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E-Book

E-Book, Englisch, 376 Seiten

Marx Oral Pathology in Clinical Dental Practice


1. Auflage 2020
ISBN: 978-0-86715-907-3
Verlag: Quintessence Publishing Co, Inc
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 376 Seiten

ISBN: 978-0-86715-907-3
Verlag: Quintessence Publishing Co, Inc
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)



While most dentists do not perform their own histologic testing, all dentists must be able to recognize conditions that may require biopsy or further treatment outside the dentist office. This book does not pretend to be an exhaustive resource on oral pathology; instead, it seeks to provide the practicing clinician with enough information to help identify or at least narrow down the differential for every common lesion or oral manifestation of disease seen in daily practice as well as what to do about them. Organized by type of lesion, mass, or disease, each pathologic entity presented includes the nature of the disease; its predilections, clinical features, radiographic presentation, differential diagnosis, and microscopic features; and the suggested course of action for the dental practitioner as well as the standard treatment regimen. In keeping with the concise nature of the text, all but the rarest disease entities include at least one photograph to illustrate the clinical condition. This book distills the comprehensive information from Dr Marx and Dr Diane Stern's award-winning pathology reference text (Oral and Maxillofacial Pathology: A Rationale for Diagnosis and Treatment, ed 2 [Quintessence, 2012]) into practical guidelines for restorative and general dentists everywhere.

Robert E. Marx, DDS, professor of surgery and chief of the Division of Oral and Maxillofacial Surgery at the University of Miami Miller School of Medicine, is well known as an educator, researcher, and innovative surgeon. He has pioneered new concepts and treatments for pathologies of the oral and maxillofacial area as well as new techniques in reconstructive surgery. As a researcher, he has made valuable contributions in the use of hyperbaric oxygen following radiation therapy, in the development of platelet rich plasma, and in elucidating the relationships between smoking and carcinogenesis. He also pioneered the clinical applications of recombinant human bone morphogenetic protein and stem cell use and was the first to identify what is now known worldwide as bisphosphonate induced osteonecrosis of the jaws. For the past 34 years, he has overseen the training of scores of residents and fellows, many of whom have themselves established distinguished careers. His many prestigious awards, including the Harry S. Archer Award, the William J. Gies Award, the Paul Bert Award, and the Donald B. Osbon Award, attest to his dedication and commitment to the field of oral and maxillofacial surgery.
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2


Red and White Lesions


Benign Hyperkeratosis

Leukoplakia

Non–Betel Nut/Slaked Lime Smokeless Tobacco Keratosis

Betel Nut/Slaked Lime Keratosis

Dyskeratosis Congenita

Epithelial Dysplasia/Carcinoma in Situ

Hypertrophic and Striaform Lichen Planus

Secondary Syphilis (Mucous Patches)

Hereditary Benign Intraepithelial Dyskeratosis

Keratosis Follicularis (Darier-White Disease)

Pachyonychia Congenita

Incontinentia Pigmenti

Proliferative Verrucous Leukoplakia (PVL)

Verrucous Carcinoma

Hypersensitivity Mucositis

Hairy Leukoplakia

Dental Lamina Rests/Epithelial Inclusions (Bohn’s Nodules and Epstein Pearls)

Nicotine Stomatitis

Oral Candidiasis

Benign Migratory Glossitis

Acute and Chronic Radiation Mucositis

Field Cancerization

Scarlet Fever

Kaposi Sarcoma

Oral Squamous Cell Carcinoma

Wavy strands of keratin above keratinocytes showing a normal progression of maturity without atypia.

Benign Hyperkeratosis


Nature of disease

A thickening of the mucosal epithelium with the production of orthokeratin without epithelial dysplasia.

Predilections

Occurs mostly in adults related to either mechanical irritation or a chemical reaction or unrelated to any observable cause. There is no sex or racial predilection. It may also be idiopathic.

Clinical features

A white patch referred to as leukoplakia. It is usually asymptomatic. It is often slightly elevated and may be thickened but will not be indurated.

Radiographic presentation

None.

Differential diagnosis

As a patch of clinical leukoplakia, it must be distinguished from premalignant dysplasia, carcinoma in situ, verrucous carcinoma, and invasive carcinoma. Additionally, lichen planus and Candida infection may be considered.

Microscopic features

A thicker-than-normal keratinocyte layer with a surface of lightly eosinophilic, wavy orthokeratin. The keratinocytes will appear to be normal without mitotic figures or nuclear pleomorphism.

Suggested course of action

Remove any obvious mechanical irritation (eg, denture irritations, toothbrush trauma, patient habits, etc) and/or chemical reaction (eg, irritating mouthwashes, certain spices or flavoring agents, etc). If there is no response or resolution within 2 weeks or if no obvious cause is noted, a biopsy is indicated.

Treatment

It is a relief to patients to hear that their benign hyperkeratosis lesion is not considered to be a cancer. However, incisional and even excisional biopsy cannot predict either regrowth or a sampling error that may result in a squamous cell carcinoma developing later. Therefore, a 6-month recall schedule is recommended even though no specific treatment is required.

Leukoplakia.

Leukoplakia


Nature of disease

A white patch on the oral mucosa. Three conditions can present as a clinically apparent white patch: acanthosis/hyperkeratosis, Candida, or fibrin.

Predilections

Can occur at any age but is more often seen in adults. There is no sex or racial predilection.

Clinical features

A white patch of oral mucosa most commonly noted on the buccal mucosa, lateral border of the tongue, or floor of the mouth.

Radiographic presentation

None.

Differential diagnosis

Clinical leukoplakia may only represent an ulcer with a fibrin base or Candida and sometimes lichen planus by virtue of its acanthosis and hyperkeratosis. However, after benign hyperkeratosis, the most serious considerations are premalignant dyplasias, carcinoma in situ, verrucous carcinoma, and invasive squamous cell carcinoma.

Microscopic features

The three entities that cause a clinical leukoplakia will appear different:

1. Fibrin: Thin strands of light eosinophilic staining over a wound base with inflammation.

2. Candida: Vertically positioned hyphae with prominent periodic acid-Schiff (PAS) or silver staining on an epithelial surface.

3. Acanthosis/hyperkeratosis:

a. Acanthosis/benign hyperkeratosis: A thickened keratinocyte layer without cellular atypia but with surface keratin.

b. Premalignant dysplasia: Various degrees of epithelial atypia above an intact basement membrane.

c. Carcinoma in situ: Severe epithelial dysplasia with nuclear pleomorphism and abnormal mitotic figures from the basal cell layer to the surface.

d. Verrucous carcinoma: A significant exophytic proliferation as well as a blunted endophytic proliferation of epithelial cells but with an intact basement membrane beneath which most often resides a dense inflammatory response.

e. Invasive carcinoma: Atypical epithelial cells forming bundles and cords through the basement membrane into the underlying tissues.

Suggested course of action

Biopsy and/or refer to an oral and maxillofacial surgeon.

Treatment

Treatment will vary according to the biopsy result. For:

? Fibrin: Wound care and treatment of the underlying etiology, as well as observation and surveillance for acanthosis/hyperkeratosis.

? Premalignant dysplasia: Excision with frozen section control.

? Carcinoma in situ: Excision with frozen section control.

? Verrucous carcinoma: Excision with frozen section control.

? Invasive carcinoma: Excision with frozen section control and evaluation for radiotherapy and/or chemotherapy.

Smokeless tobacco keratosis from chewing tobacco.

Non–Betel Nut/Slaked Lime Smokeless Tobacco Keratosis


Nature of disease

A reactive nondysplastic hyperkeratosis of the mucosa due to inflammation and stimulation from various smokeless tobacco products.

Predilections

May occur in anyone who uses such products but has a higher incidence in the western United States and the Scandinavian countries due to cultural traditions. More common in men also because of cultural acceptance. No racial predilection is known.

Clinical features

The area corresponding to the placement of the tobacco product (usually the mandibular attached gingiva and mucosa of the vestibule) will appear as an irregular and often leathery white patch referred to as a “snuffle dippers patch.” It is usually nonpainful unless the area is inflamed.

Radiographic presentation

None.

Differential diagnosis

The clinician is advised to ask the patient about use of betel nut/slaked lime use versus true smokeless tobacco products. Betel nut/slaked lime keratosis is premalignant, whereas other true tobacco-containing, topical smokeless tobacco products are not. Additionally, clinicians should also consider epithelial dysplasia, carcinoma in situ, invasive squamous cell carcinoma, and even lichen planus and hypertrophic candidiasis.

Microscopic features

Nondysplastic epithelium will be present with a thick layer of pale-staining cells occupying the superficial half of the keratinocyte layer along with significant hyperkeratosis.

Suggested course of action

Confirm that the patch is not the result of betel nut/slaked lime use. Incisional biopsy is indicated to document the absence of dysplasia. Counsel the patient about tobacco cessation, particularly as it relates to erosion of the mucosa and gingiva as well as staining of the teeth.

Treatment

No specific treatment other than cessation of smokeless tobacco use.

Trismus, buccal mucosa hyperkeratosis, and fibrosis from betel nut/slaked lime use.

Betel Nut/Slaked Lime Keratosis


Nature of disease

A dysplastic premalignant transformation of mucosal epithelial cells due to the carcinogenic effects of slaked lime. Additionally, the Areca catechu chemical in the betel nut often causes a concomitant submucosal fibrosis.

Predilections

Mostly seen in individuals from India, Sri Lanka, and East Asian countries, where the produce is called quid or pan and used for oral gratification much like chewing gum in the United States.

Clinical features

A white patch is usually seen on either buccal mucosa. There is often a limited jaw opening due to the submucosal fibrosis. Induration around the white patch is common.

Radiographic presentation

None.

Differential diagnosis

The clinician is advised to ask the patient specifically about betel nut/slaked lime use versus use of smokeless tobacco products, as the latter are not carcinogenic to a significant degree. Other considerations include squamous cell...



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