Quartz 4

Contemporary Oral Medicine A Comprehensive Approach to Clinical Practice Annotations

29 min read

Contemporary Oral Medicine: A Comprehensive Approach to Clinical Practice Annotations

Contemporary Oral Medicine A Comprehensive Approach to Clinical Practice TOC

Foreword

Clinical Evaluation of Oral Diseases

The Patient History

  • p. 139: The Patient History
  • p. 140: Description of symptoms
  • p. 140: Table 1 Elements of the new patient encounter

Diagnostic Imaging Principles and Applications in Head and Neck Pathology

Introduction

  • p. 202: Plain radiographs provide a two-dimensional overview of the region of interest, and crosssectional imaging modalities such as computed tomography (CT), cone beam computed tomography (CBCT), and magnetic resonance imaging (MRI) provide multiplanar evaluation of osseous structures of the oral and maxillofacial regio
  • p. 202: CT and MRI have the additional advantage of providing highresolution imaging of soft tissues
  • p. 202: Imaging is an adjunct to, and not a substitute for, an optimal clinical examination.

Imaging Techniques > Anatomical Techniques Using Ionizing Radiation

  • p. 203: Anatomical Techniques Using Ionizing Radiation
  • p. 203: Intraoral radiographs are readily available and provide a low cost, low radiation dose, and high spatial resolution modality for evaluating the dentoalveolar structures and specifically for detecting caries, periapical pathology, and periodontal disease
  • p. 203: In contrast, the DPT is a curved panoramic tomogram that provides an overview of the dentition, mandible, temporomandibular joints (TMJ), and maxilla and maxillary sinuses
  • p. 204: The lateral cephalogram provides a standardized assessment of the dental and skeletal relationship of the jaws as well as two-dimensional (2D) evaluation of the airway.

Imaging Techniques > Anatomical Techniques Without Ionizing Radiation

  • p. 205: The main advantages of CBCT (over MDCT) are higher resolution (0.075–0.15 mm voxel lengths as compared with 0.5–0.625 mm for MDCT) and lower radiation dose: 60–250 μSv for state-of-the-art equipment (Ludlow and Ivanovic 2008; De Vos et al. 2009; Casselman et al. 2013)
  • p. 205: Significant disadvantages include the absence of soft tissue contrast which is principally related to the lower radiation dose but also the detector design and inability to accurately measure tissue density (in Hounsfield units) as compared with the high accuracy of conventional CT
  • p. 205: Ultrasound (US)
  • p. 205: ultrasound requires a “window” that is unimpeded by bone or air
  • p. 205: For evaluation of the neck and maxillofacial region, high-frequency transducers are used, using sound waves between 7.5 and 15 MHz:
  • p. 205: Hyperechoic structures appear whiter on a gray-scale image and include bone or calculi.
  • p. 205: Isoechoic structures have the same echogenicity as their surroundings, for example, muscle.
  • p. 205: In the maxillofacial region and neck, US is an excellent initial examination for the salivary glands, thyroid, lymph nodes, congenital
  • p. 206: lesions, and miscellaneous mass lesions
  • p. 206: Magnetic resonance imaging (MRI):
  • p. 206: Most inflammatory and neoplastic lesions are waterrich and therefore are of higher signal than surrounding tissue on a T2-weighted image. Because air and cortical bone have no mobile protons, they have no signal on any MRI sequence. The presence of signal within cortical bone is always pathological apart from normal neurovascular canals and sutures.
  • p. 206: The most commonly used MRI contrast agent is gadolinium (a trivalent rare earth element) bound to a chelate.
  • p. 207: Compared with other anatomical imaging modalities, MRI has excellent contrast resolution, allowing optimal delineation of normal from abnormal tissue. Like MDCT and CBCT, MRI is now capable of submillimeter imaging which is essential for evaluation of the trigeminal and the lower cranial nerves in the evaluation of orofacial pain and optimal for the assessment of soft tissue and bone. H
  • p. 207: region. It can determine if there is arterial supply to a suspected vascular malformation

Imaging Techniques > Functional Imaging Techniques

  • p. 208: Functional Imaging Techniques
  • p. 208: They assess metabolic turnover and can be combined with anatomical imaging (MDCT or MRI).

Principal Applications of Advanced Imaging in Oral Medicine > Imaging of Mass Lesions

  • p. 210: The applications of advanced imaging techniques are discussed in various clinical scenarios below under the headings of imaging of (1) mass lesions, (2) salivary gland disease, (3) malignancy of the oral cavity, (4) osteomyelitis and osteonecrosis of the jaws, (5) temporomandibular joint disorders, (6) orofacial pain, (7) obstructive sleep apnea, and (8) headaches

Other annotations

  • p. 201: Diagnostic Imaging Principles and Applications in Head and Neck Pathology

Soft and Hard Tissue Operative Investigations in the Diagnosis and Treatment of Oral Disease

Why Perform a Biopsy?

  • p. 343: The development of a reasonable differential diagnosis is of prime importance in determining if biopsy is indicated. Furthermore, the differential diagnosis aids the clinician in selecting the appropriate technique if biopsy is necessary.
  • p. 343: A biopsy, even though it may be the gold standard for some diagnosis, is not always indicated for every oral mucosal lesion
  • p. 343: There are several main reasons why a clinician may perform a biopsy: 1. To rule out possible cancer or potentially cancerous pathology or to monitor the possible malignant transformation of an oral potentially malignant disorder (OPMD). This is especially important when one encounters white, red, indurated, and/or ulcerated lesions. 2. To help in establishing the diagnosis when the clinician has doubts, regardless of the nature of the pathology. Appropriate treatment can only
  • p. 344: Fig. 1 Flowchart for non–pigmented mucosal lesions. (Adapted from van der Waal 2010)
  • p. 344: Fig. 2 Flowchart for pigmented lesions. (Adapted from Meleti et al. 2008)
  • p. 345: Indications to perform a biopsy include: 1. Lesions (especially manifesting as a red patch or having inflammatory features) persisting for more than 2 weeks and: (a) without apparent etiopathogenic factors, and/or (b) after removal of identifiable irritating factors, and/or (c) after empirical treatment has been attempted. 2. All white hyperkeratotic lesions for which a cause is not obvious, especially speckled non-homogeneous white and red lesions. 3. Any lesion suspicious of a neoplasm (presence of growth, ulceration, induration, with or without painful symptoms). 4. Lesions interfering with function (e.g., fibroepithelial polyps). 5. Tissue from draining sinus tracts when there is no probable cause. 6. Lesions in the jaw bones that cannot be diagnosed radiographically, especially if they cause symptoms, such as pain or altered sensations.
  • p. 345: There are no absolute contraindications for performing a biopsy, yet one should keep in mind several issues that may help mitigate unwanted complications.
  • p. 345: . In case of acute pyogenic or viral infection, one should refrain from biopsy until the patient has recovered or after a course of medical treatment.
  • p. 345: anticoagulation therapy or suffers from a serious bleeding disorder
  • p. 345: The utmost attention should be exercised when performing a biopsy on a lesion involving the hard palate mucosa, so as not to puncture the greater palatine artery (a. palatina major).

When to Perform a Biopsy?

  • p. 346: Another area of caution is the gingival margin and papilla, so as not to cause dehiscence or loss of its contour.
  • p. 346: It should also be borne in mind that undertaking a biopsy of the vermillion portion of the lip, or removing large mucoceles close to the vermillion, can have cosmetic consequences
  • p. 346: Thus, one should firstly collect as much etiological and clinical data as possible.

Who should Perform a Biopsy?

  • p. 347: ypically, general dental practitioners do not have sufficient knowledge of oral diseases nor sufficient clinical experience in undertaking biopsies to routinely perform them and interpret their results for the ultimate benefit of the patien
  • p. 347: In countries where oral medicine is a recognized specialty, it would be best that these specialists undertake biopsies for suspected oral lichen planus and other non-malignant mucosal disease.

What to Do before the Biopsy?

  • p. 348: What to Do before the Biopsy?
  • p. 348: 1. Size: How large is the lesion? Does it cross anatomical boundaries? Has it changed size over time or since it was noted? 2. Shape: Has the lesion changed in shape? For example, has a blister become an ulcer? This may signify autoimmune vesicullobulous condition. 3. Progression: Is the lesion static, or has it changed over time? Has this occurred slowly or quickly, alternatively has it regressed? Have there been alternating periods of increase or decrease in size, or quiescent periods? If a lesion progresses rapidly, then it may be more sinister. This information is biased by the patient’s perception. 4. Duration: How long has the lesion been present? If the lesion has been present for years, it is more likely to be benign in nature.
  • p. 348: his provides determination of morphological and topographical features, which should be provided to the reporting pathologist. 1. Look: Determine site, shape, morphology, color, sharpness, and regularity of border, and whether the lesion is single or multiple. 2. Feel: Determine consistency (soft, firm, hard), description of surface (smooth, lobulated, irregular, verruciform), tenderness, associated symptoms (e.g., discharge) and pulsations (e.g., vascular lesions). 3. Move: Determine tethering (fixation to mucosa, skin or underlying structures). 4. Measure: Determine size (using a ruler or calipers for exact measurement). 5. Examine: Determine presence of head and neck lymph nodes (necessary part of every oral examination, always performed before biopsy). 6. Photography: Record the exact appearance and size for future reference. 7. Radiography: Perform if possible dental or bony involvement is suspected.

How to Perform a Biopsy? > Incisional Biopsy

Other annotations

  • p. 341: Soft and Hard Tissue Operative Investigations in the Diagnosis and Treatment of Oral Disease

Oral and Maxillofacial Fungal Infections

Introduction

  • p. 958: Human fungal infections caused by opportunistic fungi generally do not cause lesions in healthy individuals but rather in patients who are immunocompromised in some manner.
  • p. 958: Annotation
  • p. 958: The range of human infections caused by Candida spp. is considerable
  • p. 958: Oral candidosis is the most common mycosis of the mouth either in healthy or immunodeficient patients.

Carriage of Candida and Non-Candida Species

  • p. 959: but sometimes oral candidal infections can cause pain and discomfort, limiting nutrition in elderly or hospitalized patients
  • p. 959: It is kept under control by means of specific and non-specific host defense mechanisms and by the competition of other microorganisms in the oral flora.
  • p. 959: and the epithet “disease of the diseased” has been applied to these infections.
  • p. 959: Oral yeast carriage is not indicative of disease. In many individuals, Candida represents only a minority of their oral flora, and they have no associated clinical symptoms.
  • p. 959: These data indicate that the ill health of an individual is a predisposing factor for Candida colonization
  • p. 960: There are at least seven Candida species of major medical importance, the most important and the most frequently isolated being C. albicans. T
  • p. 960: characteristic feature of C. albicans is its ability to form true hyphae as detected by the germ tube test, although this ability is also seen i

Etiology > Virulence Factors of Candida and Non-Candida spp.

  • p. 961: Although all Candida species cause the same kind of mucositis, there are differences in their invasiveness and fungal susceptibilities

Etiology > Virulence Factors of Candida and Non-Candida spp. > Toxins

  • p. 967: Table 1 Predisposing factors to oral candidosis | Comment: Important
  • p. 967: Local predisposing factors
  • p. 967: Systemic predisposing factors
  • p. 967: Prostheses (changes in environmental conditions, trauma, denture usage, oral hygiene)
  • p. 967: Physiological (e.g., elderly, pregnancy, infancy)
  • p. 967: Endogenous epithelial changes (atrophy, hyperplasia, dysplasia)
  • p. 967: Endocrine disorders (e.g., diabetes mellitus)
  • p. 967: Qualitative (pH, glucose concentrations) and quantitative (xerostomia, Sjogren’s syndrome, radiotherapy, drug-therapy) salivary changes
  • p. 967: Nutritional deficiency (e.g., iron, folate, vitamin B12)
  • p. 967: Nutritiona
  • p. 967: Commensal flora
  • p. 967: Malignancies (e.g., leukemia, agranulocytosis, others)
  • p. 967: High-carbohydrate diet
  • p. 967: Primary immunodeficiency (e.g., DiGeorge’s syndrome)
  • p. 967: Smoking (?)
  • p. 967: Secondary immunodeficiency (e.g., HIV disease, corticosteroids, anticancer therapy)

Pathophysiology and Clinical Presentation > Candidosis > Primary > Pseudomembranous Candidosis

  • p. 970: Pathophysiology and Clinical Presentation
  • p. 970: The currently accepted classification of oral Candida infections is based on two categories: primary and secondary OC
  • p. 970: In primary OC, the oral candidal infection is confined to the oral and perioral tissues.
  • p. 970: Pseudomembranous candidosis (PC) (also known as oral thrush) usually presents as acute, although,
  • p. 971: especially in immunocompromised patients, it can become chronic
  • p. 971: The chronic form is typical in individuals who are immunosuppressed or in patients using corticosteroids topically or by aerosol
  • p. 971: Clinically this form is characterized by the presence of semi-adherent soft, whitish-yellow creamy plaques, resembling milk or cottage cheese
  • p. 971: The plaques can be removed from the mucosa with a gauze or tongue blade and, once removed, reveals erythematous and sometimes a slightly bleeding surface
  • p. 971: The possibility to remove these plaques is considered as a diagnostic feature that differentiates this form from other white oral diseases, such as oral lichen planus, proliferative verrucous leukoplakia, white sponge nevus, or morsicatio buccarum.
  • p. 971: The pseudomembranes consist of desquamated epithelial cells, tangled aggregates of fungal hyphae, fibrin, and necrotic material
  • p. 971: Table 2 Classification of oral candidosis

Pathophysiology and Clinical Presentation > Candidosis > Primary > Erythematous Candidosis

  • p. 972: Histologically, hyphae penetrate the epithelium up to the spinous cell layer. The presence of edema and microabscesses, containing polymorphonuclear leukocytes, is typical within the outer layers of epithelium
  • p. 972: The deeper parts of the epithelium show acanthosis and an inflammatory infiltrate (Fig. 2).
  • p. 972: Lesions are usually asymptomatic, although sometimes patients may complain of burning and dysphagia, especially in the oropharyngeal forms
  • p. 972: topical antifungal therapy (e.g., amphotericin B lozenge 10 mg 4 per day for 2–3 weeks or nystatin/amphotericin B suspension 4–5 times per day for 4 weeks) will accelerate the resolution of the disease

Other annotations

  • p. 957: Oral and Maxillofacial Fungal Infections

Oral and Maxillofacial Viral Infections

Introduction

  • p. 984: More recently, HPV infections have received particular attention as oncogenic types etiologically linked to increasing numbers of cases of oral squamous cell carcinoma
  • p. 984: Herpes Viruses
  • p. 984: The human herpes viruses may promote a disease state in three distinctive ways: (1) direct destruction of cells and tissues, (2) induction of immune responses, and (3) facilitation of neoplastic transformation.

Herpes Viruses > Herpes Simplex Virus (HSV-1 and HSV-2) > Clinical Features

  • p. 985: Herpes Simplex Virus (HSV-1 and HSV-2)
  • p. 985: Clinical Features
  • p. 985: l, infected patients (Arduino and Porter 2008). Primary HSV-1 infection typically affects the mouth and arises within 1–2 weeks of acquisition of the virus. The clinical features comprise initial nonspecific features of malaise, pyrexia, and lethargy followed by the eruption of widespread ulceration of the oral mucosa and gingiva (Cunningham et al. 2006).
  • p. 985: (and hence may mimic acute necrotizing ulcerative gingivitis – ANUG)
  • p. 985: ilateral cervical lymphadenopathy and occasionally a generalized macular cutaneous rash.
  • p. 985: he signs and symptoms usually spontaneously resolve within 7–10 days, although the disease can be severe and prolonged in immunocompromised individuals
  • p. 986: Secondary HSV-1 infection of the mouth affects about 30% of patients with a history of probable primary infection.
  • p. 986: Many patients present with a likely secondary disease, however, cannot recall having the primary disease

Herpes Viruses > Herpes Simplex Virus (HSV-1 and HSV-2) > Clinical Features > Diagnosis

  • p. 987: Often patients have recurrences at the exact same site each time, presumably reflecting the location of residency of the herpes simplex virus within the trigeminal ganglion.
  • p. 987: Diagnosis
  • p. 987: Managemen
  • p. 987: Despite the symptoms being distressing, the management of primary HSV-1 infection can usually be based upon symptomatic relief alone. Topical anti-inflammatory drugs such as benzydamine hydrochloride spray or mouthwash, or topical anesthetics, such as lidocaine (lignocaine) gel,

Herpes Viruses > Varicella Zoster Virus > Clinical Features > Chickenpox

  • p. 988: may reduce painful symptoms and facilitate feeding. Systemic analgesia and antipyretics such as a nonsteroidal anti-inflammatory agent such as ibuprofen, or paracetamol can be helpful.
  • p. 988: Varicella Zoster Virus
  • p. 988: Varicella zoster virus (VZV, HHV-3) gives rise to a primary infection termed chickenpox and a secondary infection known as shingles. Infection is transmitted via droplets or close contact with lesions (i.e., the cutaneous rash of chickenpox).

Herpes Viruses > Ramsay Hunt Syndrome > Diagnosis

  • p. 990: Unlike primary HSV infection, antiviral therapy is almost always warranted for orofacial shingles. Oral acyclovir (e.g., 800 mg, 5 times daily for 7 days) is a typical therapy but sometimes valacyclovir or famciclovir can be used, especially if patients have difficulty in taking medication so frequently and/or the disease is atypical or prolonged.

Coxsackie Viruses > Hand, Foot, and Mouth Disease

  • p. 994: Hand, foot, and mouth disease (HFMD) is a common viral and exanthematous illness, typically affecting infants and children between 3 and 10 years of age. The most common virus involved is coxsackie virus A16, but other viruses such as coxsackie viruses A5, A7, A9, A10, B2, B5, and enterovirus 71 can also cause HFMD (Solomon et al. 2010).
  • p. 994: The transmission takes place through fecal-oral contact or via inhalation of respiratory droplets; however the direct interaction with cutaneous lesions can also cause disease transmission.

Other annotations

  • p. 983: Oral and Maxillofacial Viral Infections

Oral Ulcerative Lesions

Ulcerative Lesions of the Mouth > Infective Ulcerative Conditions

  • p. 1035: Recurrent Aphthous Stomatitis (RAS)
  • p. 1035: common oral mucosal disease affecting 10–20% of the general population.

Recurrent Aphthous Stomatitis (RAS) > Epidemiology

  • p. 1036: characterized by recurring ulcers of the oral mucosa usually manifesting first in childhood or adolescence in patients with no other systemic diseases.
  • p. 1036: minor, major, herpetiform, and severe
  • p. 1036: RAS usually initially develops in individuals between 10 and 19 years of age and becomes less common with time (
  • p. 1036: Cases of RAS that become more severe with age may be

Recurrent Aphthous Stomatitis (RAS) > Etiopathogenesis

  • p. 1037: indicative of an underlying systemic condition | Comment: Case pres
  • p. 1037: The incidence of RAS ranges between 5% and 50% and is dependent on the socioeconomic status and ethnicity of patients
  • p. 1037: The etiology of RAS is multifactorial and not yet well understood
  • p. 1037: infections, such as varicella zoster virus (VZV), cytomegalovirus (CMV), and human herpes virus (HHV) 6 and 7, oral streptococci, and Helicobacter pylori, although none of these have been confirmed and data remain inconclusive (Lin et al. 2005; Pedersen and Hornsleth 1993; Victoria et al. 2003).
  • p. 1037: Heredity may play a role as both twins and children with parents affected by RAS are more prone to develop the disease (Miller et al. 1980).
  • p. 1037: however specific abnormalities of the immune system have not yet been identified
  • p. 1037: Immunoglobulin serum levels and natural killer cells are usually within normal ranges in patients with RAS
  • p. 1037: Studies have shown defects of cell-mediated immunity with an alteration in the CD4+:CD8+ T lymphocyte ratio (Preeti et al. 2011). Specifically, CD4+ cells are more frequent in the pre-ulcer and healing phases, while CD8+ cell levels are higher when the ulcer is present (Bachtiar et al. 1998; Sun et al. 2000).

Recurrent Aphthous Stomatitis (RAS) > Diagnosis and Clinical Presentation

  • p. 1038: A dysfunction of the mucosal cytokine cascade has been associated with RAS with a subsequent increased cell-mediated immune response and local ulceration of the oral mucosa. Increased levels of interleukin-2 (IL-2), IL-4, IL-5, interferon-γ, and tumor necrosis factor-α in aphthous ulcers and raised levels of circulating IL-6 have been found in patients with RAS
  • p. 1038: Other possible precipitating factors for RAS include nutritional deficiencies, psychological stress, anxiety, hormonal fluctuations, allergy to certain foods, and sodium lauryl sulfatecontaining toothpaste (
  • p. 1038: Conditions that may present with RAS include micronutrient deficiencies, Behçet disease, celiac disease, inflammatory bowel disease, and HIV disease
  • p. 1038: The diagnosis of RAS is generally made through the patient’s history and clinical presentation
  • p. 1038: Biopsy is not indicated, although it may be helpful in atypical cases to rule out other condition
  • p. 1038: In some rare cases, the severity and frequency of RAS can increase in the elderly.
  • p. 1038: Crunchy, spicy, acidic food and certain beverages may make eating, speaking, and swallowing uncomfortabl

Recurrent Aphthous Stomatitis (RAS) > Management

  • p. 1039: Severe aphthous ulcers (Fig. 13) are a variant in which patients are almost never ulcer-free, and they are often associated with chronic pain, malnutrition, and weight loss. Patients typically develop new ulcers when the previous ones are healing. Both the keratinized and nonkeratinized mucosa may be affected. In HIV patients, severe recurrent aphthous ulcers are often larger than 1.0 cm in diameter.
  • p. 1039: typical RAS (such as in older individuals with new episodes or in patients with other/new systemic symptoms), laboratory tests may be helpful. A blood workup might be indicated if hematologic deficiencies are suspected (e.g., low serum levels of vitamin B12, folate, ferritin, and iron) or in HIV patients with a CD4 count below 100/mm3 (Crivelli et al. 1988)
  • p. 1039: Management
  • p. 1039: The management of RAS depends on the frequency and severity of the lesions. In many cases (especially for the minor form) treatment is not necessary as the pain is tolerable and does not interfere with the daily life activities of the patient
  • p. 1039: The main therapeutic goal for severe and painful cases is to reduce the frequency of the episodes and control the pain.
  • p. 1039: atients who report one to two outbreaks a year may be instructed to use over-the-counter local anesthetics (such as 10% benzocaine), viscous lidocaine, or mucoadhesive agent
  • p. 1040: able 3 Topical anesthetics and immunosuppressive agents used for management of recurrent aphthous stomatiti
  • p. 1040: Annotation

Pigmented Lesions of the Oral Mucosa

Introduction

Focal Pigmentation > Freckle/Ephelis > Epidemiology

  • p. 1195: Oral melanocytes are regularly interspersed between basal keratinocytes, and melanin from the melanocytes are transported and transmitted to epithelial cells via dendritic migration of melanosomes (melanin-containing vesicles).
  • p. 1195: There are no numerical or structural differences in oral melanocytes between light-skinned and dark-skinned individuals except that in the latter, the melanosomes are larger and more numerous
  • p. 1195: Focal Pigmentation
  • p. 1195: Freckle/Ephelis
  • p. 1195: Epidemiology
  • p. 1195: A freckle (ephelis) is a hyperpigmented macule commonly observed on the facial and perioral skin.
  • p. 1195: Etiology
  • p. 1195: Freckles are thought to be developmental in origin
  • p. 1195: Pathophysiology
  • p. 1195: Freckles are due to an increase in melanin production without an increase in the number of melanocytes and become more pronounced after sun exposur
  • p. 1195: Clinical-Pathologic Features
  • p. 1195: Freckles appear as a uniformly tan- or browncolored, oval or round macule, between 1 and 3 mm in size on sun-exposed cutaneous surfaces
  • p. 1195: appear on the perioral skin and vermillion border of the lips with increased frequency on the lower lip (H

Focal Pigmentation > Freckle/Ephelis > Patient Management

  • p. 1196: Patient Management
  • p. 1196: Treatment is typically not indicated for freckles in childhood or adolescence (Hatch 2005)
  • p. 1196: Oral/Labial Melanotic Macule
  • p. 1196: Epidemiology
  • p. 1196: A melanotic macule is a benign pigmented lesion that may occur on intraoral mucosal surfaces (oral melanotic macule) or on the lips (labial melanotic macule) (Tarakji et al. 2014)
  • p. 1196: the most common oral mucosal lesions of melanocytic origin and are also termed focal melanosis (
  • p. 1196: Oral/labial melanotic macules are present in up to 3% of the population, are typically observed in patients in the fourth and fifth decades, and have a 2:1 female predilection
  • p. 1196: Annotation
  • p. 1196: Etiology
  • p. 1196: not been definitively determined
  • p. 1196: Pathophysiology
  • p. 1196: Oral/labial melanotic macules are caused by an increased production and deposition of melanin within the basal cell layer, the lamina propria, or both (Meleti et al. 2008)
  • p. 1196: sun exposure does not appear to be a precipitating factor
  • p. 1196: Clinical-Pathologic Features
  • p. 1196: Features
  • p. 1196: solitary, wellcircumscribed lesions that are typically less than 1 cm in diameter
  • p. 1196: Overall, labial melanotic macules are the most common type of macules observed with the lower lip vermillion border predominantly affected
  • p. 1196: 2011).
  • p. 1196: In contrast to freckles, labial melanotic macules do not darken after exposure to the sun
  • p. 1196: are most commonly observed on the buccal mucosa, gingiva, and palate

Focal Pigmentation > Oral/Labial Melanotic Macule > Patient Management

  • p. 1197: Histopathological analysis of melanotic macules reveals an increase in melanin in the basal and parabasal layers of normal stratified squamous epithelium without an increase in number of melanocytes
  • p. 1197: Patient Management
  • p. 1197: Oral/labial melanotic macules are considered benign lesions without malignant potential
  • p. 1197: Since early malignant melanoma may have a similar clinical appearance and exhibits a predilection for the maxillary alveolar mucosa and palate, it is strongly advisable to perform an excisional biopsy for any suspected oral/labial melanotic macule for histopathologic analysis

Focal Pigmentation > Oral Melanoacanthoma > Patient Management

  • p. 1199: Melanocytic Nevu
  • p. 1199: Epidemiology
  • p. 1199: Melanocytic nevi, commonly referred to as “moles,” represent a group of benign tumors that develop due to melanocytic growth and proliferation (Alawi 2013; Hatch 2005)
  • p. 1199: The intramucosal nevus is the most frequently observed type of oral nevus followed by the blue nevus, compound nevus, junctional nevus, and combined nevus, in decreasing order of frequency (Alawi 2013)
  • p. 1199: Etiology
  • p. 1199: In general, melanocytic nevi are acquired lesions with both environmental and genetic factors thought to play a role in the development of cutaneous lesion
  • p. 1199: Sun exposure is a well-recognized environmental factor for development of cutaneous nevi (
  • p. 1199: Pathophysiology
  • p. 1199: The pathogenesis of melanocytic nevi, including oral melanocytic nevi, is poorly understood
  • p. 1199: Blue nevi are melanocytic lesions that typically appear slate blue to blue black and account for up to 35% of all oral nevi (Pinto et al. 2003). They are categorized into the common type and the less frequently encountered cellular type, and while each has specific characteristic histopathologic features, both types harbor melanin particles deep to the surface so that reflected light appears blue to the observer
  • p. 1199: Clinical-Pathologic Features
  • p. 1199: Cutaneous junctional nevi commonly appear as a sharply demarcated macule less than 6 mm in diameter with brown or blue coloration
  • p. 1199: Compound nevi may be macular or slightly elevated, soft with a relatively smooth surface, while intradermal (cutaneous counterpart to intramucosal) nevi exhibits loss of pigmentation and a papillomatous surface with possible central hair growth (Alawi 2013)

Focal Pigmentation > Melanocytic Nevus > Clinical-Pathologic Features

  • p. 1200: no distinguishing clinical characteristics; however, they are usually asymptomatic, solitary, well circumscribed, less than 1 cm, macular or nodular in appearance, and brown or blue in color (

Focal Pigmentation > Melanocytic Nevus > Patient Management

  • p. 1201: Patient Management
  • p. 1201: Treatment of cutaneous lesions are typically not indicated unless a cosmetic concern exists and there is a tendency for lesion regression with advancing age (Alawi 2013)
  • p. 1201: A biopsy is necessary to confirm the diagnosis of oral melanocytic nevi as the clinical presentation resembles other focally pigmented lesions, such as malignant melanoma
  • p. 1201: Oral melanocytic nevi are indicated for complete, conservative surgical excision with recurrence rarely reported
  • p. 1201: The number of melanocytic nevi represents an independent risk factor for development of melanoma, with greater than 50 nevi increasing the risk of melanoma approximate

Other annotations

  • p. 1193: Pigmented Lesions of the Oral Mucosa
  • p. 1193: Oral health-care providers must assess several parameters associated with pigmented lesions, such as location, shape, color, and size.
  • p. 1193: Annotation

White and Red Lesions of the Oral Mucosa

Developmental Conditions > White Sponge Nevus (Cannon White Sponge Nevus, Familial White Folded Dysplasia) > Etiology and Pathophysiology

  • p. 1210: White Sponge Nevus (Cannon White Sponge Nevus, Familial White Folded Dysplasia)
  • p. 1210: White sponge nevus is caused by mutation in genes associated with keratin-4 (KRT4) or keratin-13 (KRT13), resulting in keratin instability and abnormal aggregation of tonofilaments, which in turn promotes abnormal proliferation and thickening of the oral epithelium (
  • p. 1210: The lesions of white sponge nevus appear at birth, early childhood, or adolescence
  • p. 1210: sually present in a bilateral, symmetric fashion as asymptomatic, thick, white, spongy plaques, usually on the buccal mucosa, ventral tongue, lip mucosa, and soft palate
  • p. 1210: There may also be esophageal, upper airway, and genital lesions, but the skin is not affected.
  • p. 1210: Diagnosis is established through a biopsy because other conditions such as chronic traumatic keratoses may appear clinically similar.
  • p. 1210: ere is no effective treatment. Cases that have reportedly responded to antibiotics or antibacterial mouth rinses are not likely to represent this condition but instead a reactive keratosis.

Reactive Lesions > Chemical Desquamation > Patient Management

  • p. 1212: Leukoedema
  • p. 1212: a process caused by mild local irritation, such as from cigarette or marijuana smoking, the use of some toothpastes and mouth rinses, and from physical trauma such as sucking (Heyl and Raubenheimer 1987
  • p. 1212: Its prevalence differs between gender and racial groups ranging from 0.96% to 90% of the
  • p. 1212: highest prevalence in African-American males
  • p. 1212: Leukoedema presents as asymptomatic, white-gray translucent linear reticulations, most frequently seen on the buccal mucosa and to a lesser extent, the lip mucosa and ventral tongue.
  • p. 1212: he complete disappearance of these pale reticulations upon stretching the mucosa (the so-called “stretch test”)
  • p. 1212: A biopsy is rarely necessary although the reticulations may be mistaken for those of lichen planus, prompting a biopsy.
  • p. 1212: he patient should be reassured as to the benign nature of the condition. If there is an associated smoking habit, it is a good opportunity to discuss habit cessation.

Reactive Lesions > Contact Stomatitis > Patient Management

  • p. 1217: Nicotinic Stomatitis (Stomatitis Nicotina)
  • p. 1217: icotinic stomatitis (NS) is an inflammatory condition of the hard palatal mucosa presenting as thickened and hyperkeratotic alteration of the palatal mucosa, commonly seen with pipe, cigar, or reverse smokers
  • p. 1217: Reverse smoking lesions which are the most severe form of nicotinic stomatitis

Reactive Lesions > Nicotinic Stomatitis (Stomatitis Nicotina) > Etiology and Pathophysiology

  • p. 1218: Etiology and Pathophysiology
  • p. 1218: NS is a misnomer because the lesions develop in response to the intense heat associated with smoking habits and not from nicotine.
  • p. 1218: It has also been reported in patients who habitually consume extremely hot beverages. As a result of chronic exposure to heat, the palatal mucosa becomes hyperkeratotic and thickened, and the orifices of excretory salivary ducts become inflamed.
  • p. 1218: NS is more common in males in the fifth decade and older, and is usually asymptomatic
  • p. 1218: The palatal mucosa is diffusely whitened, and established lesions are fissured, with a cobblestone or “dried mud” appearance.
  • p. 1218: he surface often contains scattered 1–3 mm, red punctuate papules that represent the inflamed orifices of minor salivary gland ducts
  • p. 1218: Because these lesions are fairly uniform appearing and symmetric, any localized area that appears raised, warty, or fleshy must be viewed with suspicion and biopsied.
  • p. 1218: Early NS lesions may regress on cessation of pipe smoking; however, patients with persistent
  • p. 1218: esions should be followed up regularly to monitor for malignant transformation, particularly reverse smokers
  • p. 1218: benign oral condition characterized by marked elongation of filiform papillae resulting in a hairlike appearance or a matted/coated appearance of the tongue dorsum.
  • p. 1218: Etiology and Pathophysiology
  • p. 1218: HT is caused by retention or accumulation of keratin on the filiform papillae and/reduced normal desquamation;
  • p. 1218: he first is usually caused by dehydration, and the second by poor diet (Manabe et al. 1999).
  • p. 1218: This is most frequently seen in patients who have salivary gland hyposalivation from taking anticholinergic medications, not drinking sufficient water, with chronic anxiety or as a result of smoking tobacco.
  • p. 1218: Less frequent causes of hyposalivation include head and neck radiation for cancer and Sjogren’s syndrome
  • p. 1218: Fig. 8 Nicotinic stomatitis: diffuse whiteness of the palatal mucosa with cobblestone appearance and red puncta (Image courtesy of Dr Ivan Stojanov, Case Western Reserve University, Cleveland, Ohio, USA)

Reactive Lesions > Hairy/Coated Tongue > Clinical-Pathologic Features

  • p. 1219: Clinical-Pathologic Features
  • p. 1219: HT is generally seen in adults because it is strongly associated with hyposalivation and chronic illness, and there may be a male predilection
  • p. 1219: usually asymptomatic
  • p. 1219: These matted papillae may be stained by the natural color of foods, food dyes, tobacco, or pigment produced by pigment-producing (chromogenic) bacteriae on the tongue.
  • p. 1219: Patient Management
  • p. 1219: HT is self-limiting with no serious sequelae, and patients should be reassured that they do not have an infection
  • p. 1219: Improved hydration, eating a diet containing fresh fruits and vegetables, and reducing habits that cause dehydration of the mucosa (such as smoking and using alcoholic mouth rinses) will improve this condition.
  • p. 1219: Brushing the tongue gently with a soft toothbrush or gentle use of a tongue scraper helps to remove the retained keratin and promote desquamation, but should be used sparingly so as not to cause further irritation to the dorsal tongue epithelium

Other annotations

  • p. 1207: White and Red Lesions of the Oral Mucosa

Unmapped Annotations

  • p. C1: Contemporary Oral Medicine

Graph View

Backlinks