Читать книгу Clinical Cases in Periodontics - Группа авторов - Страница 60

A. According to the 2017 World Workshop on the Classification of Periodontal and Peri‐Implant Diseases and Conditions, the etiology of the non‐plaque‐induced gingival lesions can be divided into several categories [1]. It should be emphasized that even though the direct cause of the lesions in these cases is not plaque, the severity of the inflammation often depends on the interaction with the bacterial plaque present.

 Genetic/developmental disorders (e.g. hereditary gingival fibromatosis)

 Specific infections (e.g. bacterial, viral, fungal)

 Inflammatory and immune conditions and lesions (e.g. hypersensitivity reactions, autoimmune diseases of skin and mucous membranes, granulomatous inflammatory conditions)

 Reactive processes (e.g. epulides)

 Neoplasms (e.g. premalignant, malignant)

 Endocrine, nutritional, and metabolic diseases (e.g. vitamin deficiencies)

 Traumatic lesions (e.g. physical/mechanical insults, chemical [toxic] insults, thermal insults)

 Gingival pigmentation

Arriving at a specific diagnosis may be a complex process and requires taking a detailed history along with the specific clinical presentation of a particular patient.

B. Desquamative gingivitis (DG) is a clinical term used to describe a condition characterized by intense erythema, desquamation, and/or ulceration of the gingiva [2]. A variety of different conditions can manifest as DG, but it is most often associated with one of the vesiculoerosive diseases (see answer to Question C).

Plaque‐induced gingivitis is a response to inadequate oral hygiene practices and generally presents with inflammation at the gingival margin. This inflammation often causes the tissue to become erythematous and edematous. There is commonly bleeding on probing and an increase in gingival crevicular fluid or exudate. The clinical signs and symptoms of plaque‐induced gingivitis are usually reversed after removing the primary etiology of bacteria‐laden plaque. Refer to Chapter 1, Case 2 for a detailed description of plaque‐induced gingivitis.

C. DG may be a manifestation of multiple dermatologic conditions, most commonly LP, mucous membrane pemphigoid, or pemphigus vulgaris [3]. Other conditions that can present as DG include linear immunoglobulin A disease, dermatomyositis, or mixed connective tissue disease [4]. Once a clinical diagnosis of DG is rendered, a definitive diagnosis must be established.

D. Regardless of the underlying cause of DG, it has been shown that improved oral hygiene can decrease the severity of the lesions [5]. However, this will not bring about complete resolution and, more importantly, does not address the underlying cause. A biopsy of the lesion must be taken to establish a definitive diagnosis. The biopsy should include intact epithelium because the center of an ulcer histologically reveals only nonspecific granulation tissue. A second specimen submitted for immunofluorescence studies may aid in the diagnosis.

The symptoms of DG are managed based on the underlying cause of the condition. In most cases, the oral lesions themselves may be managed with topical corticosteroids. A common first line of treatment is 0.05% fluocinonide gel, which may be applied to the lesions four times daily. This may be delivered directly to the gingiva or, in the case of diffuse gingival involvement, placed in a custom‐fabricated tray comparable to a bleaching tray typically used for tooth whitening. Alternatively, a dexamethasone elixir may be prescribed for patients to swish and expectorate three times daily. It is important to monitor the patients for signs of oral candidiasis that may develop in the setting of steroid use.

Patients diagnosed with mucous membrane pemphigoid should be referred to an ophthalmologist who is familiar with the ocular lesions of this condition to guard against vision loss. Although corticosteroid therapy has helped to reduce the mortality rate associated with pemphigus vulgaris to less than 10% [6], patients with this diagnosis should be evaluated by their primary care physicians or dermatologists for the evaluation of cutaneous lesions.

E. Oral LP is one of the most common mucocutaneous diseases manifesting on the gingiva. Oral involvement alone is common; concomitant skin lesions develop in patients with oral lesions in approximately 15% of cases [7]. Most patients who present with oral LP are middle aged. Children are rarely affected [8]. A predilection for women is shown in most series of cases by a ratio of 3 : 2 over men. The prevalence of oral LP in various populations has been found to be 0.1–4% [9].

Different classifications have been used for oral LP, and a recent classification groups lesions into three categories: reticular, atrophic, and ulcerated [10]. The reticular form is most common and often goes unnoticed by the patient. It generally involves the posterior buccal mucosa bilaterally, but any area of the oral mucosa may be affected. Reticular LP is named because of its characteristic pattern of interlacing white lines (Wickham striae). Erosive/erythematous and ulcerated LP are less common but more significant for the patient because the lesions are usually symptomatic. The periphery is usually bordered by the fine white radiating striae of reticular LP. Erythema with or without ulcers involving the gingiva are characteristic features of DG.

F. The most characteristic clinical manifestations of oral LP are white interlacing white striae appearing bilaterally on the posterior buccal mucosa [11]. A diagnosis of reticular LP can often be made based on simply the clinical presentation of the lesions. Erosive and ulcerated LP can be more challenging to diagnose based on clinical features alone. Unilateral lesions or presentations lacking typical radiating white striae may be difficult to distinguish from other ulcerative or erosive diseases. If the diagnosis is in question after clinical examination, a biopsy is necessary to confirm a diagnosis.

G. The etiology of most oral LP cases is idiopathic. Oral lichenoid lesions can also be associated with various types of medications including nonsteroidal anti‐inflammatory drugs, antihypertensive agents, antimalarials, gold salts, and penicillamine [12]. Unilateral oral lichenoid lesions are rare and may be secondary to contact with amalgam dental restorations.

H. Oral LP presents histologically with varying degrees of orthokeratosis and/or parakeratosis. There is disruption of the basal cells and transmigration of T lymphocytes into the basal and parabasal cell layers of the epithelium. Degenerating keratinocytes termed Civatte bodies (colloid bodies) are often found at the junction of the epithelium and connective tissue. There is typically a subepithelial bandlike accumulation of T lymphocytes and macrophages characteristic of a type IV hypersensitivity reaction [13] (Figure 1.3.2). These features are characteristic but not specific to oral LP. Other interface processes including lupus erythematosus and chronic ulcerative stomatitis have similar histopathologic presentations.

I. Reticular LP often causes no symptoms and need not be treated. The first line of treatment for symptomatic erosive LP is topical corticosteroids. Fluocinonide gel applied to the most symptomatic areas or dexamethasone elixir used as a mouth rinse up to four times per day is often sufficient to induce healing within one to two weeks. Patients should be informed that the lesions will likely return and the corticosteroids should be reapplied. Patients should be monitored for their response and for the possibility of candidiasis induced by use of the steroids. Another important part of the therapeutic regimen in patients with DG is meticulous plaque control, which results in significant improvement in many patients [14].

Figure 1.3.2 Characteristic histopathology of lichen planus demonstrates parakeratinized and/or orthokeratinized stratified squamous epithelium with sawtooth‐shaped rete ridges, squamatization of basal cells, and a bandlike infiltrate of lymphocytes in the superficial connective tissue.

J. LP is a chronic condition with lesions that wax and wane over time. The erosive form should be monitored and treated as necessary to improve patient comfort. There has long been controversy over the malignant potential of LP. Recent studies suggest malignant transformation appears to be more common in older females, often with erythematous LP, and the rate has been reported to range from 0.9 to 1.1% [15,16].