|
| A) | Patients are asymptomatic. | ||
| B) | It is accompanied by a foul odor. | ||
| C) | Patients always present with a high fever. | ||
| D) | Involvement predominates in the posterior teeth. |
The classic identifying lesion associated with ANUGP is a painful, necrotic ulceration that originates in the interdental papilla. The lesion is often accompanied by a grey-white pseudomembrane—a necrotic layer of debris. The removal of this pseudomembrane will yield an underlying layer of tissue that bleeds profusely and is extremely sensitive to any environmental stimulus. Anterior teeth are involved more than posterior teeth, with a variance in the number of teeth and surfaces involved [2]. Erythema and edema of the adjacent tissue is extensive, and a bright red margin is peripheral to the lesion. The process begins at the tips of the interdental papilla and can continue to involve the entire interdental gingiva. The necrotic tissue produces a foul odor (fetor oris) that is another diagnostic feature. Elevation in body temperature will occur in some, but not all, patients. Localized lymphadenopathy, increased salivation, and malaise may also accompany these outbreaks [3].
| A) | resolves spontaneously within 14 days. | ||
| B) | always has suppuration as a diagnostic feature. | ||
| C) | is more common in the maxillary arch than the mandible. | ||
| D) | usually occurs via direct extension of a contiguous infection. |
Osteomyelitis of the jaws (OMJ) begins as an inflammatory process of the medullary bone. Extension of this infection outward to the cortical bone and periosteum leads to destruction and necrosis of bone and osseous remodeling of the affected areas [10]. There are varied classifications for this condition that reflect origin, duration, and the presence or absence of suppuration from the involved area(s).
It is rare, but possible, for a pathogenic organism to cause OMJ via the hematogenous route. However, most cases develop by non-hematogenous means via an extension of a contiguous oral infection [11]. Acute osteomyelitis occurs for 30 days or less, while the chronic form continues for more than 30 days. Osteomyelitis that presents with an absence of intraoral or external suppuration or fistulas in the affected area is categorized as non-suppurative; the presence of these features indicates the suppurative form [11,12].
| A) | usually die because of systemic sepsis. | ||
| B) | are afebrile upon clinical presentation. | ||
| C) | present with multiple areas of suppuration. | ||
| D) | have a bilateral cellulitis with involvement of the submental, sublingual, and submandibular fascial spaces. |
Few acute diseases demonstrate the potentially fatal consequences of odontogenic infections as Ludwig angina, which was first described in 1836 by Wilhelm Friedrich von Ludwig [16]. By definition, this is a rapidly advancing cellulitis that features bilateral involvement of the submandibular and sublingual fascial spaces posteriorly and the submental fascial space anteriorly [17,18]. The origin of approximately 90% of Ludwig angina cases is odontogenic; usually, carious and/or periodontally involved lower molars are the source of the initial oral infection [19]. The clinical presentation is of diffuse cellulitis. Infection and edema from bilateral involvement of the submandibular space causes an indurated swelling of both sides of the neck above the hyoid bone [18]. When bilateral involvement of the sublingual spaces occurs, the posterior aspect of the tongue becomes enlarged. Edema and swelling in the floor of the mouth cause the tongue to be elevated above the level of the mandibular teeth [18,20]. When this occurs, swallowing saliva is difficult for patients and drooling becomes common. Speaking may also be difficult as basic movements of the tongue are severely restricted [18]. Despite the swelling, intraoral and facial suppuration is rarely seen. The areas involved in Ludwig angina can extend to the clavicles and even to the superior aspect of the chest. The skin overlying these sites can appear erythematous. The most critical concern for patients afflicted with Ludwig angina is airway compromise. Death is more common from airway obstruction than from systemic sepsis [21]. Many patients are febrile upon clinical presentation.
| A) | do not cross midline. | ||
| B) | usually occur in older adults. | ||
| C) | are curable with antibiotic therapy. | ||
| D) | affect both the keratinized and non-keratinized oral mucosa. |
The initial infection with herpes simplex virus type 1 (HSV-1) can occur at any age, but it is most frequently seen in infants and young children [25]. Intraoral lesions are most prominent in this initial presentation, called primary herpetic gingivostomatitis. Occasionally, the skin around the lips also becomes infected. The oral lesions of primary herpetic gingivostomatitis affect both the keratinized and non-keratinized oral mucosa [26]. Vesicles may form but can rupture quickly to produce non-specific ulcers. The initial outbreak can be very painful, with accompanying fever, lymphadenopathy, and malaise. Swallowing can be difficult when palatal lesions are involved [25]. Palliative support with analgesics, antipyretics, and nutritional support usually allow for recovery within two weeks. The disappearance of these initial lesions is not equated with a complete eradication of this disease. Instead, the virus migrates to a regional nerve ganglion. The trigeminal ganglion is the usual reservoir for HSV-1, where it can lie dormant for years. Reactivation of HSV-1 can occur at any time with exposure to certain stimuli; stress, illness, sunlight, and immunosuppression are considered among the many factors that can end viral dormancy [25,27]. As opposed to the primary herpetic gingivostomatitis, recurrent lesions occur most often on the junction of the lips and skin and are known as recurrent herpes labialis. These lesions begin with formation of minute vesicles that coalesce to form several large lesions. Most patients experience a prodromal sensation characterized by itching, burning, tingling, or tightness of the skin in the area that will feature the herpetic outbreak [25]. The lesions of herpes labialis rupture, form scabs, and ultimately heal within two weeks without scar formation (Image 1). Patients should be advised not to touch these recurrent lesions as the vesicles contain a multitude of viral particles, and upon inoculation into the skin of a fingertip, the condition known as herpetic whitlow can develop. The virus is also highly contagious during outbreaks, and patients should take steps to prevent infecting close contacts. The affected area can be subjected to a lifetime of recurrent painful herpetic outbreaks.
| A) | usually heal without scar formation. | ||
| B) | contain the live virus and should not be touched. | ||
| C) | may have a prodromal sensation prior to their eruption. | ||
| D) | All of the above |
The initial infection with herpes simplex virus type 1 (HSV-1) can occur at any age, but it is most frequently seen in infants and young children [25]. Intraoral lesions are most prominent in this initial presentation, called primary herpetic gingivostomatitis. Occasionally, the skin around the lips also becomes infected. The oral lesions of primary herpetic gingivostomatitis affect both the keratinized and non-keratinized oral mucosa [26]. Vesicles may form but can rupture quickly to produce non-specific ulcers. The initial outbreak can be very painful, with accompanying fever, lymphadenopathy, and malaise. Swallowing can be difficult when palatal lesions are involved [25]. Palliative support with analgesics, antipyretics, and nutritional support usually allow for recovery within two weeks. The disappearance of these initial lesions is not equated with a complete eradication of this disease. Instead, the virus migrates to a regional nerve ganglion. The trigeminal ganglion is the usual reservoir for HSV-1, where it can lie dormant for years. Reactivation of HSV-1 can occur at any time with exposure to certain stimuli; stress, illness, sunlight, and immunosuppression are considered among the many factors that can end viral dormancy [25,27]. As opposed to the primary herpetic gingivostomatitis, recurrent lesions occur most often on the junction of the lips and skin and are known as recurrent herpes labialis. These lesions begin with formation of minute vesicles that coalesce to form several large lesions. Most patients experience a prodromal sensation characterized by itching, burning, tingling, or tightness of the skin in the area that will feature the herpetic outbreak [25]. The lesions of herpes labialis rupture, form scabs, and ultimately heal within two weeks without scar formation (Image 1). Patients should be advised not to touch these recurrent lesions as the vesicles contain a multitude of viral particles, and upon inoculation into the skin of a fingertip, the condition known as herpetic whitlow can develop. The virus is also highly contagious during outbreaks, and patients should take steps to prevent infecting close contacts. The affected area can be subjected to a lifetime of recurrent painful herpetic outbreaks.
| A) | The initial clinical presentation is shingles. | ||
| B) | It causes oral lesions but not cutaneous lesions. | ||
| C) | It can lie dormant for decades before reactivation. | ||
| D) | It is characterized by a bilateral distribution of lesions. |
The varicella zoster virus (VZV) has a pathogenesis that is similar to that of HSV-1. The initial infection caused by this virus is chickenpox and is most frequently seen in children. After this infection resolves, VZV migrates to dorsal root and cranial nerve ganglia, where it can lie dormant forever or until its reactivation, the clinical presentation of which is known as shingles [4,29]. Although less common than cutaneous lesions, both chickenpox and shingles can have oral manifestations.
The initial infection of chickenpox is a highly contagious disease that is spread through direct contact of infected secretions such as respiratory droplets. A rash with macular, vesicular, and pustular stages is seen predominantly on the head, neck, and trunk. These lesions resolve approximately two weeks after their emergence [2]. Oral lesions are less common but can occur and feature vesicles that rupture quickly and form small, non-specific ulcers (Image 2). When these occur on the soft palate, swallowing and eating can be painful. Systemic analgesics and topical anesthetic preparations can palliate some of these symptoms. The primary infection of chickenpox resolves uneventfully for most patients. However, immunocompromised children and adults who contract this illness for the first time can have severe systemic involvement and even succumb from its complications.
Many years after the resolution of the initial outbreak of chickenpox, the reactivation of VZV causes the development of shingles. Similar to chickenpox, the head and thorax are the most common areas of involvement. The rash is similar in appearance to that of chickenpox, but the stabbing and radiating pain that accompanies these outbreaks distinguishes between these two diseases.
Shingles primarily affects older adults and the immunocompromised but can occur in any age group. When present, the oral and maxillofacial manifestations of shingles can be severe and cause intense, prolonged pain. Oral manifestations of shingles commonly involve the ophthalmic, maxillary, and mandibular division of the trigeminal nerve. Unilateral distribution is a classic feature, as the cutaneous and intraoral lesions of shingles do not cross midline [30,31]. Vesicles form and rupture to form painful ulcers in the affected areas, which can take two weeks or longer to heal. The pain that accompanies the intraoral lesions can make eating and swallowing extremely difficult. Topical anesthetic solutions may offer some relief from this pain. Systemic anti-inflammatory medications and narcotic analgesics are often needed to subdue the associated pain. Cutaneous lesions of the maxillofacial region are also very painful, and involvement of the ophthalmic division of the trigeminal nerve can produce corneal ulceration and resultant loss of vision [32]. Viral involvement of the facial nerve can cause Ramsay Hunt syndrome. This features cutaneous vesicle eruptions of the ear and facial nerve dysfunction with weakness and paralysis of the affected side [29,33]. VZV can even cause osteonecrosis of the alveolar bone, possibly the result of vasoconstriction with subsequent ischemia to the involved area. Tooth loss can also occur [34].
| A) | shingles. | ||
| B) | chickenpox. | ||
| C) | recurrent herpes labialis. | ||
| D) | primary herpetic gingivostomatitis. |
Shingles primarily affects older adults and the immunocompromised but can occur in any age group. When present, the oral and maxillofacial manifestations of shingles can be severe and cause intense, prolonged pain. Oral manifestations of shingles commonly involve the ophthalmic, maxillary, and mandibular division of the trigeminal nerve. Unilateral distribution is a classic feature, as the cutaneous and intraoral lesions of shingles do not cross midline [30,31]. Vesicles form and rupture to form painful ulcers in the affected areas, which can take two weeks or longer to heal. The pain that accompanies the intraoral lesions can make eating and swallowing extremely difficult. Topical anesthetic solutions may offer some relief from this pain. Systemic anti-inflammatory medications and narcotic analgesics are often needed to subdue the associated pain. Cutaneous lesions of the maxillofacial region are also very painful, and involvement of the ophthalmic division of the trigeminal nerve can produce corneal ulceration and resultant loss of vision [32]. Viral involvement of the facial nerve can cause Ramsay Hunt syndrome. This features cutaneous vesicle eruptions of the ear and facial nerve dysfunction with weakness and paralysis of the affected side [29,33]. VZV can even cause osteonecrosis of the alveolar bone, possibly the result of vasoconstriction with subsequent ischemia to the involved area. Tooth loss can also occur [34].
| A) | shingles. | ||
| B) | Kaposi sarcoma. | ||
| C) | recurrent herpes labialis. | ||
| D) | primary herpetic gingivostomatitis. |
Although the oral and cutaneous lesions heal, many patients with shingles develop postherpetic neuralgia. This debilitating pain syndrome originates in the area affected by the vesicular rash and can persist for years after the area has healed. Approximately 50% of patients older than 60 years of age with shingles experience this problem [29]. Because many of these patients will have narcotic analgesics and/or antidepressant medications prescribed, healthcare professionals should use caution in dispensing any additional medication that could have harmful interactions.
| A) | is usually painful. | ||
| B) | features easily removable plaques. | ||
| C) | predominantly affects the buccal mucosa. | ||
| D) | is caused by the reactivation of the Epstein-Barr virus. |
Oral hairy leukoplakia features bilateral areas of epithelial hyperplasia on the lateral and ventral surface of the tongue found upon oral examination (Image 3). Corrugated in texture, these lesions are adherent to the underlying tissue and are asymptomatic for the patient. The emergence of oral hairy leukoplakia in patients with HIV is caused by the reactivation of the Epstein-Barr virus as the efficacy of the immune system continues to decrease. While oral antiviral medication can resolve these lesions, they have a tendency to recur upon the cessation of therapy. Occasionally, the size of these lesions can be large enough to be traumatized during occlusion. Because these lesions appear when the CD4+ count has diminished to levels of approximately 300/mcL, this reflects continued deterioration of the immune system and a less favorable overall prognosis for the patient [50].
| A) | involvement of the interdental papilla only. | ||
| B) | a decrease in the tendency for gingival bleeding. | ||
| C) | rapid resolution with basic oral hygiene procedures. | ||
| D) | an intense, finely demarcated zone of gingival erythema. |
An early manifestation of the gingival involvement is that of linear gingival erythema. Formerly called HIV-associated gingivitis, this problem has a unique clinical presentation in patients with HIV infection. This condition features an intense zone of inflammation that is finely demarcated and involves the free and attached gingiva and extends into the interdental papilla [51]. The tendency for gingival bleeding is increased. These areas reflect minimal or no resolution despite excellent oral hygiene and conventional periodontic treatment. Consideration has been given that this could represent an unusual distribution and chronic infection with C. albicans[48].
| A) | are an AIDS-defining illness. | ||
| B) | are only found in patients with HIV/AIDS. | ||
| C) | feature cutaneous lesions but not intraoral lesions. | ||
| D) | usually occur early in the course of HIV infection. |
Once a rare malignancy that most frequently occurred in elderly men of the Mediterranean region and certain regions of Africa, Kaposi sarcoma is now the most common malignant disease in patients with HIV/AIDS [53]. In patients without HIV, Kaposi sarcoma grows slowly and is usually seen as cutaneous lesions on the extremities. The lesions associated with HIV/AIDS tend to grow rapidly and can disseminate to cause multiple organ involvement. Lesions may arise within the endothelium of small blood vessels and cause cutaneous and intraoral lesions. Kaposi sarcoma was the first pathologic entity to be identified as an AIDS-defining illness [54,55].
Although cutaneous lesions are more common, oral lesions of Kaposi sarcoma affect approximately one-third of patients [56]. Initial oral lesions are asymptomatic, and their red-to-violet color can resemble ecchymosis within the mucosal and gingival tissues (Image 4). An incisional biopsy must be completed to establish a definitive diagnosis. The most common intraoral site affected by Kaposi sarcoma is the hard palate [57]. However, lesions have been seen on all other intraoral sites. As the condition progresses, the flat appearance of the early lesions changes to a more raised appearance (in the case of a single lesion) or multiple lobules of a larger lesion. The color can vary and may be a composite of red, blue, purple, or brown. Enlargement of the lesions can cause difficulty in eating, speaking, and swallowing [57]. Partial or complete dentures may be difficult to fit and/or wear as these lesions will change tissue topography. If surgery is performed to remove these lesions, alterations in tissue contour would require that a new prosthesis be made. New Kaposi sarcoma lesions perpetuate this cycle, and patients may be unable to wear a prosthesis.
| A) | can occur on any mucosal surface. | ||
| B) | usually are invasive and erythematous. | ||
| C) | occur only in patients with HIV/AIDS. | ||
| D) | are adherent to the tissues and cannot be removed. |
The clinical presentation of oropharyngeal candidiasis can have four different appearances, the most common of which is pseudomembranous candidiasis [61]. The lesions typical of pseudomembranous candidiasis consist of white-to-yellow flecks or plaques with a smooth and slightly raised appearance. The surface of these lesions can be removed easily, leaving an erythematous base that may bleed. These plaques occur on any mucosal surface.
| A) | 30% | ||
| B) | 50% | ||
| C) | 70% | ||
| D) | 90% |
There are several factors that can result in C. albicans becoming an oral pathogen and manifesting in varied clinical presentations. Diseases such as HIV/AIDS that decrease the normal immune response allow a normal oral inhabitant such as C. albicans to flourish and can cause not only oropharyngeal candidiasis, but also esophageal candidiasis. Among patients who have advanced to AIDS, 90% will experience this fungal pathology [63]. Patients who undergo chemotherapy for systemic malignancies develop problems with granular and agranular leukocytes, both of which are essential components of a healthy immune system, and may subsequently present with symptoms of candidiasis [61].
| A) | Immunosuppression | ||
| B) | The use of systemic antibiotics | ||
| C) | Any illness or medication that can decrease salivary flow | ||
| D) | All of the above |
Oropharyngeal candidiasis can develop quickly in immunocompromised patients and pose a serious problem if organisms are disseminated systemically. Because these patients may also be experiencing mucositis related to chemotherapy, the presence of denuded mucosal surfaces can facilitate systemic access for fungal organisms [61]. Systemic fungal infections that develop in this fashion have a fatality rate that is twice that of similarly disseminated bacterial infections [64].
Decreases in salivary production from medical procedures, such as radiotherapy for oral cancer, or autoimmune diseases, such as Sjögren syndrome, can cause a change in the oral environment that is favorable to the development of candidiasis. Both of these possible causes will result in long-term problems as radiation-induced damage to salivary glands is irreversible and most autoimmune disorders, including Sjögren syndrome, are incurable diseases. Saliva contains immunoglobulins that promote the proper function of B-lymphocytes, a component of the immunologic response toward C. albicans[65]. When the lubricating and cleansing action of the saliva are diminished, microorganism adherence to the mucosal surfaces is enhanced. Increased exposure time and decreased immune function allow for the development of opportunistic infections such as candidiasis. This is a problem that will resolve for patients undergoing chemotherapy after their regimen ends and the formed elements of human blood return to their appropriate levels.
Medications can be another source of changes to the oral environment [61]. Antibiotics such as amoxicillin or penicillin can alter the composition of the oral microflora. Because these medications are bactericidal, they will decrease the number of bacteria that would normally compete with C. albicans for the available nutrient supply. This decrease in competitive inhibition can allow for candidiasis to develop in susceptible individuals. Fungal infections triggered by antibiotic use usually resolve with the cessation of antibiotic therapy but can recur if the same or similar antibiotic regimen is used again. In addition, numerous medications can cause a decrease in salivary flow, which may also contribute to fungal overgrowth.
| A) | can recur at any time. | ||
| B) | are of fungal or viral origin. | ||
| C) | occur on keratinized mucosa only. | ||
| D) | are not associated with a genetic predisposition. |
Recurrent aphthous stomatitis, ulcerative lesions also known as recurrent aphthous ulcers or more commonly as canker sores, features painful ulcerative lesions that generally heal without scarring in immunocompetent patients but can recur at any time (Image 5). The size is a demarcation for the categorization of these lesions. Minor aphthae are less than 1 cm at the greatest diameter; major aphthae exceed this dimension. Each type of lesion only involves nonkeratinized tissues, such as the buccal and labial mucosa, the soft palate, and the surface layer of the floor of the mouth. Movement of the mucosa affected by lesions of either size is painful and can interfere with speaking, eating, and swallowing. Major aphthae tend to have irregular shapes and borders and ulcers with more depth. The numbers of both can vary, although solitary lesions are uncommon. Lesions of aphthous stomatitis feature a shallow yellow base and an intense erythematous halo peripherally.
The incidence of these lesions varies from 20% to 60% and can reflect the actual population studied. Many patients develop the condition during the first two decades of life [68]. There has yet to be a bacterial, viral, or fungal etiology that can be attributed to the origin of these lesions. A genetic predisposition to the occurrence is possible. When both parents have a history of these lesions, there is a 90% chance that their children will be similarly affected [69]. Common predisposing factors include physical and emotional stress and sensitivity to ingredients in toothpaste and/or mouthwash, such as sodium lauryl sulfate and alcohol [70,71]. Tissue manipulation during dental or medical procedures, during which the oral tissues are stretched or manipulated by instruments, is a source of local trauma that can cause the development of these ulcers. Nutritional deficiencies in folic acid, iron, and vitamin B12 are other potential etiologies of these lesions [71]. Systemic chemotherapy and radiotherapy targeting malignant lesions of the oropharynx can cause the development of overlapping aphthous ulcers of considerable size that can serve as areas of systemic access of pathogenic organisms. Occasionally, these ulcers occur as part of a disease such as Behçet syndrome. In patients with Behçet syndrome, major aphthae are more frequent than minor aphthae and occur simultaneously on the nonkeratinized oral mucosa, uvula, and genitals [4,71]. Sensitivity to certain medications, including nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, and bisphosphonates, may produce an aphthous-like tissue reaction. Given the multitude of medications available and potential untoward effects that can occur in the patients who take them, this could be a potential issue for numerous medications.
| A) | Aphthous ulcers | ||
| B) | Oral lichen planus | ||
| C) | Recurrent herpes labialis | ||
| D) | Pseudomembranous candidiasis |
The incidence of these lesions varies from 20% to 60% and can reflect the actual population studied. Many patients develop the condition during the first two decades of life [68]. There has yet to be a bacterial, viral, or fungal etiology that can be attributed to the origin of these lesions. A genetic predisposition to the occurrence is possible. When both parents have a history of these lesions, there is a 90% chance that their children will be similarly affected [69]. Common predisposing factors include physical and emotional stress and sensitivity to ingredients in toothpaste and/or mouthwash, such as sodium lauryl sulfate and alcohol [70,71]. Tissue manipulation during dental or medical procedures, during which the oral tissues are stretched or manipulated by instruments, is a source of local trauma that can cause the development of these ulcers. Nutritional deficiencies in folic acid, iron, and vitamin B12 are other potential etiologies of these lesions [71]. Systemic chemotherapy and radiotherapy targeting malignant lesions of the oropharynx can cause the development of overlapping aphthous ulcers of considerable size that can serve as areas of systemic access of pathogenic organisms. Occasionally, these ulcers occur as part of a disease such as Behçet syndrome. In patients with Behçet syndrome, major aphthae are more frequent than minor aphthae and occur simultaneously on the nonkeratinized oral mucosa, uvula, and genitals [4,71]. Sensitivity to certain medications, including nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, and bisphosphonates, may produce an aphthous-like tissue reaction. Given the multitude of medications available and potential untoward effects that can occur in the patients who take them, this could be a potential issue for numerous medications.
| A) | are considered to be of autoimmune origin. | ||
| B) | occur most frequently on the hard and soft palate. | ||
| C) | have a high transformation rate to oral squamous cell carcinoma. | ||
| D) | can be wiped away from the tissue and will leave an erythematous base in the process. |
Lichen planus is a chronic autoimmune condition with cutaneous and oral manifestations [72]. Although the actual prevalence of the condition in the United States is unknown, lichen planus is estimated to affect approximately 1% to 3% of the adult population [72]. The classic presentation of lichen planus lesions on the oral mucosa are fine, well-demarcated, adherent white lines called Wickham striae that can involve varying amounts of the posterior buccal mucosa. Occasionally, lichen planus may involve the dorsum of the tongue and appear as adherent white plaques on the anterior two-thirds of the tongue. These forms of oral lichen planus are usually asymptomatic and are often discovered during a clinical dental or medical examination. However, exacerbations from this asymptomatic state to erosive lichen planus can occur. Patients with erosive oral lichen planus present with symptoms that range from minimal discomfort to a burning sensation [71]. The buccal mucosa, tongue, and gingiva can be involved in these outbreaks. The irregularly-shaped lesions of erosive lichen planus can involve large areas of tissue and appear as patchy white areas interspersed with erythematous zones of inflamed or denuded tissue. Secondary infection by C. albicans can increase discomfort and make the diagnosis and treatment of the involved areas a challenge.
| A) | Salivary flow is increased. | ||
| B) | The euphoric state lasts one hour or less. | ||
| C) | The re-uptake of cerebral neurotransmitters is enhanced. | ||
| D) | There is an increased craving for sugar-laden carbonated beverages. |
Beyond its pharmacotherapeutic realm, methamphetamine has gained popularity among drug abusers for several reasons. The manufacturing process of methamphetamine is inexpensive and uncomplicated. Once produced, it may be smoked, snorted, swallowed as a pill, or injected. The euphoria produced by methamphetamine can last approximately 12 hours, compared to the 1-hour duration for cocaine [78]. The neurophysiologic basis for this euphoric state is that methamphetamine blocks the re-uptake of the cerebral neurotransmitters such as dopamine, norepinephrine, and serotonin [79]. Repeated use of this drug can induce cerebral damage, including edema, hemorrhage, strokes, and persistent hallucinations. A potent stimulant, methamphetamine can also cause elevation of both systolic and diastolic blood pressure [80].
The teeth are not spared from the problems caused by the abuse of this drug. As use of this drug increased, an aggressive and rapidly progressing form of dental caries called "meth mouth" was identified. Use of this drug causes several physiologic changes and behaviors that result in this rampant form of caries.
As a stimulant of the alpha-adrenergic receptors within the salivary gland vasculature, methamphetamine causes vasoconstriction and a reduction in salivary flow. Repetitive abuse of this potent stimulant can result in hyposalivation [81]. A chronic lack of salivary flow causes a decrease in the mechanical cleansing of plaque from the teeth and an increase in the retention of cariogenic organisms. There is also a commensurate decrease in salivary immunoglobulins and bactericidal enzymes.
| A) | Oral hygiene deteriorates. | ||
| B) | There is an increased tendency for grinding and clenching. | ||
| C) | The affected areas are difficult to reach for basic oral hygiene. | ||
| D) | The most common areas affected are the buccal surfaces of the teeth and the interproximal areas of anterior teeth. |
Behaviorally, methamphetamine induces a craving for sugar-laden carbonated beverages, and prolonged exposure of these beverages on the teeth promotes dental caries. Those who abuse this drug also have a tendency for clenching and grinding (bruxing) the teeth. These forces on already weakened teeth further fractures and cause weakening of the remaining tooth structure. After the enamel has fractured away, the softer underlying dentin is more prone to decay and less resilient to fracture.
| A) | perimylolysis. | ||
| B) | parotid gland enlargement. | ||
| C) | oropharyngeal soft tissue trauma. | ||
| D) | All of the above |
The teeth and soft tissues are adversely affected by the repetitive episodes of induced vomiting characteristic of bulimia. Erosion, the loss of tooth structure via a chemical process, can occur as gastric contents deliberately expelled after a binging episode contain hydrochloric acid. The repetitious episodes of binging and vomiting result in an extended cumulative exposure of tooth enamel to this acidic mixture. A unique pattern of erosion called perimylolysis develops.
The enamel of the lingual, occlusal, and incisal surfaces of the maxillary and mandibular teeth is gradually eroded by the gastric acid (Image 6). The erosion extends through the enamel and into the dentin and yields a surface that is smooth and glossy. Sensitivity to temperature and sweets can develop when the superficial dentinal tubules are uncovered. This erosive process can also undermine existing amalgam or bonded restorations. Exposed dentin is a softer material than enamel and is more prone to caries. Tooth structure that previously served as a contact point for occlusion can be minimized or lost. Changes in both the occlusal pattern and the vertical dimension of occlusion can develop. Tooth structure and tooth contour used for a partial denture clasp can change configurations that preclude the proper contact. This can make a partial denture difficult to wear or unusable. If patients have concurrent bruxing or other parafunctional habits, further erosion and abrasion can accelerate the loss of the remaining tooth structure. It may take two or more years for the purgative episodes to develop the erosive patterns [86]. Thickness of the enamel, oral hygiene, and the frequency of the purgative episodes can alter this interval.
The mucosa of the oropharyngeal region can also be traumatized when fingers or objects are used to induce vomiting. Frequent occurrences of these episodes can delay healing of the affected areas and increase the potential for localized infections. The soft palate and the pharynx are the areas most often traumatized.
The parotid glands frequently undergo bilateral enlargement in patients with bulimic and binge eating disorders ("chipmunk facies"). The massive quantities of food ingested during episodes of binge eating cause a commensurate increase in the amount of salivary production. Hypertrophy of the glandular elements causes an increase in the overall size of the gland that can alter the external facial appearance. The duct to the parotid gland remains patent, and salivary flow is unaltered [87].