cells, and the epithelium and connective tissue interface is flat
92
Q

Inflamed dentigerous cyst:

A
  • fibrous wall is more collagenized, with a variable infiltration of chronic inflammatory cells
  • epithelial lining may show varying amounts of hyperplasia with the development of rete ridges and more definite squamous features a
  • keratinized surface is sometimes seen, but these changes must be differentiated from those observed in the OKC
  • focal areas of mucous cells may be found in the epithelial lining
93
Q

Eruption cyst:

Definition:

A

The soft tissue analogue of the dentigerous cyst

94
Q

Eruption cyst:

Cause:

A

Develops as a result of separation of the dental follicle from around the crown of an erupting tooth that is within the soft tissues overlying the alveolar bone

95
Q

Eruption cyst:

Characteristics:

A
  • Soft, often translucent swelling in the gingival mucosa
  • overlying the crown of an erupting deciduous or permanent tooth
96
Q
A

Eruption cyst

97
Q

Eruption cyst:

Affected sites:

A

May occur with any erupting tooth, the lesion is most commonly associated with the deciduous mandibular central incisors, the first permanent molars, and the deciduous maxillary incisors

98
Q

Eruption hematomas:

A

Surface trauma may result in a considerable amount of blood in the cystic fluid, which imparts a blue to purple-brown color. Such lesions sometimes are referred to as eruption hematomas

99
Q

Eruption cyst:

Histopathologic Features:

A
  • Surface oral epithelium on the superior aspect
  • The underlying lamina propria shows a variable inflammatory cell infiltrate
  • The deep portion of the specimen, which represents the roof of the cyst, shows a thin layer of nonkeratinizing squamous epithelium
100
Q

Odontogenic keratocyst (OKC):

Definition:

A

Α distinctive form of developmental odontogenic cyst that deserves special consideration because of its specific histopathologic features and clinical behavior

101
Q

OKCs are significant for three reasons:

A
  • Greater growth potential than most other odontogenic cysts
  • Higher recurrence rate
  • Possible association with the nevoid basal cell carcinoma syndrome
102
Q

Odontogenic keratocyst (OKC):

Age:

A

Infancy to old age - 60% between 10y and 40y Slight male predilection

103
Q

Odontogenic keratocyst (OKC):

Affected site:

A
  • Mandible: 60%-80% - posterior body and ramus
  • Small OKCs: are usually asymptomatic
  • Larger OKCs: may be associated with pain, swelling, or drainage. Some extremely large cysts, however, may cause no symptoms
104
Q

Odontogenic keratocyst (OKC):

Area of growth:

A

Tend to grow in an anteroposterior direction within the medullary cavity of the bone without causing obvious bone expansion

105
Q

Odontogenic keratocyst (OKC):

Multiple OKCs:

A

may be present - nevoid basal cell carcinoma (Gorlin) syndrome

106
Q

Odontogenic keratocyst (OKC):

Diagnosis:

A

Radiographic findings are not diagnostic - The diagnosis is based on the histopathologic features

107
Q
A

OKCs

108
Q
A

OKCs

109
Q
A

OKCs

110
Q

OKCs

Histopathologic features:

A
  • The epithelial lining is composed of a uniform layer of stratified squamous epithelium - six to eight cells in thickness
  • The luminal surface shows flattened parakeratotic epithelial cells, which exhibit a wavy or corrugated appearance
  • On occasion, isolated foci of orthokeratin production may be found in addition to the parakeratin
  • The basal epithelial layer is composed of a palisaded layer of cuboidal or columnar epithelial cells, which are often hyperchromatic
  • The granular cell consist of compact layer of having keratohyaline granules in large amount
    7% to 26%: small satellite cysts, cords, or islands of odontogenic epithelium may be seen within the

fibrous wall

Inflammatory changes, the typical

features of the OKC may be altered:

  • The parakeratinized luminal surface

may disappear

  • The epithelium may proliferate to

form rete ridges

  • Loss of the characteristic palisaded basal layer
  • The diagnosis of OKC cannot be confirmed unless other sections show the typical features described earlier
111
Q

Gingival (alveolar) cyst of the newborn:

Definition:

A

Small, superficial, keratin-filled cysts

112
Q

Gingival (alveolar) cyst of the newborn:

Characteristics:

A

Appear as multiple whitish papules on the mucosa overlying the alveolar processes of neonates

113
Q
A

Gingival (alveolar) cyst of the newborn

114
Q

Gingival (alveolar) cyst of the newborn:

Size:

A

< 2-3mm in diameter

115
Q

Gingival (alveolar) cyst of the newborn:

Origin:

A

Arise from remnants of the dental lamina

116
Q

Gingival (alveolar) cyst of the newborn:

Age:

A

Common lesions - 50% of all newborns

117
Q

Gingival (alveolar) cyst of the newborn:

Lesion progression:

A

The lesions seldom are noticed or sampled for biopsy because they disappear spontaneously by rupture into the oral cavity

118
Q

Gingival (alveolar) cyst of the newborn:

Histopathologic Features:

A
  • Thin, flattened epithelial lining
  • Parakeratotic luminal surface
  • Lumen contains keratinaceous debris
119
Q

Calcifying odontogenic cyst:

Characteristics of lesion:

A

Part of a spectrum of lesions characterized by odontogenic epithelium containing “ghost cells,” which then may undergo calcification.

120
Q

Calcifying odontogenic cyst:

Affected area:

A

Equally in both jaws - 65% incisor/canine area

121
Q

Calcifying odontogenic cyst:

Age:

A

Mean age: 30 years

122
Q

Calcifying odontogenic cyst:

Radiograph:

A

Usually unilocular, well-defined radiolucency

  • 30-50% of cases: radiopaque structures within the lesion
  • 30% of cases: associated with an unerupted tooth (canine)
123
Q
A

Calcifying odontogenic cyst

124
Q

Calcifying odontogenic cyst:

Histopathologic Features:

A
  • fibrous capsule and a lining of odontogenic epithelium of four to ten cells in thickness.

basal cells may be cuboidal or columnar, similar to ameloblasts

  • “ghost cells”: altered epithelial cells that are characterized by the loss of nuclei with preservation of the basic cell outline (most characteristic histopathologic feature)

calcification within the ghost cells is common / dentinoid

  • several variants of the cystic type
  • intraosseous and extraosseous solid dentinogenic ghost cell tumors
  • ghost cells and juxtaepithelial dentinoid differentiate these lesions from ameloblastoma
125
Q

Glandular odontogenic cyst:

Definition:

A

Rare type of developmental odontogenic cyst that can show aggressive behavior

126
Q

Glandular odontogenic cyst:

Origin:

A

Although it is generally accepted as being of odontogenic origin, it also shows glandular or salivary features that presumably are an indication of the pluripotentiality of odontogenic epithelium

127
Q

Glandular odontogenic cyst:

Age:

A

Middle-aged adults (mean age 46-51)

128
Q

Glandular odontogenic cyst:

Most affected site:

A

75% mandible

129
Q

Glandular odontogenic cyst:

Size:

A
  • Size can vary from small lesions less than 1 cm to large destructive lesions that may involve most of the jaw
  • Large cysts often produce clinical expansion - sometimes can be associated with pain or paresthesia
130
Q

Glandular odontogenic cyst:

Radiograph:

A

Radiographically, the lesion presents as either a unilocular or multilocular radiolucency - well defined margins with a corticated rim

131
Q

Cleft Lip and Palate:

Embryology:

A
  • Craniofacial development represents a complex interaction of cell patterning, migration, proliferation, and differentiation. Much of the facial tissue originates by cell migration from the embryonic neural crest, which is governed by regulatory, structural, and positional genes
132
Q

Cleft lip:

A
  • Normally, complete closure of the lip is accomplished by 35 days postconception as the lateral nasal, median nasal, and maxillary mesodermal processes merge**. **Failure of closure of any one of the three normal sites of fusion can produce unilateral (most common), bilateral (less common), or median (rare) lip clefting
  • CL is considered incomplete when only the upper lip is affected and complete when the defect extends to the nose
133
Q

Cleft palate:

A
  • CP occurs when midline fusion of the palatal shelves fails to occur
  • CP can occur with CL or alone; the latter is possible because palatal closure is not completed until 56 to 58 days postconception, well after closure of the lip, and because the etiology may differ
134
Q

Cleft Lip and Palate:

Etiology:

A

Most oral clefts are nonsyndromic. However, syndromes account for approximately 30% of cases of CL/P and 50 percent of cases of CP.

135
Q

Nonsyndromic clefting:

A

a genetically complex event with gene-gene and gene-

environment interactions:

  • Genes that control cell patterning, cell proliferation, extracellular communication, and differentiation
  • Over 30 candidate genes have been identified
  • Genetic overlap between nonsyndromic and syndromic etiologies
136
Q

Cleft Lip and Palate:

Environmental factors:

A
  • Drugs, Cigarette smoking, Folate deficiency, Maternal obesity, Amniotic band sequence,
  • Other (viral infection, radiation, significant metabolic perturbation)
137
Q

Micrognathia - Pierre Robin sequence:

a.k.a Pierre Robin syndrome

A
  • Occurance: Hypoplasia of the mandible that occurs before the 9th week of development
  • Etiology: The etiology of Pierre Robin sequence is uncertain. Possible mechanisms include genetic disorders, oligohydramnios (which may limit chin growth), myotonia, or connective tissue disease
  • Type of abnormality: Pierre Robin sequence often is an isolated abnormality
  • Associations: One-third of the patients with associated malformations had Stickler syndrome or velocardiofacial syndrome (VCFS).
138
Q

Micrognathia - Pierre Robin sequence:

Clinical features:

A
  • Micrognathia, glossoptosis, and cleft palate
  • The tongue tends to prolapse backward, leading to airway obstruction that can be life threatening
  • Respiratory compromise can lead to hypoxia, cardiopulmonary arrest, pulmonary hypertension, and failure to thrive. Feeding problems are common
139
Q

Macrognathia – Acromegaly:

A
  • Cause: Excessive secretion of growth hormone (GH)
  • Annual incidence: 6-8/ 1000000
  • Mean age of diagnosis: 40-45
  • Most common cause:
  • somatotroph (GH-secreting)
  • adenoma of the anterior pituitary
  • Onset: insidious onset, very slow progression
  • Characteristic findings: enlarged jaw (macrognathia) and enlarged, swollen hands and feet
  • Maxillofacial area: Macrognathia, Enlarged lips, Enlarged tongue, Supraorbital bulging, Enlarged nose
140
Q

Progressive Hemifacial Atrophy (Parry-Romberg Syndrome):

A
  • Slowly progressive hemifacial atrophy of the skin, subcutaneous tissue, fat, and, in severe cases, underlying muscle and bone
  • Prevalence: m=f
  • Onset: first 20 years of life
  • Progression: over a 2- to 10- years self limited period
  • Spontaneous stabilisation
  • Unknown pathogenesis - is most often described as an autoimmune condition on the same spectrum as localised scleroderma en coup de sabre
141
Q

Progressive Hemifacial Atrophy (Parry-Romberg Syndrome):

Oral involvment:

A

Oral involvement affects the tongue, gingiva and soft palate

  • Dental involvement includes delayed dental eruption, dental root exposure and resorption
142
Q

Eagle Syndrome:

A
  • Elongated stylohyoid process and/or calcification of stylohyoid ligament
  • Symptoms: Recurrent episodes of dull and persistent throat pain, pharyngeal foreign body sensation, dysphagia, referred otalgia, and facial and neck pain
143
Q

Classical stylohyoid syndrome:

A

is found after tonsillectomy or trauma and is characterized by pharyngeal, cervical, facial pain, and headache

144
Q

Styloid process-carotid syndrome:

A

is the consequence of pericarotid sympathetic fibers irritation and compression on the carotid artery

145
Q

Condylar Hyperplasia:

A
146
Q

Fordyce Granules:

A
  • Fordyce granules are sebaceous glands that occur on the oral mucosa
  • Similar lesions also have been reported on the genital mucosa
147
Q

What are Fordyce Granules considered to be?

A

Because sebaceous glands typically are considered to be dermal adnexal structures, those found in the oral cavity often have been considered to be “ectopic.” However, because Fordyce granules have been reported in more than 80% of the population, their presence must be considered a normal anatomic variation.

148
Q

Fordyce Granules:

Clinical Features:

A
  • Fordyce granules appear as 1- to 3-mm multiple yellow or yellow-white papules that are most common on the buccal mucosa and the lateral portion of the vermilion of the upper lip. Occasionally, these glands also may appear in the retromolar area and anterior tonsillar pillar
  • They are more common in adults than in children, probably as a result of hormonal factors; puberty appears to stimulate their development
  • The lesions are typically asymptomatic, although patients may be able to feel a slight roughness to the mucosa
  • Considerable clinical variation may exist; some patients may have only a few lesions, whereas others may have literally hundreds of these “granules”
     They can become hyperplastic and adenomatous
149
Q
A

Fordyce Granules

150
Q

Paramedian Lip Pits:

A
  • Rare congenital invaginations of the lower lip
  • Arise from persistent lateral sulci on the embryonic mandibular arch
  • Bilateral** and **symmetric fistulas on either side of the midline of the vermilion of the lower lip
  • Depth of 1.5 cm and may express salivary secretion
151
Q

Paramedian Lip Pits:

Genetic relation:

A
  • The greatest significance of paramedian lip pits is that they usually are inherited as an autosomal dominant trait and in combination with cleft lip (CL) and/or cleft palate (CP) consists Van der Woude syndrome
  • Interferon regulatory factor 6 (IRF6), which has been mapped to chromosome locus 1q32-q41
152
Q

Double Lip:

A
  • Rare oral anomaly characterized by a redundant fold of tissue on the mucosal side of the lip
  • Most often it is congenital in nature, but it may be acquired later in life as: - a component of Ascher syndrome, or - a result from trauma or oral habits, such as sucking on the lip
153
Q

Double Lip:

Clinical Features:

A
  • Upper lip is affected much more often than the lower lip; occasionally, both lips are involved
  • With the lips at rest, the condition is usually unnoticeable, but when the patient smiles or when the lips are tensed, the excess fold of tissue is visible
154
Q

Macroglossia:

A
  • Macroglossia is an uncommon condition characterized by enlargement of the tongue
  • Caused by: a wide variety of conditions, including: congenital malformations and acquired diseases
  • Most frequent causes: are vascular malformations and muscular hypertrophy
  • In edentulous patients: the tongue often appears elevated and tends to spread out laterally because of loss of the surrounding teeth; as a result, wearing a denture may become difficult
155
Q

Macroglossia:

Tongue appearance:

A

The tongue usually has a multinodular appearance :

  • Amyloidosis
  • Neurofibromatosis
  • Multiple Endocrine Neoplasia, type 2B

The tongue shows a diffuse, smooth, generalized enlargement:

  • Hypothyroidism
  • Beckwith-Wiedemann syndrome
  • Neuromuscular disorders
156
Q

Macroglossia:

Clinical Features:

A
  • Macroglossia most commonly occurs in children and can range from mild to severe
  • In infants, macroglossia may be manifested first by:
  • noisy breathing drooling
  • difficulty in eating
  • The tongue enlargement may result in a lisping speech
  • The pressure of the tongue against the mandible and teeth can produce:
  • crenated lateral border to the tongue
  • open bite
  • mandibular prognathism
  • If the tongue constantly protrudes from the mouth, it may ulcerate and become secondarily infected or may even undergo necrosis
  • Severe macroglossia can produce airway obstruction
157
Q

Microglossia:

A
  • Uncommon developmental condition of unknown cause that is characterized by an abnormally small tongue may be missing
  • Associated with hypoplasia of the mandible, and the lower incisors
  • Most cases have been associated with one of a group of overlapping conditions known as oromandibular-limb hypogenesis syndromes
  • These syndromes feature associated limb anomalies, such as hypodactylia (i.e., absence of digits) and hypomelia (i.e., hypoplasia of part or all of a limb)
158
Q

Melkersson–Rosenthal syndrome (MRS):

Clinical characteristics:

A
  • MRS in children is a rare condition

Clinically characterised by a triad of synchronous or metachronous symptoms:

  • recurrent peripheral facial palsy (can be on one side or both)
  • relapsing orofacial oedema
  • and a fissured tongue
159
Q

Melkersson–Rosenthal syndrome (MRS):

Aetiology:

A
  • The aetiology of this disease is still unclear.
  • However, genetic factors, as well as alterations in immune functions, infections, and allergic reactions have been postulated
160
Q

Nevoid basal cell carcinoma syndrome or Gorlin - Goltz Syndrome:

A
  • Gorlin and Goltz, in the year 1960, described the triad which includes multiple basal cell carcinoma, odontogenic keratocysts (OKC), and bifid ribs characteristic of the syndrome
  • Nevoid basal cell carcinoma syndrome (Gorlin-Goltz syndrome) due to its high variability in expression are often not diagnosed as the syndrome and often managed same as that of odontogenic keratocyst
161
Q

Nevoid basal cell carcinoma syndrome or Gorlin - Goltz Syndrome:

Causes:

Prevalence:

A
  • Generally is inherited as an autosomal dominant trait
  • It is caused by mutations to patched PTCH1 which is a tumor suppressor gene located on 9q22, 3-q31
  • 1 in 57,000 to 1 in 256,000
  • Male to female ratio is 1:1
162
Q

Nevoid basal cell carcinoma syndrome or Gorlin - Goltz Syndrome:

Diagnosis:

A
  • OKCs are the first ones likely to get diagnosed as they can be detected during the first decade of life. They occur almost in 80% NBCCSs.
  • Early diagnosis of the syndrome is very important due to the susceptibility to neoplasm, and the syndrome can become very destructive as age progresses
  • There is great variability in the expressivity of nevoid basal cell carcinoma syndrome, and no single component is present in all patients
163
Q
A

Nevoid basal cell carcinoma syndrome or Gorlin - Goltz Syndrome:

164
Q

Nevoid basal cell carcinoma syndrome or Gorlin - Goltz Syndrome:

The features of the syndrome include:

A
165
Q

Treacher Collins Syndrome (Mandibulofacial Dysostosis):

A
  • Patients with mild forms of mandibulofacial dysostosis may not require treatment
  • In _more severe case_s the clinical appearance can be improved with _cosmetic surgery_. Because of the extent of facial reconstruction required, multiple surgical procedures usually are necessary. Individual operations may be needed for the eyes, zygomas, jaws, ears, and nose.
  • Combined orthodontic therapy** is needed along with the **orthognathic surgery
166
Q

Peutz - Jegers Syndrome:

A
  • Peutz-Jeghers syndrome is a relatively rare but well recognized condition
  • 1 in 50,000 to 200,000 births
  • Characterized by freckle - like lesions of the hands, perioral skin, and oral mucosa, in conjunction with intestinal polyposis and predisposition to develop cancer (GΙ tract, pancreas, lungs, breast, ovaries, testicles)
167
Q

Peutz - Jegers Syndrome:

causes:

A
  • Is inherited as an autosomal dominant trait
  • Mutation of the tumor suppressor gene, STK11 (also known as LKB1) is responsible for most cases of Peutz-Jeghers syndrome
  • This gene, which encodes for a serine/threonine kinase, is located on chromosome 19p13.3
  • Positive correlation between number of mutant STK11 copies and phenotypic severity of PJS
168
Q

Peutz - Jegers Syndrome:

oral involvment:

A
  • Pigmentation can also occur intraorally** (particularly on the buccal mucosa) and on the **skin** of the **extremities
  • The oral lesions present as 1- to 4-mm brown to blue-gray macules primarily affect the vermilion zone, the labial and buccal mucosa, and the tongue; they are seen in more than 90% of these patients
  • The oral and perioral pigmentation persists throughout life. Some degree of fading may be noted during adolescence. Does not require treatment however, laser therapy can be performed if the patient elects cosmetic intervention
169
Q

Treacher Collins Syndrome (Mandibulofacial Dysostosis)

differential diagnosis:

A

The differential diagnosis for this pattern of oral and perioral pigmentation includes Laugier–Hunziker syndrome (LHS), although the pigmentation in that condition does not occur until adulthood

170
Q

Rendu-Osler-Weber Syndrome (Hereditary Hemorrhagic Telangiectasia):

Diagnosis:

A

A diagnosis of HHT can be made if a patient has 3 of the following 4 criteria:


  1. Recurrent spontaneous epistaxis
  2. Telangiectasias of the mucosa and skin
  3. Arteriovenous malformation involving the lungs, liver, or CNS
  4. Family history of HHT
171
Q

Sturge Weber:

A
  • Sturge-Weber Syndrome is a congenital, non-familial disorder of unknown incidence
  • Recently was shown to be related to a somatic activating mutation of the GNAQ gene on chromosome 9q21
172
Q

Sturge Weber:

Characteristics:

A

It is characterized by a congenital hemangiomatous facial lesion (a port wine stain) in the distribution of the trigeminal nerve associated with similar lesion intracranially and neurological abnormalities

  • Other symptoms associated with Sturge-Weber can include eye and internal organ irregularities
  • Each case of Sturge-Weber Syndrome is unique and exhibits the characterizing findings to varying degrees
173
Q

Sturge Weber:

Intraoral involvement:

A
  • Intraoral involvement in Sturge-Weber syndrome is common, resulting in hypervascular changes to the ipsilateral mucosa
  • The gingiva may exhibit slight vascular hyperplasia or a more massive hemangiomatous proliferation that can resemble a pyogenic granuloma
  • Destruction of the underlying alveolar bone has been reported in rare instances
174
Q

Papillon-Lefèvre Syndrome:

Cause:

A
  • Autosomal recessive inheritance pattern
  • Mutation and loss of function of the cathepsin C gene located on chromosome 11q14-q21
  • This gene is important in the structural growth and development of the skin and is critical for appropriate immune response of myeloid and lymphoid cells
  • Loss of appropriate function of the cathepsin C gene results in an altered immune response to infection and may affect the integrity of the junctional epithelium surrounding the tooth
175
Q

Papillon-Lefèvre Syndrome:

Characteristics:

A
  • Is characterized by premature loss of the primary and permanent teeth and hyperkeratosis of the palms, soles, and sometimes of the knees and elbows
  • The periodontal inflammation begins soon after eruption of the primary teeth
  • The periodontal inflammation begins soon after eruption of the primary teeth
  • Bone loss is rapid and severe; primary teeth are lost by 3 to 5 years of age and permanent teeth within a few years of eruption
176
Q

Papillon-Lefèvre Syndrome:

Radiographic image:

A

FLOATING IN AIR TEETH”—DESTRUCTION OF ALVEOLAR BONE

177
Q

Papillon-Lefèvre Syndrome:

severity of disease:

Molecular mechanisms:

A
  • The severity of disease may be related to immunologic and microbiologic factors. Patients with PLS have abnormalities in neutrophil and natural killer cell function.
  • Molecular mechanisms implicated in the periodontal pathogenesis include the deficient processing and lack of cathelicidin (LL37) in gingival fluid.
178
Q

Papillon-Lefèvre Syndrome:

organisms typically cultured:

A

The organisms typically cultured from the gingival sulcus of patients with PLS are similar to those cultured from children who have neutropenia, and include:

  • A. actinomycetemcomitans, Capnocytophaga species, Fusobacterium nudeatum, E. corrodens, and Aggregatibacter actinomycetemcomitans
179
Q

Desquamative Gingivitis:

A
  • Most > 40-year-old female
  • Not a Diagnosis but Clincial Term for an underlying manifestation Clinical Features
  • Smooth erythema, loss of stippling, desquamation, and erosion of the gingiva are common signs of DG, irrespective of the etiopathogenesis
  • Generally involves the attached and free gingiva
  • Chronic onset all over mouth
  • Multifocal or generalized pattern
  • Goes hand in hand with vesicle/bulla formation filled with clear fluid or blood
  • Mostly asymptomatic, when symptomatic ranges from mild burning sensation to pain
  • DG is considered as a clinical disorder that can be easily recognized by the examiner on the dental chair.
  • DG has no association with loss of attachment and alveolar bone destruction
  • Is a possible risk factor for long-standing periodontal health
180
Q

Desquamative Gingivitis:

manifestation:

other diagnosis:

A
  • DG has a wide range of manifestations, which may imitate other conditions
  • The process almost always represents a manifestation of one of several different vesiculoerosive diseases, usually mucous membrane pemphigoid. Some clinicians broaden the definition to include patients with atrophic and erosive gingival lesions without true peeling of the epithelium.
  • In such cases, lichen planus is diagnosed most frequently
  • Other diagnoses that are made less frequently include linear IgA disease, pemphigus vulgaris, epidermolysis bullosa acquisita, systemic lupus erythematosus (SLE), chronic ulcerative stomatitis, and paraneoplastic pemphigus
  • For definitive diagnosis biopsy immunofluorescence are necessary
181
Q

Necrotizing Ulcerative Gingivitis (NUG):

Factors

A
  • Has a distinctive pattern of gingival pathologic changes

Occurs in the presence of psychologic stress. Other factors have been related to an increased frequency of NUG: Immunosuppression

  • Smoking
  • Local trauma
  • Poor nutritional status
  • Poor oral hygiene
  • Inadequate sleep
  • Recent illness
  • Immunocompromised status associated with acquired immunodeficiency syndrome (AIDS)
182
Q

Necrotizing Ulcerative Gingivitis (NUG):

Clinical features:

A
  • The interdental papillae are highly inflamed, edematous, and hemorrhagic
  • Typically, the affected papillae are blunted and demonstrate areas of “punched-out,” craterlike necrosis that are covered with a gray pseudomembrane. Early cases may be missed easily because the ulceration initially involves only the tip of the interdental papilla
  • A fetid odor, pain, spontaneous hemorrhage, and
  • Lymphadenopathy, fever, and malaise accumulations of necrotic debris usually are noted
183
Q

Necrotizing Ulcerative Gingivitis (NUG):

Treatment:

A
  • Débridement by scaling, curettage, or ultrasonic instrumentation (except when contraindicated, as in HIV- positive patients)
  • Topical or local anesthetic often is required before the Frequent rinses with chlorhexidine, diluted hydrogen
  • clinician can débride the tissues adequately peroxide are beneficial in increasing the therapeutic response
  • Antibiotic medications: metronidazole and penicillin have been suggested as the drugs of choice
184
Q

Acute herpetic gingivostomatitis (primary herpes):

Age:

Onset:

cause:

A
  • 90% of cases are caused by HSV-1
  • From 6 months to 5 years old, with the peak prevalence occurring between 2 and 3 years of age
  • The onset is abrupt and often accompanied by anterior cervical lymphadenopathy, chills, fever, nausea, anorexia, irritability, and sore mouth lesions. The manifestations vary from mild to severely debilitating
185
Q

Acute herpetic gingivostomatitis (primary herpes):

affected sites

A
  • Initially the affected mucosa develops numerous pinhead vesicles, which rapidly collapse to form numerous small, red lesion. These lesions enlarge slightly and develop central ulceration covered by yellow fibrin
  • Both the movable and attached oral mucosa can be affected
  • Self-inoculation of the fingers, eyes, and genital areas can occur.
  • Mild cases usually resolve within 5 to 7 days; severe cases may last 2 weeks
  • Rare complications include kerato-conjunctivitis, esophagitis, pneumonitis, meningitis, and encephalitis
186
Q

Acute herpetic gingivostomatitis (primary herpes):

initial symptoms are:

A

Primary infection in adults may cause pharyngotonsillitis. The initial symptoms are:

  • sore throat
  • fever
  • malaise
  • headache
  • Numerous small vesicles develop on the tonsils and posterior pharynx. The vesicles rapidly rupture to form shallow ulcers, which often coalesce and develop an overlying diffuse, gray-yellow exudate.
  • Involvement of the oral mucosa anterior to Waldeyer ring occurs in less than 10% of cases
187
Q

Acute herpetic gingivostomatitis (primary herpes):

Therapy:

A
188
Q

Hand-Foot-And-Mouth Disease:

cause:

A

Usually is caused by coxsackievirus A16, but also may arise from coxsackievirus A5, A9, or A10; echovirus 11; or enterovirus 71

189
Q

Hand-Foot-And-Mouth Disease:

Affected sites:

A
  • The name fairly well describes the location of the lesions
  • Oral and hand lesions almost always are present
  • The oral lesions arise without prodromal symptoms and precede the development of the cutaneous lesions. Sore throat and mild fever usually are present also
  • The cutaneous lesions range from a few to dozens and primarily affect the borders of the palms and soles and the ventral surfaces and sides of the fingers and toes. Rarely other sites, especially the buttocks, external genitals, and legs, may be involved. They begin as erythematous macules that develop central vesicles and heal without crusting. In some cases, nail loss or ridges (Beau lines) may ensue after several weeks
190
Q

Hand-Foot-And-Mouth Disease:

oral lesions:

A

The oral lesions resemble those of herpangina but may be more numerous and more frequently involve anterior regions of the mouth. The number of lesions ranges from 1 to 30. The buccal mucosa, labial mucosa, and tongue are the most common sites, but any area of the oral mucosa may be involved. The individual lesions typically measure 2 to 7 mm in diameter but may be larger than 1cm. The lesions rapidly ulcerate and then typically heal within 1 week

191
Q

Hand-Foot-And-Mouth Disease:

Diagnosis:

Thearpy:

A
  • Is diagnosed based upon the clinical manifestations
  • Therapy is directed toward symptomatic relief; nonaspirin antipyretics and topical anesthetics, such as dyclonine hydrochloride, often are beneficial
192
Q

Herpangina:

cause:

A
  • Usually is produced by coxsackievirus A1 to A6, A8, A10, or A22. However, it also may represent infection by coxsackievirus A7, A9, or A16; coxsackievirus B2 to B6; echovirus 9, 16, or 17; or enterovirus 71

05-08/2015: 10.210 children diagnosed with herpangina in China

193
Q

Herpangina:

Onset:

Lesions:

A
  • Begins with an acute onset of sore throat, dysphagia, and fever, occasionally accompanied by cough, rhinorrhea, anorexia, vomiting, diarrhea, myalgia, and headache. Most cases, however, are mild or subclinical
  • Typically a small number of lesions (usually two to six) develop on the soft palate or tonsillar pillars. The lesions begin as red macules, which form fragile vesicles that rapidly ulcerate. The ulcerations average 2 to 4 mm in diameter. The systemic symptoms resolve within a few days; the ulcerations usually take 7 to 10 days to heal
194
Q

Herpangina:

Therapy:

A

Therapy is directed toward symptomatic relief; non aspirin antipyretics and topical anesthetics, such as dyclonine hydrochloride, often are beneficial.