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Good oral health is important for your total well-being. The condition of the tissues and structures of your mouth affect your general physical condition, ability to chew and speak, appearance, and personal relations.

To help prevent tooth decay and gum disease, practice proper brushing and flossing and see your dentist regularly. Ask your dentist or dental hygienist to show you proper brushing technique. Also, you may want to ask your dentist about additional ways to prevent tooth decay, such as sealants for teeth and fluoride treatments.

Brush your teeth correctly for at least 2 minutes at least twice a day. The most important time to brush is before you go to sleep. It is also a good idea to brush or rinse after meals. Floss between your teeth once a day.

Brushing your teeth

The American Dental Association suggests that you brush your teeth in the following manner:

• Position the head of the toothbrush against your teeth, with the tips of the bristle angled against the gum line at a 45-degree angle.
• Move the brush in a gentle, circular scrubbing motion. Brush the outer surfaces of each tooth, upper and lower, keeping the bristles angled against the gum line.
• Use the same motion to brush the inside surfaces of the teeth.
• Scrub chewing surfaces of all teeth. Only the tips of the bristles on the toothbrush can clean the teeth. Use a light pressure so that the bristles do not bend. Let the bristles reach into the grooves of the teeth. Change the position of the toothbrush often.
• To clean inside the front teeth, tilt the brush vertically and make gentle up and down strokes with the front part of the brush over the teeth and gum tissue of the upper and lower jaws.
• Brush the tongue to refresh your breath and remove bacteria.

A brush with soft, end-rounded or polished bristles is less likely to injure gum tissues than one with hard bristles. A brush with hard bristles can cause abrasion to the teeth. Abrasion is the wearing away of the tooth structure, especially along the gumline. Abrasions make it easier for bacteria and acids to damage the tooth because the hard, protective enamel layer has been brushed away. The hard bristles can also cause damage by making the gum line recede (push back) away from the tooth.

Replace your brush at the first sign that the bristles have become splayed or matted. Store your brush uncovered in a dry place so that it can dry out between brushings. Never share your toothbrush with anyone. It contains bacteria that can be passed from one person to another no matter how well you clean the brush.

Some electric toothbrushes can clean better than manual brushes. People with handicaps and young children may find an electric toothbrush easier to use. Ask your dentist which type of brush will clean your teeth more effectively.

Flossing your teeth

Flossing is the best way to remove food and plaque from between the teeth, an area the toothbrush cannot reach. Use the following technique:

• Cut off about 18 inches of floss and wind most of it around the middle finger of one hand. Wind the rest around the middle finger of your other hand, to take up the floss as you use it.
• Gently, using a sawing motion, pull the floss between 2 of your teeth, being careful not to snap it into the gums.
• When the floss reaches the gum line, curve it into a C-shape against one tooth and slip it into the space between the tooth and the gum until you feel resistance.
• Holding the floss tightly against the tooth, move it up and down away and toward the gum, scraping the side of the tooth.
• Wind the floss around the middle finger, so that a fresh section is in position and repeat for all teeth. Not using a fresh section of floss can spread bacteria and could cause a gum infection (gingivitis).
• Remember to floss the backs of your rear 4 teeth.

If you keep having bleeding from your gums, it is a sign that something is not healthy. It should be looked at by your dentist if it continues for more than 5 days.

Buying dental products

Look for the American Dental Association (ADA) seal of acceptance when determining the effectiveness of a product.

Always buy toothpastes with fluoride. The fluoride helps prevent cavities. You can buy toothpastes with special ingredients for controlling tartar or for whitening teeth.

Mouthwashes are generally used to temporarily freshen bad breath. Some mouthwashes may help reduce plaque levels. Fluoride mouthwashes also help protect the teeth against decay. If your breath odor is not caused by food, such as garlic or onions, it may be a warning sign of decay, gum abscess, or a medical problem. Ask your dentist to determine why you have bad breath.

Preventing decay with a healthy diet

Decay occurs only when the inside of the mouth is acidic. This happens when you eat starchy or sugary foods (carbohydrates). You can help prevent decay by avoiding highly sugary or sticky foods or brushing your teeth right after you eat these foods. Rinsing with water after you eat or drink sugar-containing foods can also help reduce the amount of acid and help wash away food plaque from the teeth.

Snacks to avoid include:

• candy, cookies, cake, pie
• soda pop and other sugary liquids
• gum sweetened with sugar, including high fructose corn syrup
• crackers, breadsticks, chips
• dried fruits; raisins are not only sweet but also sticky and cling to the teeth.

Snacks to choose include:

• fresh fruit (However, because some fruit, such as oranges, pineapples, and peaches, are high in natural sugar and acid; frequent fruit snacks may damage your teeth. It is best to rinse your mouth with water after eating these fruits and not brush your teeth until 45 minutes after you ate the fruit.)
• fresh vegetables
• cheese
• unsalted nuts
• unsweetened fruit juices
• popcorn (unsalted)
• hard-boiled eggs
• bean dips.

A healthy diet is the cornerstone of dental health. A diet rich in fresh fruits and vegetables and whole grains is healthy for teeth and gums. Foods such as raw apples help clean the teeth and make good snacks. Milk is a good snack and a good mealtime drink. Drink it with sweet foods to help wash sugar from your mouth.

Chewing sugarless gum after meals promotes production of saliva, a natural mouth rinse, and helps neutralize tooth-decaying acids in plaque. It is good to brush your teeth after eating, but if you can’t, chewing sugarless gum is an alternative. Chewing gums sweetened with Xylitol can reduce and control the amount of bacteria that cause decay.

Dental care during pregnancy

Women who are pregnant may notice that their gums are swollen and bleed when they brush or floss their teeth. The bleeding is usually related to the increased blood flow to the gums caused by hormonal changes during pregnancy. The increased bleeding usually goes away after delivery. In the meantime, be sure to floss every day and brush your teeth with a soft toothbrush. You can use a mouthwash that has no alcohol or use just warm water to cleanse your mouth and gums.

Try to visit the dentist at least once during your pregnancy to have your teeth examined. Tell the dentist that you are pregnant. Most dental work can be done safely while you are pregnant, but some procedures and treatments may need to be postponed until after pregnancy. It may be a good idea to have your dentist call your pregnancy healthcare provider to help determine which tests and treatments are safe for you. Antibiotics, pain medicines, or even X-rays are often necessary for some special dental problems during pregnancy. Your dentist can consult with your pregnancy healthcare provider before proceeding with treatment.
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What is a dentist?

Dentists are healthcare professionals trained to help you care for your teeth, gums, and all of the soft tissues of your mouth. They have had several years of training in dental medicine. A dentist has 1 of 2 possible degrees: a DDS (doctor of dental surgery) or DMD (doctor of dental medicine) degree. There is no difference between the 2 degrees. The degree a dentist has depends on the school he or she attended.

How do I start my search for a dentist?

Here are a few tips on finding a good dentist:

• Ask family, friends, or a coworker for recommendations.
• Ask your family doctor or local pharmacist.
• Call or write the local dental society to see if they provide referrals.
• Ask faculty members of local dental schools.
• If you are moving, ask your current dentist for recommendations.
• If you have dental insurance, ask for a list of dental providers on your plan.

If you are looking for charitable or low-cost dental care, check with your state dental society to see if there are community health centers, assistance programs, or a dental school clinic in your area. Dental schools often have clinics that allow dental students to gain experience treating patients while providing very good care for a lower cost. Experienced, licensed dentists closely supervise the students. You can also contact your state or local health department to find out what services are offered in your area.

What should I check?

Look for a dentist in a location easy for you to get to, either from home or from work. Call the dentist’s office and ask if they are taking new patients. Ask about office hours and appointments, payment policy, and insurance coverage. When you visit the office, check for neatness and cleanliness.

You and your dentist are partners in maintaining your oral health. Take the time to ask questions.

• Ask how long the dentist has been in practice in the community.
• Find out how dental emergencies are handled.
• Ask how you will be told about fees and payment before treatments.
• If you are comparing the fees charged by different dentists, ask what the cost is for X-rays and a preventive dental visit that includes an oral exam and teeth cleaning.
• If you know others who have seen this dentist, ask them if the dentist is easy to talk to. Does the dentist take time to explain treatment choices and teach ways to prevent dental health problems?

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Pain of Odontogenic Origin

Tooth Eruption

Discomfort is commonly associated with the eruption of primary or deciduous teeth in infants. Irritability, drooling, and decreased intake are commonly associated findings. An associated low-grade fever (37.9°C/100.2°F) and diarrhea are more controversial findings. No scientific data support an association of teething, fever, and diarrhea. One must be careful in attributing either to tooth eruption. Other sources for fever must be carefully sought.² Table 242-2 lists common causes of orofacial pain.

Table 242-2 Differential Diagnosis of Orofacial Pain

As with the primary dentition, eruption of permanent teeth, especially third molars, or wisdom teeth, may result in significant pain. Gingival irritation and inflammation associated with tooth eruption are common and must be distinguished from pericoronitis. Pericoronitis is inflammation of the operculum, or the gingival tissue overlying the occlusal surface of an erupting tooth. Impaction of food and debris beneath the operculum results in a severe inflammatory response. Without intervention this progressive inflammatory process will result in frank infection. Because of the close proximity of the masticator space (comprised of the masseteric space, pterygomandibular space, and the superficial and deep temporalis space) to third molars, associated trismus is common and portends the potential for extension into the communicating parapharyngeal spaces. Treatment consists of appropriate antibiotic therapy with penicillin VK 500 mg PO qid, erythromycin 250 mg PO qid, or clindamycin 300 mg PO qid, local irrigation of food and debris from underneath the operculum, saline mouth rinses, and analgesic therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) and opiate preparations as appropriate. Referral to a general dentist or an oral and maxillofacial surgeon within 24 to 48 h is essential. If pericoronitis is related to trauma from an opposing tooth during mastication, as is frequently the case with third molars, concomitant extraction of the opposing tooth and antibiotic therapy will bring marked relief within 24 h. Definitive treatment is extraction of the associated tooth by a general dentist or oral and maxillofacial surgeon.

Dental Caries and Pulpal Pathology

Dental caries represents the loss of integrity of the tooth enamel secondary to dissolution of hydroxyapatite from prolonged exposure to the acidic metabolic by-products of plaque bacteria. Caries most commonly occurs in areas where plaque accumulates such as pits and fissures of the occlusal surface, interproximally, and along the gingival margins. When a sufficient breach of enamel integrity has occurred, sensitivity to cold or sweet stimulus may result. With dentinal involvement, carious progression occurs more rapidly, spreading along dentinal microtubules. At this stage, direct communication between the oral environment and the vital dental pulp has been established, and inflammatory changes in the pulpal tissue are evident histologically.

The pulpal inflammatory process is initially reversible, but with continued stimuli, the pulp’s ability to respond and repair is jeopardized. Irreversible pulpitis can be distinguished from reversible pulpitis by the duration of symptoms. Both require a stimulus to initiate a painful response; however, in reversible pulpitis, the duration of pain is short, lasting seconds, as compared with irreversible pulpitis, in which the pain may last for minutes to hours. The most common stimulus is thermal, although sweet or sour stimuli also can elicit a painful response. Spontaneous odontogenic pain most frequently represents pulpal death or necrosis. Pain elicited with heat stimulus is most commonly associated with pulpal necrosis. Determining a particular tooth’s position in this continuum of disease is impractical for the emergency physician. Treatment focuses on providing adequate analgesia and referral to a general dentist. The definitive treatment for irreversible pulpitis and pulpal necrosis is root canal therapy or dental extraction.

Periradicular Pathology

The most common cause of severe odontogenic pain is periapical pathology. Periapical granuloma, more appropriately termed periradicular periodontitis, is the most common periapical lesion. This lesion is not a true granuloma but rather slowly expanding granulation tissue associated with the root apex. Most commonly, periradicular periodontitis is a result of pulpal inflammation or necrosis, but it can be associated with trauma. Periapical or radicular cyst and periradicular abscess are clinically and radiographically indistinguishable from periradicular periodontitis, yet histologically separate entities. A periapical cyst has an epithelial lining originating embryologically from the rest of Malassez, and a periradicular abscess merely represents the accumulation of associated inflammatory cell. All three lesions are only associated with teeth with severely inflamed or necrotic pulps and may cause significant pain. Radiographically, these periapical lesions appear as a slight widening of the periodontal ligament space, a thinning of the lamina dura, or a frank radiolucent area associated with the root apex on a periapical dental radiograph (Figure 242-4). Radiographic evaluation with a Panorex panoramic x-ray machine is rarely useful for identification of all but the most extensive periradicular lesions, but can be important in identifying other more significant painful osseous pathology.

View Large Fig. 242-4. Add to ‘My Saved Images’ A. The radiographic appearance of a healthy tooth with a normal periodontal ligament space and distinct lamina dura compared with the radiographic appearance of a periapical abscess, periradicular periodontitis, and periradicular cyst. B. A periapical radiolucency. C. Subtle radiographic loss of the periapical lamina dura and widening of the periodontal ligament space. (Courtesy of Gary M. Beaudreau, DMD.)

Pain of dental origin may be diffuse in nature, presenting as a headache, sinus pain, eye pain, or jaw or neck pain, or may be localized to a single tooth. One must remember to consider myocardial infarction as an etiology of jaw pain. Identification of the offending tooth is best accomplished by eliciting pain with percussion of the suspected teeth with a dental mirror handle or similar metallic object. A small swelling of the gingiva with a draining fistula adjacent to the affected tooth is known as a parulis, and can help identify the involved tooth. Erosion of a periradicular abscess through the cortical bone and subperiosteal extension results in intraoral or facial swelling and fluctuance that, if possible should be incised and drained intraorally. The emergency physician should treat dental abscesses or other periapical lesions with oral antibiotics such as penicillin VK 500 mg PO qid, clindamycin 300 mg PO qid, or erythromycin 500 mg PO qid, and should provide adequate analgesia with an NSAID. Opioid analgesia may be indicated in the first 24 to 48 h. Prompt referral to a dentist for definitive treatment such as root canal therapy or extraction is indicated.

Facial Cellulitis

Spread of odontogenic infections into the various facial spaces is relatively common. Buccal extension of a periapical infection of the mandibular teeth will involve the buccinator space. Maxillary labial extension of infection primarily will involve the infraorbital space. Perforation through the lingual cortical bone of mandibular molars, particularly the second and third molars, usually occurs below the mylohyoid ridge and involves the submandibular space. Lingual spread of periapical infections associated with mandibular anterior teeth will affect the lingual space. The submandibular space and lingual space communicate with each other at the posterior border of the mylohyoid muscle.

Cellulitis of bilateral submandibular spaces and the lingual space is called Ludwig angina (see Chap. 243) and is potentially life-threatening. Clinically, Ludwig angina is a rapidly spreading cellulitis that results in brawny induration of the suprahyoid region and elevation of the tongue. Involvement of the floor of the mouth pushes the tongue posteriorly. As these spaces and the masticator spaces ultimately communicate with the parapharyngeal space, involvement of the epiglottis is not uncommon. As a result, airway compromise is the immediate primary concern. The primary focus of initial management is maintenance of a patent airway. Timely intravenous administration of high-dose penicillin and metronidazole or cefoxitin is essential. An aminoglycoside may be added to extend coverage, and in the penicillin-sensitive person, clindamycin may be substituted. Immediate oral and maxillofacial surgical consultation and hospitalization for incision and drainage and intubation as indicated are necessary.

Infection of the infraorbital space may have a potentially devastating outcome if retrograde spread via the ophthalmic veins occurs, and the cavernous sinus becomes involved. Cavernous sinus thrombosis presents as an infraorbital or periorbital cellulitis with rapidly developing meningeal signs, sepsis, and coma. Early recognition and treatment with a high-dose IV antibiotic as above are essential in decreasing morbidity and mortality.

Postextraction Alveolar Osteitis

Pain in the initial 24 to 48 h after dental extraction, termed periosteitis, is common and responds well to analgesics. Depending on the tooth removed, density of the bone, and amount of associated trauma that occurred during extraction, significant discomfort can occur. Postextraction alveolar osteitis, or dry socket, usually occurs on the second or third postoperative day and is associated with exquisite oral pain. Displacement of the clot from the socket or fibrinolytic dissolution of the clot results in exposure of the alveolar bone to the oral environment. This initiates an inflammatory response resulting in a localized osteomyelitis of the exposed bone. Risk factors for developing postextraction alveolar osteitis include smoking, preexisting pericoronitis or periodontal disease, a traumatic extraction, a prior history of alveolar osteitis, and hormone replacement therapy.³

The incidence of postextraction alveolar osteitis is 2 to 5 percent of all extractions but is considerably higher (20 to 35 percent) among impacted third molar extractions. Dental radiographs should be taken to ensure the absence of a retained root tip or other foreign body. Thorough irrigation of the dental socket with sterile normal saline and packing it with oil of cloves- or eugenol-impregnated gauze results in an almost immediate improvement in level of comfort. Dental anesthesia may be necessary to adequately irrigate and pack a dry socket. Antibiotic therapy is indicated in the most severe cases, and daily packing changes are important. Thus, referral to a dentist within 24 h is indicated.^3,4

Managing postoperative dentoalveolar sequelae is in the realm of emergency medicine. Postoperative pain requiring analgesics, is a common presentation. Pain immediately postoperative is most commonly related to the trauma of surgery. Postoperative edema such as with extraction of third molars peaks within the first 24 to 48 h and is best managed with ice packs and elevation of the head of the bed to 30 degrees. Trismus, also common postoperatively, can result from infection, direct injury to the temporomandibular joint, injury to the muscles of mastication during administration of the inferior alveolar nerve block or during the surgery, and most commonly, normal perioperative inflammation. Trismus peaks in the first 24 h and usually decreases thereafter unless an infective process is the etiology. Postoperative trismus persisting for greater than 1 week will usually require stretching exercises prescribed by the oral and maxillofacial surgeon.^3,4

Postrestorative Pain

Pain may occur after a dental restorative procedure. Normal trauma from mechanical instrumentation of the tooth or direct exposure of the pulpal tissue during instrumentation may result in pain. Pain associated primarily with mastication may be a result of improper occlusion of the new restoration. After endodontic therapy, patients may experience exquisite pain secondary to instrumentation or a buildup of gaseous pressure in the pulp chamber. Providing analgesia and referral to the patient’s general dentist are the treatment of choice.

Periodontal Pathology

Periodontal Disease

Gingival inflammation and bleeding, or gingivitis, results from the accumulation of plaque along the gingival margins. Hormonal variations of puberty, adolescence, and pregnancy, as well as many medications such as phenytoin, may exacerbate gingival inflammation. As the inflammatory process progresses, destruction of the periodontal attachment apparatus occurs, and the gingival sulcus deepens, resulting in periodontal pockets and periodontitis. Periodontal pockets create a favorable environment for plaque accumulation, maturation, and mineralization into calculus. Further destruction of the periodontal attachment results. Eventually, sufficient bone loss causes tooth mobility and tooth loss.^1,5

The pathogenesis of periodontal disease is uncertain, but there is a very strong association between adult periodontitis and Bacteroides gingivalis. Many other specific bacteria have been shown to have a role in periodontitis. Destruction of tissue collagens, proteoglycans, and the connective tissue matrix is a major feature of gingivitis and periodontitis. Three theories for the etiology of this destruction have been proposed. Tissue destruction may occur as a result of the direct effects of bacterial plaque and their metabolic products, an accelerated host immune response, or immune deficiencies involving neutrophil function or the autologous mixed lymphocyte response.^1,5

Four distinctive types of periodontal disease have been identified. These include adult, rapidly progressing, juvenile, and prepubertal periodontitis.⁵ Etiology, age and gender predilection, and clinical course of disease vary by type. A definite association between juvenile periodontitis and Actinobacillus actinomycetemcomitans exists. More severe and rapidly progressing periodontitis, especially those types affecting a younger population such as the prepubertal and juvenile periodontitis, appears to be associated with decreased neutrophil chemotaxis or phagocytosis. Systemic illnesses such as human immunodeficiency virus (HIV) infection, diabetes, lazy leukocyte syndrome, Down syndrome, and cyclic neutropenia are associated with severe periodontal disease.¹

Periodontal disease usually progresses painlessly but may present as gingival bleeding or tender, swollen gingival tissue. Treatment is directed at slowing or arresting the progression of disease primarily by the removal of plaque and its by-products.¹ Antibiotics may play a role in treatment. Referral to a dentist for definitive treatment is indicated because the treatment involves extensive dental cleaning, instruction and improvement in oral hygiene, and in some cases, periodontal surgery.

Periodontal Abscess

When plaque and debris are entrapped in the periodontal pocket, a periodontal abscess may form, resulting in severe pain. Small periodontal abscesses respond to local therapy with warm saline rinses and antibiotics such as penicillin VK 500 mg PO qid or erythromycin 250 mg PO qid. Larger periodontal abscesses require incision and drainage. Saline mouth rinses four times a day are useful. Analgesics are essential.

Acute Necrotizing Ulcerative Gingivitis

Acute necrotizing ulcerative gingivitis (ANUG) is an aggressively destructive process (Figure 242-5). Also known as Vincent disease or trench mouth, it is part of a spectrum of disease ranging from localized ulceration of the gingiva to often fatal noma, in which localized ulceration and necrosis spread to the adjacent tissues of the cheeks, lips, and underlying facial bones.^6,7 The diagnostic triad includes pain, ulcerated or “punched out” interdental papillae, and gingival bleeding. Secondary signs include fetid breath, pseudomembrane formation, “wooden teeth” feeling, foul metallic taste, tooth mobility, lymphadenopathy, fever, and malaise.^7,8

View Large Fig. 242-5. Add to ‘My Saved Images’ Acute necrotizing ulcerative gingivitis. (Courtesy of Philip J. Hanes, DDS.)

The differential diagnosis for ANUG is quite extensive, but herpes gingivostomatitis is most difficult to differentiate. Herpes gingivostomatitis usually has smaller vesicular eruptions, less bleeding, more systemic signs, and lack of interdental papilla involvement.^7,8

The etiology of ANUG is still poorly understood. It appears to be an opportunistic infection in a host with lowered resistance. It is believed that suppression of the humoral and cell-mediated immune response in HIV infection, severe malnourishment, and perhaps stress may be responsible for a lowered host resistance. Anaerobic bacteria such as Treponema, Selenomonas, Fusobacterium, and Prevotella are uniformly identified. These bacteria appear to invade otherwise healthy tissue, resulting in an aggressively destructive disease process.^7,8

The most important predisposing factor is HIV infection. Previous necrotizing gingivitis infection is the second most important predisposing factor. Other contributing factors include poor oral hygiene, unusual emotional stress, poor diet, inadequate sleep, white heritage, age less than 21 years, poor socioeconomic status, recent illness, alcohol use, tobacco use, acatalasia, and various infections such as malaria, measles, and intestinal parasites.^7,8

Treatment consists primarily of bacterial control. Chlorhexidine oral rinses bid, professional debridement and scaling, and adjunctive antibiotic therapy with metronidazole 250 mg PO tid are the mainstay of treatment. Reduction in pain can be expected within 24 h of institution of this regimen. Identification and resolution of the predisposing factors, and supportive therapy with a soft diet rich in protein, vitamins, and fluids are important in establishing and maintaining a disease-free state.⁷

Cranial Neuralgias

Trigeminal neuralgia is the most common of the cranial neuralgias. Others include postherpetic neuralgia, glossopharyngeal and vagal neuralgia, and superior laryngeal neuralgia. Trigeminal neuralgia is undoubtedly one of the most painful entities involving the face. Most commonly affecting adults 30 to 60 years of age, females constitute 60 percent of the patients. Trigeminal neuralgia is almost always unilateral, following the anatomic distribution of the involved cranial nerve. The maxillary branch of the fifth cranial nerve is most commonly affected. Recurrent episodes of excruciating, electric shock like paroxysmal pain of short duration, separated by pain-free periods are characteristic. Associated contraction of the facial and masticatory muscles is typical, resulting in the term tic douloureux. Physical stimulation of a trigger point is the usual inciting event.⁹

The pathogenesis of trigeminal neuralgia is still uncertain. Diagnosis is clinical, requiring the exclusion of organic pathology such as acoustic neuroma or a nasopharyngeal carcinoma. Thus referral to a neurologist is important.⁹

Trigeminal neuralgia may respond well to the administration of carbamazepine (100 mg PO bid initially and gradually increasing as needed to a maximum dose of 1200 mg daily). Surgery is reserved for patients who do not respond to medications.⁹

Nonparoxysmal pain of neuropathic origin may develop 1) in patients who have had long-standing neuralgias, 2) secondary to surgical trauma along the distribution of the affected nerve branch, and 3) in association with viral infections, drugs, or heavy metal intoxication. Other neuropathies such as alcoholic and diabetic sensory neuropathies also may affect the oral cavity.
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Orofacial Pain

Pain of Odontogenic Origin Tooth Eruption Discomfort is commonly associated with the eruption of primary or deciduous teeth in infants. Irritability, drooling, and decreased intake are commonly associated findings. An associated low-grade fever (37.9°C/100.2°F) and diarrhea are more controversial findings. No scientific data support an association of teething, fever, and diarrhea. One must be careful in attributing either to tooth eruption. Other sources for fever must be carefully sought.2 Table 242-2 lists common causes of orofacial pain. Table 242-2 Differential Diagnosis of Orofacial Pain As with the primary dentition, eruption of permanent teeth, especially third molars, or wisdom teeth, may result in significant pain. Gingival irritation and inflammation associated with tooth eruption are common and must be distinguished from pericoronitis. Pericoronitis is inflammation of the operculum, or the gingival tissue overlying the occlusal surface of an erupting tooth. Impaction of food and debris beneath the operculum results in a severe inflammatory response. Without intervention this progressive inflammatory process will result in frank infection. Because of the close proximity of the masticator space (comprised of the masseteric space, pterygomandibular space, and the superficial and deep temporalis space) to third molars, associated trismus is common and portends the potential for extension into the communicating parapharyngeal spaces. Treatment consists of appropriate antibiotic therapy with penicillin VK 500 mg PO qid, erythromycin 250 mg PO qid, or clindamycin 300 mg PO qid, local irrigation of food and debris from underneath the operculum, saline mouth rinses, and analgesic therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) and opiate preparations as appropriate. Referral to a general dentist or an oral and maxillofacial surgeon within 24 to 48 h is essential. If pericoronitis is related to trauma from an opposing tooth during mastication, as is frequently the case with third molars, concomitant extraction of the opposing tooth and antibiotic therapy will bring marked relief within 24 h. Definitive treatment is extraction of the associated tooth by a general dentist or oral and maxillofacial surgeon. Dental Caries and Pulpal Pathology Dental caries represents the loss of integrity of the tooth enamel secondary to dissolution of hydroxyapatite from prolonged exposure to the acidic metabolic by-products of plaque bacteria. Caries most commonly occurs in areas where plaque accumulates such as pits and fissures of the occlusal surface, interproximally, and along the gingival margins. When a sufficient breach of enamel integrity has occurred, sensitivity to cold or sweet stimulus may result. With dentinal involvement, carious progression occurs more rapidly, spreading along dentinal microtubules. At this stage, direct communication between the oral environment and the vital dental pulp has been established, and inflammatory changes in the pulpal tissue are evident histologically. The pulpal inflammatory process is initially reversible, but with continued stimuli, the pulp’s ability to respond and repair is jeopardized. Irreversible pulpitis can be distinguished from reversible pulpitis by the duration of symptoms. Both require a stimulus to initiate a painful response; however, in reversible pulpitis, the duration of pain is short, lasting seconds, as compared with irreversible pulpitis, in which the pain may last for minutes to hours. The most common stimulus is thermal, although sweet or sour stimuli also can elicit a painful response. Spontaneous odontogenic pain most frequently represents pulpal death or necrosis. Pain elicited with heat stimulus is most commonly associated with pulpal necrosis. Determining a particular tooth’s position in this continuum of disease is impractical for the emergency physician. Treatment focuses on providing adequate analgesia and referral to a general dentist. The definitive treatment for irreversible pulpitis and pulpal necrosis is root canal therapy or dental extraction. Periradicular Pathology The most common cause of severe odontogenic pain is periapical pathology. Periapical granuloma, more appropriately termed periradicular periodontitis, is the most common periapical lesion. This lesion is not a true granuloma but rather slowly expanding granulation tissue associated with the root apex. Most commonly, periradicular periodontitis is a result of pulpal inflammation or necrosis, but it can be associated with trauma. Periapical or radicular cyst and periradicular abscess are clinically and radiographically indistinguishable from periradicular periodontitis, yet histologically separate entities. A periapical cyst has an epithelial lining originating embryologically from the rest of Malassez, and a periradicular abscess merely represents the accumulation of associated inflammatory cell. All three lesions are only associated with teeth with severely inflamed or necrotic pulps and may cause significant pain. Radiographically, these periapical lesions appear as a slight widening of the periodontal ligament space, a thinning of the lamina dura, or a frank radiolucent area associated with the root apex on a periapical dental radiograph (Figure 242-4). Radiographic evaluation with a Panorex panoramic x-ray machine is rarely useful for identification of all but the most extensive periradicular lesions, but can be important in identifying other more significant painful osseous pathology. View Large Fig. 242-4. Add to ‘My Saved Images’ A. The radiographic appearance of a healthy tooth with a normal periodontal ligament space and distinct lamina dura compared with the radiographic appearance of a periapical abscess, periradicular periodontitis, and periradicular cyst. B. A periapical radiolucency. C. Subtle radiographic loss of the periapical lamina dura and widening of the periodontal ligament space. (Courtesy of Gary M. Beaudreau, DMD.) Pain of dental origin may be diffuse in nature, presenting as a headache, sinus pain, eye pain, or jaw or neck pain, or may be localized to a single tooth. One must remember to consider myocardial infarction as an etiology of jaw pain. Identification of the offending tooth is best accomplished by eliciting pain with percussion of the suspected teeth with a dental mirror handle or similar metallic object. A small swelling of the gingiva with a draining fistula adjacent to the affected tooth is known as a parulis, and can help identify the involved tooth. Erosion of a periradicular abscess through the cortical bone and subperiosteal extension results in intraoral or facial swelling and fluctuance that, if possible should be incised and drained intraorally. The emergency physician should treat dental abscesses or other periapical lesions with oral antibiotics such as penicillin VK 500 mg PO qid, clindamycin 300 mg PO qid, or erythromycin 500 mg PO qid, and should provide adequate analgesia with an NSAID. Opioid analgesia may be indicated in the first 24 to 48 h. Prompt referral to a dentist for definitive treatment such as root canal therapy or extraction is indicated. Facial Cellulitis Spread of odontogenic infections into the various facial spaces is relatively common. Buccal extension of a periapical infection of the mandibular teeth will involve the buccinator space. Maxillary labial extension of infection primarily will involve the infraorbital space. Perforation through the lingual cortical bone of mandibular molars, particularly the second and third molars, usually occurs below the mylohyoid ridge and involves the submandibular space. Lingual spread of periapical infections associated with mandibular anterior teeth will affect the lingual space. The submandibular space and lingual space communicate with each other at the posterior border of the mylohyoid muscle. Cellulitis of bilateral submandibular spaces and the lingual space is called Ludwig angina (see Chap. 243) and is potentially life-threatening. Clinically, Ludwig angina is a rapidly spreading cellulitis that results in brawny induration of the suprahyoid region and elevation of the tongue. Involvement of the floor of the mouth pushes the tongue posteriorly. As these spaces and the masticator spaces ultimately communicate with the parapharyngeal space, involvement of the epiglottis is not uncommon. As a result, airway compromise is the immediate primary concern. The primary focus of initial management is maintenance of a patent airway. Timely intravenous administration of high-dose penicillin and metronidazole or cefoxitin is essential. An aminoglycoside may be added to extend coverage, and in the penicillin-sensitive person, clindamycin may be substituted. Immediate oral and maxillofacial surgical consultation and hospitalization for incision and drainage and intubation as indicated are necessary. Infection of the infraorbital space may have a potentially devastating outcome if retrograde spread via the ophthalmic veins occurs, and the cavernous sinus becomes involved. Cavernous sinus thrombosis presents as an infraorbital or periorbital cellulitis with rapidly developing meningeal signs, sepsis, and coma. Early recognition and treatment with a high-dose IV antibiotic as above are essential in decreasing morbidity and mortality. Postextraction Alveolar Osteitis Pain in the initial 24 to 48 h after dental extraction, termed periosteitis, is common and responds well to analgesics. Depending on the tooth removed, density of the bone, and amount of associated trauma that occurred during extraction, significant discomfort can occur. Postextraction alveolar osteitis, or dry socket, usually occurs on the second or third postoperative day and is associated with exquisite oral pain. Displacement of the clot from the socket or fibrinolytic dissolution of the clot results in exposure of the alveolar bone to the oral environment. This initiates an inflammatory response resulting in a localized osteomyelitis of the exposed bone. Risk factors for developing postextraction alveolar osteitis include smoking, preexisting pericoronitis or periodontal disease, a traumatic extraction, a prior history of alveolar osteitis, and hormone replacement therapy.3 The incidence of postextraction alveolar osteitis is 2 to 5 percent of all extractions but is considerably higher (20 to 35 percent) among impacted third molar extractions. Dental radiographs should be taken to ensure the absence of a retained root tip or other foreign body. Thorough irrigation of the dental socket with sterile normal saline and packing it with oil of cloves- or eugenol-impregnated gauze results in an almost immediate improvement in level of comfort. Dental anesthesia may be necessary to adequately irrigate and pack a dry socket. Antibiotic therapy is indicated in the most severe cases, and daily packing changes are important. Thus, referral to a dentist within 24 h is indicated.3,4 Managing postoperative dentoalveolar sequelae is in the realm of emergency medicine. Postoperative pain requiring analgesics, is a common presentation. Pain immediately postoperative is most commonly related to the trauma of surgery. Postoperative edema such as with extraction of third molars peaks within the first 24 to 48 h and is best managed with ice packs and elevation of the head of the bed to 30 degrees. Trismus, also common postoperatively, can result from infection, direct injury to the temporomandibular joint, injury to the muscles of mastication during administration of the inferior alveolar nerve block or during the surgery, and most commonly, normal perioperative inflammation. Trismus peaks in the first 24 h and usually decreases thereafter unless an infective process is the etiology. Postoperative trismus persisting for greater than 1 week will usually require stretching exercises prescribed by the oral and maxillofacial surgeon.3,4 Postrestorative Pain Pain may occur after a dental restorative procedure. Normal trauma from mechanical instrumentation of the tooth or direct exposure of the pulpal tissue during instrumentation may result in pain. Pain associated primarily with mastication may be a result of improper occlusion of the new restoration. After endodontic therapy, patients may experience exquisite pain secondary to instrumentation or a buildup of gaseous pressure in the pulp chamber. Providing analgesia and referral to the patient’s general dentist are the treatment of choice. Periodontal Pathology Periodontal Disease Gingival inflammation and bleeding, or gingivitis, results from the accumulation of plaque along the gingival margins. Hormonal variations of puberty, adolescence, and pregnancy, as well as many medications such as phenytoin, may exacerbate gingival inflammation. As the inflammatory process progresses, destruction of the periodontal attachment apparatus occurs, and the gingival sulcus deepens, resulting in periodontal pockets and periodontitis. Periodontal pockets create a favorable environment for plaque accumulation, maturation, and mineralization into calculus. Further destruction of the periodontal attachment results. Eventually, sufficient bone loss causes tooth mobility and tooth loss.1,5 The pathogenesis of periodontal disease is uncertain, but there is a very strong association between adult periodontitis and Bacteroides gingivalis. Many other specific bacteria have been shown to have a role in periodontitis. Destruction of tissue collagens, proteoglycans, and the connective tissue matrix is a major feature of gingivitis and periodontitis. Three theories for the etiology of this destruction have been proposed. Tissue destruction may occur as a result of the direct effects of bacterial plaque and their metabolic products, an accelerated host immune response, or immune deficiencies involving neutrophil function or the autologous mixed lymphocyte response.1,5 Four distinctive types of periodontal disease have been identified. These include adult, rapidly progressing, juvenile, and prepubertal periodontitis.5 Etiology, age and gender predilection, and clinical course of disease vary by type. A definite association between juvenile periodontitis and Actinobacillus actinomycetemcomitans exists. More severe and rapidly progressing periodontitis, especially those types affecting a younger population such as the prepubertal and juvenile periodontitis, appears to be associated with decreased neutrophil chemotaxis or phagocytosis. Systemic illnesses such as human immunodeficiency virus (HIV) infection, diabetes, lazy leukocyte syndrome, Down syndrome, and cyclic neutropenia are associated with severe periodontal disease.1 Periodontal disease usually progresses painlessly but may present as gingival bleeding or tender, swollen gingival tissue. Treatment is directed at slowing or arresting the progression of disease primarily by the removal of plaque and its by-products.1 Antibiotics may play a role in treatment. Referral to a dentist for definitive treatment is indicated because the treatment involves extensive dental cleaning, instruction and improvement in oral hygiene, and in some cases, periodontal surgery. Periodontal Abscess When plaque and debris are entrapped in the periodontal pocket, a periodontal abscess may form, resulting in severe pain. Small periodontal abscesses respond to local therapy with warm saline rinses and antibiotics such as penicillin VK 500 mg PO qid or erythromycin 250 mg PO qid. Larger periodontal abscesses require incision and drainage. Saline mouth rinses four times a day are useful. Analgesics are essential. Acute Necrotizing Ulcerative Gingivitis Acute necrotizing ulcerative gingivitis (ANUG) is an aggressively destructive process (Figure 242-5). Also known as Vincent disease or trench mouth, it is part of a spectrum of disease ranging from localized ulceration of the gingiva to often fatal noma, in which localized ulceration and necrosis spread to the adjacent tissues of the cheeks, lips, and underlying facial bones.6,7 The diagnostic triad includes pain, ulcerated or “punched out” interdental papillae, and gingival bleeding. Secondary signs include fetid breath, pseudomembrane formation, “wooden teeth” feeling, foul metallic taste, tooth mobility, lymphadenopathy, fever, and malaise.7,8 View Large Fig. 242-5. Add to ‘My Saved Images’ Acute necrotizing ulcerative gingivitis. (Courtesy of Philip J. Hanes, DDS.) The differential diagnosis for ANUG is quite extensive, but herpes gingivostomatitis is most difficult to differentiate. Herpes gingivostomatitis usually has smaller vesicular eruptions, less bleeding, more systemic signs, and lack of interdental papilla involvement.7,8 The etiology of ANUG is still poorly understood. It appears to be an opportunistic infection in a host with lowered resistance. It is believed that suppression of the humoral and cell-mediated immune response in HIV infection, severe malnourishment, and perhaps stress may be responsible for a lowered host resistance. Anaerobic bacteria such as Treponema, Selenomonas, Fusobacterium, and Prevotella are uniformly identified. These bacteria appear to invade otherwise healthy tissue, resulting in an aggressively destructive disease process.7,8 The most important predisposing factor is HIV infection. Previous necrotizing gingivitis infection is the second most important predisposing factor. Other contributing factors include poor oral hygiene, unusual emotional stress, poor diet, inadequate sleep, white heritage, age less than 21 years, poor socioeconomic status, recent illness, alcohol use, tobacco use, acatalasia, and various infections such as malaria, measles, and intestinal parasites.7,8 Treatment consists primarily of bacterial control. Chlorhexidine oral rinses bid, professional debridement and scaling, and adjunctive antibiotic therapy with metronidazole 250 mg PO tid are the mainstay of treatment. Reduction in pain can be expected within 24 h of institution of this regimen. Identification and resolution of the predisposing factors, and supportive therapy with a soft diet rich in protein, vitamins, and fluids are important in establishing and maintaining a disease-free state.7 Cranial Neuralgias Trigeminal neuralgia is the most common of the cranial neuralgias. Others include postherpetic neuralgia, glossopharyngeal and vagal neuralgia, and superior laryngeal neuralgia. Trigeminal neuralgia is undoubtedly one of the most painful entities involving the face. Most commonly affecting adults 30 to 60 years of age, females constitute 60 percent of the patients. Trigeminal neuralgia is almost always unilateral, following the anatomic distribution of the involved cranial nerve. The maxillary branch of the fifth cranial nerve is most commonly affected. Recurrent episodes of excruciating, electric shock like paroxysmal pain of short duration, separated by pain-free periods are characteristic. Associated contraction of the facial and masticatory muscles is typical, resulting in the term tic douloureux. Physical stimulation of a trigger point is the usual inciting event.9 The pathogenesis of trigeminal neuralgia is still uncertain. Diagnosis is clinical, requiring the exclusion of organic pathology such as acoustic neuroma or a nasopharyngeal carcinoma. Thus referral to a neurologist is important.9 Trigeminal neuralgia may respond well to the administration of carbamazepine (100 mg PO bid initially and gradually increasing as needed to a maximum dose of 1200 mg daily). Surgery is reserved for patients who do not respond to medications.9 Nonparoxysmal pain of neuropathic origin may develop 1) in patients who have had long-standing neuralgias, 2) secondary to surgical trauma along the distribution of the affected nerve branch, and 3) in association with viral infections, drugs, or heavy metal intoxication. Other neuropathies such as alcoholic and diabetic sensory neuropathies also may affect the oral cavity.

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What are other names for this remedy?

Type of medicine: natural remedy

Scientific and common names: Capsicum frutescens, Capsicum annum, capsicum, cayenne pepper, capsaicin, red pepper, African chili, Tabasco pepper, paprika, Mexican chili, pimento, garden pepper

What is capsicum?

Capsicum is a small annual shrub that grows in tropical America and around the world. It produces an oblong fruit (peppers). The fruit of the plant is used to make medicine.

What is it used for?

Besides being used in food as a pepper or spice, capsicum has been used in medicines. The active, medicinal ingredient used from the pepper is called capsaicin.

Capsaicin is used in skin creams to treat:

• pain from shingles, arthritis, fibromyalgia
• nerve pain in people with diabetes or AIDS.

It also may be used on the hands to prevent thumb-sucking or nail biting.

Capsaicin is also taken by mouth to treat:

• cramps
• diarrhea
• toothache
• blood clots
• fever
• nausea
• malaria
• high cholesterol
• heart disease

It is also used to stimulate digestion.

Capsaicin is used as a nasal spray to treat:

• hay fever
• sinusitis
• cluster headaches
• migraine headaches.

Capsaicin is the ingredient used in pepper spray for self-defense.

How is it taken?

Capsicum comes in the form of peppers, capsules, seasoning, and as a tincture for use by mouth. It is also available in creams, ointments, and lotions for use on the skin, and as a nasal spray.

Follow the directions printed on the product label or given by your healthcare provider.

What if I overdose?

Symptoms of an acute overdose have not been reported.

What should I watch out for?

Do not use creams or ointments containing capsaicin if you have:

• an allergy to pepper
• broken or irritated skin.

Do not take capsicum by mouth if you have:

• an allergy to pepper
• stomach problems such as ulcers or irritable bowel syndrome.

Keep ointments or creams containing capsaicin away from your eyes, nose, and mouth. If some gets into your eyes, nose, or mouth, flush them with a weak vinegar solution or lots of cool water.

Do not use tight bandages over skin that has been treated with capsicum because it will make the burning sensation worse. Do not use with a heating pad or apply right before or after a hot shower.

Eating too much capsicum could cause stomach pain and kidney and liver damage. Do not take capsicum by mouth in large doses or for a long time.

If you need emergency care, surgery, or dental work, tell the healthcare provider or dentist that you are taking this remedy. It may cause you to bleed more.

Females of childbearing age: Do not take this remedy by mouth if you are pregnant or breast-feeding without your healthcare provider’s approval.

Talk to your healthcare provider or pharmacist about any natural remedy that you are using or thinking about using. If your provider does not tell you how to take it, follow the directions that come with the package. Do not take more or take it longer than recommended. Ask about anything you do not understand. Remember:

• Natural remedies are not always safe.
• Do not take them if you are pregnant or breast-feeding without your healthcare provider’s approval. They should not be taken by infants, children, or older adults without your provider’s approval.
• They affect your body and may interact with prescription medicines that you take.
• Natural remedies are not standardized and may be contaminated. They may have different strengths and effects.

What are the possible side effects?

Along with its desirable effects, this remedy may cause some unwanted side effects. Some side effects may be very serious. Some side effects may go away as your body adjusts to the remedy. Tell your healthcare provider if you have any side effects that continue or get worse.

When you eat the hot peppers you may have an intense burning feeling in your mouth and stomach. It may cause you to sweat and feel flushed. This burning feeling can be reduced by removing the seeds from the pepper pod before you eat the pepper or by eating bananas with the peppers.

Side effects from putting capsicum products on your skin may include a burning sensation, minor redness, or swelling on the area where you put the cream or powder, especially if the area is bandaged tightly.

Side effects from taking capsicum by mouth may include stomach upset, sweating, flushing, or runny nose.

What products might interact with this remedy?

When you take this remedy with other medicines, it can change the way the remedy or the medicines work. Vitamins and certain foods may also interact. Using these products together might cause harmful side effects. Before taking this remedy, talk to your healthcare provider if you are taking:

• medicine that reduces the chance of blood clots forming such as aspirin, warfarin (Coumadin), heparin, enoxaparin (Lovenox), dalteparin (Fragmin), and clopidogrel (Plavix)
• herbs such as angelica, anise, arnica, asafoetida, celery, chamomile, clove, fenugreek, garlic, ginger, ginkgo, Panax ginseng, horse chestnut, horseradish, licorice, onion, papain, passionflower, red clover, turmeric, and willow
• medicines to treat lung disease such as theophylline
• nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Motrin, Motrin IB, Advil, Nuprin), naproxen (Naprosyn, Anaprox, Aleve, Naprelan), ketoprofen, nabumetone (Relafen), indomethacin (Indocin), ketorolac (Toradol), sulindac (Clinoril), piroxicam (Feldene), diclofenac (Voltaren, Cataflam), and oxaprozin (Daypro)

Keep a list of all your medicines with you. List all the prescription medicines, nonprescription medicines, supplements, natural remedies, and vitamins that you take. Be sure that you tell all healthcare providers who treat you about all the products you are taking
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Oral Somesthesia Somatosensory innervation of the oral cavity is provided by the maxillary and mandibular branches of the trigeminal nerve and by the glossopharyngeal nerve. The mandibular nerve branches to innervate the oral mucosa of the cheek, anterior two thirds of the tongue, mandibular dentition, PDL, gingiva, and anterior mandibular vestibule. Branches of the maxillary nerve innervate the hard and soft palate, the oral mucosa of the maxillary vestibule, and the maxillary dentition, gingiva, and PDL. Somatosensory innervation of the back of the tongue and oropharynx is provided by the glossopharyngeal nerve. Although the entire oral cavity is densely innervated with sensory fibers, considerable evidence indicates that the innervation is not uniform. Specialized oral tissues, including the lips, teeth, PDL, tongue, and palate, each display specific patterns of sensitivity. Although specific parts of the oral cavity rival the hand in terms of absolute psychophysical thresholds for tactile and thermal sensitivity, the structure/function somesthetic correlations so painstakingly deduced for the hand have little predictive veracity in the mouth.

Overall, the anterior oral cavity displays greater tactile sensitivity than does the posterior oral structure.^[61][203] The tip of the tongue is particularly sensitive, with a discriminative capability equivalent to that of the digits ( Figure 62-1 ). The midline of the palate and tongue are more sensitive than lateral regions. A similar pattern of sensitivity applies to the teeth.^[149] Adults with complete dentition could detect a 1-g von Frey hair applied to the anterior (midline) teeth but required nearly 10 g to detect stimulation of the first molar. The sensitivity to warm and cold stimuli also varies widely across oral tissues. Sensitivity to warm stimuli is relatively high on the tip of tongue but not particularly so on either the palate or buccolabial surfaces.^[89][268] In contrast, the sensitivity to a cool stimulus is less differentiated within the oral cavity, and the sensitivity of the tongue tip, palate, and buccolabial surfaces are essentially equal. In general, the sensitivity to cool stimuli is greater compared with warm stimuli.

Figure 62-1 Spatial discrimination of tactile detection thresholds from a number of studies. Numbers represent mean threshold in milligrams weight. (From Rath EM, Essick GK: J Oral Maxillofac Surg 48:1181–1190, 1990.)

Recording from single human lingual fibers innervating the anterior tongue^[257] confirms the small receptive fields and high sensitivity to low-threshold forces observed psychophysically ( Figure 62-2 ). Based on their small receptive fields and low thresholds, lingual fibers could be divided into those innervating the superficial (mucosal) surface of the tongue and those innervating deeper muscle tissue. The majority of the superficial fibers were rapidly adapting—a characteristic in common with other highly sensitive structures used in exploratory activity (e.g., the hand). In contrast, the deeper receptors were all slowly adapting and may provide information about the position of the tongue.

Figure 62-2 Receptive field properties of superficial mechanoreceptive afferents recorded from the human lingual nerve. A, Size and location of receptive fields of three types of mechanoreceptors: rapidly adapting (RA), slowly adapting (SA), and slowly adapting irregular. B, Receptive field area. C, Receptive field threshold. Small squares indicate corresponding data from human median nerve.[70]. Vertical bars indicate SE. (From Trulsson M, Essick GK: J Neurophysiol 77:737–748, 1997.)

Trigeminal endings mediating somesthetic and thermal sensitivity of the tongue and palate range from free nerve endings to an intermediate group of “semi-organized” endings^[151] to more highly organized endings variously referred to as Krause end bulbs,^[78] mucocutaneous end organs,^[151] or coiled terminations.^[66] All investigators agree that there are no Pacinian corpuscles in the oral mucosa. Based on ultrastructural criteria, Munger^[170] refers to many highly organized oral mucosa endings as Meissner corpuscles, similar to those found in glabrous skin of the hand. However, despite all this variation in nomenclature, many of the illustrations of the specialized endings are quite similar and show “finely wound nonmyelinated fibers” without a clearly defined capsule.^[151] Ultrastructural studies further reveal that some of these organized endings in the palate (but not the lingual epithelium) send axonal processes into the overlying epithelial pegs and are associated with Merkel cells.^[170][241] In the hand, Merkel cells are correlated physiologically with slowly adapting mechanoreceptors; however, a similar correlation has not been made in the palate, and their apparent absence in the lingual epithelium does not preclude slowly adapting mechanoreceptors in this structure (see Figure 62-2 ). Thus, unlike the hand, a correlation between the morphology of oral receptor endings and their response properties as rapidly or slowly adapting has not been demonstrated.

Mechanoreceptors in the PDL have been studied in some detail (see reviews by Jacobs and Steenberghe^[119] and Maeda and colleagues^[148]). In addition to detecting forces directed against the teeth, PDL receptors initiate oral reflexes of jaw opening and salivation and, together with receptors in the temporomandibular joint, contribute to interdental discrimination and oral stereognosis.^[118][119] As many as six varieties of receptor morphology are found in the PDL, ranging from complex Ruffini-like branched endings to free nerve endings.^[31][33] The cell bodies for PDL receptors are located peripherally in the trigeminal ganglion and centrally in the mesencephalic trigeminal nucleus.^[123] Mesencephalic trigeminal innervation of the PDL is primarily in the apical region near the root and consists mostly of small myelinated Ruffini-like endings.^[34] Trigeminal ganglion innervation extends from the apical region to the more superficial region and includes small unmyelinated nerve endings.

Both rapidly and slowly adapting mechanoreceptors are found in the PDL, and it is likely that it is the location of the receptor in the ligament that determines its response characteristic. Because the tooth rotates about its fulcrum, forces directed laterally to the crown will translate to greater stretch at the root of the tooth compared with the fulcrum. Thus, it is perhaps not surprising that lower-threshold fibers are found near the root and that they tend to be slowly adapting compared with receptors located near the fulcrum.^[42] In addition, individual Ruffini’s endings are not uniformly distributed around the tooth and thus display directional sensitivity to the force required to activate them. Recordings from human nerves (microneurography) demonstrate the directional sensitivity of PDL receptors^[259] ( Figure 62-3 ) and further indicate mechanical coupling between the teeth. Single fibers respond to stimulation of multiple (adjacent) teeth; however, there is no anatomic evidence that individual fibers innervate multiple teeth.^[256]

Figure 62-3 Responses of a single human periodontal afferent fiber to a force (?250 mN) from various directions. The cell responded best to a force from the distal (Di) direction. Directions: lingual (Li), labial (La), mesial (Me), downward (Do), upward (Up). (From Trulsson M, Johansson RS: Behav Brain Res 135:27–33, 2002.)

The differential innervation of the PDL by the trigeminal ganglion and mesencephalic trigeminal nucleus has functional significance. Mesencephalic receptors are primarily medium and rapidly adapting receptor types, many with directional sensitivity. The central termination of these mesencephalic force detectors includes inhibitory connections to trigeminal jaw closer motoneurons via the supratrigeminal area.^[129] Thus, these receptors serve a protective role in preventing potentially damaging tooth contact during mastication. In contrast, trigeminal ganglion receptors include slowly adapting mechanoreceptors (position detectors) and high-threshold C fibers (nociceptors) in addition to rapidly adapting mechanoreceptors. Because these periodontal receptors from the trigeminal ganglion terminate centrally in the sensory trigeminal complex, the source for the ascending sensory pathway to the thalamus and cortex, they provide information about tooth displacement and dental pain to the forebrain.

Although mechanoreceptors in the PDL are not encapsulated, their response characteristics are influenced by the elastic properties of the ligament. When the attachment of the ligament is compromised (e.g., during periodontitis that loosens the connective attachments of the ligament), a corresponding loss in interdental force discrimination is observed.^[261] Periodontal receptors also contribute to the regulation of bite force. Individuals with dentures could not bite as hard as normal dentulous subjects and could not perceive variations in their own bite force.^[118][258] Similar results were obtained by anesthetizing the inferior alveolar nerve.^[264] In contrast, anesthetizing the temporomandibular joint does not affect bite force discrimination but does impair jaw-positioning performance. Thus, different populations of oral receptors may regulate sensing jaw position and controlling bite force during mastication.

Common Chemical Sense Stimulation of the oral cavity with high concentrations of salts, acids, alkaloids, and other compounds elicits intense taste sensations, but also evokes nontaste sensations ranging from stinging and burning to warm, cool, and painful. This sensitivity of the oral cavity, mediated by nonspecialized free nerve endings and shared by all mucosal membranes, is referred to as the common chemical sense or chemesthesis and should not be confused with taste. Although free nerve endings respond to many traditional gustatory stimuli, they typically display a much lower sensitivity. Electrophysiologic recordings from the lingual nerve, for example, indicate that single fibers require concentrations of sodium chloride (NaCl) 1000× higher than those necessary to elicit a response from a gustatory fiber in the chorda tympani nerve (reviewed by Bryant and Silver^[26]). Much lower concentrations of other types of chemical stimuli (e.g., menthol [10^-4]), however, are adequate to elicit a response in trigeminal nerve fibers. The types of chemical stimuli that elicit low-threshold responses in trigeminal fibers suggest that one function of the common chemical sense is to protect the oral cavity. Responses to common chemical stimuli include reflex salivation and coughing that function to diffuse and remove offending stimuli from the mouth. The common chemical sense is not purely protective, however. Spices such as horseradish, ginger, and red pepper are effective stimuli for trigeminal afferent fibers and contribute to the flavor of food. One of the receptors for chemesthetic stimulation was recently cloned.^[43] A member of the TRP family of G-protein-coupled receptors, the vanilloid receptor termed “VR1″ responds to both noxious heat and low concentrations of protons in addition to vanilloid compounds, such as capsaicin found in chili pepper. Stimulation of this receptor results in the opening of a cation channel, thus depolarizing the afferent fiber.

Dental Pain Persons usually describe dental pain as either dull/burning or sharp.^[3] Sensations of dull burning pain are associated with stimulation of C fibers terminating in the pulp chamber, whereas sharp “bright” dental pain is associated with A-delta fiber innervation that extends a short distance into the dentinal tubules matrix interposed between the pulp chamber and the enamel covering of the tooth (reviewed in Burgess and colleagues^[28]). Unmyelinated C fibers constitute the majority of pulpal innervation (50% to 75%); however, endings within the pulp chamber may be unmyelinated terminals of A-delta (myelinated) afferent fibers. Polymodal C fibers innervating the pulp chamber respond to thermal stimuli and, in particular, to inflammatory mediators including histamine and bradykinin, endogenous factors associated with pulp pathology. C fibers innervating the pulp chamber contain neuropeptides such as substance P and calcitonin gene-related peptide.^[100] The peripheral release of these neuropeptides upon C fiber activation produces local vasodilation, thus increasing the pressure within the rigid pulp chamber, further augmenting C fiber activation (i.e., peripheral sensitization). The release of substance P in infected teeth has been directly measured in human patients using microdialysis, and patients with irreversible pulpitis had significantly higher levels of substance P in the pulp chamber compared with noninfected teeth.^[22] Although the release of neuropeptides augments pain, there is evidence that it may also reduce inflammation and promote recovery. In experiments with animals, eliminating the afferent terminal release of neuropeptides by denervating the teeth reduced wound healing after lesions were experimentally induced.^[35]

Sharp pain is mediated by A-delta fibers extending 0.2 to 0.3 mm into the dentinal tubules encasing the pulp chamber.^[32] These nerve fibers respond to heat, mechanical, and osmotic stimuli applied to the distal end of the dentinal tubules that become exposed to environmental stimuli when the enamel layer is breached.^[177] Because the dentinal tubules are filled with a fluid, the fluid transmits mechanical, thermal, and osmotic stimuli to the proximal end of the dentinal tubules where the nerve endings are located. This “hydrodynamic” theory of dental pain has gained anatomic, physiologic, and psychophysical support and further offers an explanation of dentinal hypersensitivity. When the dentinal tubules are exposed by a cavity or other lesion, patients report sharp pain in response to innocuous stimuli such as mild temperature or osmotic stimuli (e.g., sweet compounds). However, the theory predicts that if the tubules are covered, thus limiting exposure to environmental stimuli, stimulated pain should be reduced. This had been experimentally assessed in human volunteers in whom a small cavity in a tooth was prepared (in a tooth scheduled for removal) and a conical chamber positioned over the cavity through which regulated air pressure could be delivered.^[2] Creating a smear layer of amorphous tooth particles in the cavity, or dissolving it away with solvents, controlled the interface between the exposed dentinal tubules and the air pressure stimulus. When the smear layer was intact, covering the dentinal tubules, it took more air pressure to induce the perception of sharp pain than when the smear layer was dissolved.

Central Projections of Trigeminal System Afferent fibers of the trigeminal nerve enter the brainstem in the pons, bifurcate, and terminate in either the principal sensory nucleus or descend to terminate in the spinal trigeminal complex in the medulla. The bifurcation of the trigeminal nerve at the level of the pons reflects a tendency toward a segregation of function.^[128] In general, low-threshold mechanoreceptors predominate in the principal trigeminal sensory nucleus, indicative of a tactile discriminative function. In contrast, considerable evidence implicates the subnucleus caudalis in orofacial pain mechanisms, and many neurons in the subnucleus caudalis respond to noxious stimuli applied to the head and neck.^[218] These neurons include those specifically activated by noxious stimuli (nociceptive-specific neurons) and wide-dynamic-range neurons, responsive to both low- and high-intensity stimulation.

Because the receptive fields for many nociceptive neurons in the subnucleus caudalis are large and include responses to nociceptive stimuli applied to the masticatory muscles, tooth pulp, and temporomandibular joint, a role for these neurons in referred pain has been suggested.^[219] Anatomic studies confirm that afferent fibers innervating the oral cavity, tooth pulp, oropharynx, temporomandibular joint, masticatory muscles, and superficial skin all converge in the subnucleus caudalis.^[40][224] In many patients, lesions in mandibular teeth have a high likelihood of producing referred pain to the maxillary region, the cheek, and the ear, in addition to the mandible itself.^[223] Likewise, lesions in the maxillary teeth are often referred to the mandible as well as the maxilla, temple, and orbital region.

In addition to subnucleus caudalis, other parts of the sensory trigeminal complex are also involved in trigeminal pain. Nociceptive responses have been obtained from extensive areas of the sensory trigeminal complex, and destruction of the subnucleus caudalis does not prevent all trigeminal pain function (reviewed in Sessle^[218]). Case studies of patients who have undergone trigeminal tractotomy for intractable pain associated with cancer are completely analgesic on the face, but pulpal pain is intact.^[272] Likewise, when the principal trigeminal nucleus and subnucleus oralis were damaged after a stroke, oral and perioral pain sensitivity was diminished, as well as normal tactile sensitivity from these structures.^[88]

Neurons in both the rostral sensory trigeminal complex (subnucleus oralis) and the subnucleus caudalis may also form a substrate for “central sensitization” in which central neurons in the pain pathway have their response characteristics magnified as a result of peripheral stimulation.^[267] These changes can last a variable amount of time and potentially contribute to both short-term hyperalgesia and long-term chronic pain. Fundamental to the concept of central sensitization is that neurons initially only responsive to high-threshold (nociceptor) input become responsive to low-threshold, non-nociceptive input. The increased responsiveness is thought to be mediated by A-? (non-nociceptive) input that only becomes functionally active after intense peripheral nociceptor input. One neural mechanism for the nascent response to non-nociceptive input has been studied in great detail. An intense afferent barrage of nociceptor input, following peripheral tissue damage or inflammation “sensitizes” a central neuron via structural modification of an N-methyl-D-aspartate (NMDA) glutamate receptor. NMDA receptors are voltage sensitive and will not pass current, even in the presence of a ligand, unless the cell is sufficiently depolarized. The central release of a neuropeptide (e.g., substance P) by nociceptor afferents, however, may provide sufficient depolarization to modify NMDA glutamate receptors via intracellular signaling pathways, thereby allowing glutamate released by non-nociceptive (A-?) input to activate central neurons. A-? activation of a central nociceptor thus provides a neural mechanism for allodynia. Similar mechanisms have been demonstrated in the brainstem sensory trigeminal complex and may provide a substrate for chronic oral and facial pain.^[218] Experimental studies demonstrate that neuropharmacologically blocking NMDA receptors prevents temporomandibular joint or tooth pulp afferents from inducing hyperactivity in central trigeminal neurons (i.e., central sensitization).^[50][273]

Somatosensory information reaches the ventrobasal complex of the thalamus from all major subdivisions of the trigeminal sensory complex.^[218] Many cells in the ventrobasal complex respond to low-intensity stimulation, indicative of a tactile discriminatory function; however, other neurons require high-intensity stimulation. The small receptive fields of both these types of neurons suggest a role in localization. Other nuclei, including the posterior thalamic nuclei and the nucleus submedius, respond preferentially to high-intensity stimulation and may be involved in affective components of pain.^[59] Both nociceptive and non-nociceptive trigeminally activated neurons from the thalamus project to the somatosensory cortex. Electrophysiologic mapping studies in primates indicate a complex, sometimes discontinuous somatotopic map of the facial and oral region.^[120] In general, the face is represented medially on the cortical surface adjacent to the representation of the hand, with successively lateral representations of the teeth and tongue. Magnetic resonance imaging (MRI) in humans confirms this somatotopic representation

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Traditional Dental Insurance Plans

Some people are fortunate enough to have access to employer-paid traditional dental insurance,  Usually the employee must pay into the plan but the employer pays something as well.  Dental insurance is available only through group plans and cannot be purchased by an individual.  Most insurance does not cover everything.  If anything is covered completely it will be basic services like exams, root canals, cleanings and some fillings.  Advanced treatments, like orthodontics, periodontics and crown and bridge treatment, may be payable at a lower rate (50 – 80%) if at all.
With a traditional dental insurance plan, the patient goes to the dentist of his or her choice and services are covered according to the plan chosen by the employer to the extent charges are “reasonable” and “Customary.”  Since the insurance  company decides the amount that is reasonable and customary,  the dentists fee may not be covered and the patient will owe the remainder.  Usually, a yearly deductible is not payable and there is a yearly limit.
Some traditional plans are PPOs, or preferred provider organizations.  This means that dentists who “participate” in the plan can only charge the amount allowed by the plan and cannot charge you more.  If you go to a dentist outside the plan, that dentist will charge whatever insurance does not pay.  Why would anyone go to a non-participating dentist?  The answer is that you may not find a dentist on the list in your area that you want to see.  Dentists join and quit all the time.
In my opinion, many plans pay so little that dentists cannot spend adequate time to do their best work.  It may be better to go to a non-participating dentist with whom you are happy and pay the difference.  In my own case,  I once joined a plan that paid less for a cleaning that I paid my hygienist to do it.  The only way I could stay a participant would be to ask her to do a faster and less thorough job.  Maybe some dentists can keep up the quality and take a lower fee but I could not.

HMO Dental Plans

These are also provided to groups of employees.  A list of dentists is provided and if the patient goes outside the plan, the HMO pays nothing.  Dentists are paid a certain amount per patient each month as long as the patient is enrolled at that dentist’s patient.  The dentist,  for this fee, is supposed to provide all basic services, exams, x-rays, cleanings, fillings.  The patient may be charged for more complicated work but only to the extent allowed.  My own opinion of these plans is that the dentist has very little incentive to do a through job and find all the problems that need to be addressed since the dentist is paid the same amount regardless of the work done.

Discount Dental Plans

These are the plans that can be joined by individuals and families.  They are not provided by employers.  They are not really insurance plans and they work a different way:  The patient pays a yearly fee.  In return, the patient can visit participating dentists who bill according to a discounted fee schedule.  The dentist joins and takes a lower fee and, in return, the plan sends patients to him or her.
Discount Dental Plans can be found on the Internet and they are sponsored by traditional insurance companies.  They work very well as long as you can find dentists in your area that you want to see who are participating.  Also,  the dentist should be supplying you with the same care that non-plan patients are getting.

Dental Plans: the Standard of Care
A dentist owes all patients treatment that is up recognized standards.  Legally, the same standard of care is owed to a patient who pays full fee and one for which the dentist is reimbursed less that his/her regular fee.  Unfortunately, dentists do not always understand this concept.  If they have to cut corners, do work faster, take less x-rays, do a less thorough cleaning on plan patients in order to make ends meet, they should not stay members.   Also,  the plan patients should be treated with the same courtesy, recalled as frequently as regular patients and should not be giving only unpopular appointment times.

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The Future of the Dental Devices Market to 2015 : New Company and Market Analysis

The Future of the Dental Devices Market to 2015

Summary

Global Markets Direct’s ?The Future of the Dental Care Devices Market to 2015? report provides key data, information and analysis on the global dental devices market. The report provides market landscape, competitive landscape and market trends information on Crowns and Bridges, Dental Chairs and Equipment, Dental Implants, Dental Lasers, Dental Supplies, Digital Dental X-Ray Systems and Orthodontic Materials and Products market categories. The report provides comprehensive information on the key trends affecting these categories, and key analytical content on the market dynamics. The report reviews the competitive landscape in terms of mergers and acquisitions, pipeline products and technology offerings.

Scope – The report covers data and analysis on the dental devices market in the leading geographies of the world comprising of the United States, Canada, UK, Germany, France, Italy, Spain, Japan, China, India, Australia, and Brazil. – The report covers global market size and company share data for 7 dental devices market categories – crowns and bridges, dental chairs and equipment, dental implants, dental lasers, dental supplies, digital dental X-ray systems and orthodontic materials and products. – Annualized market revenues data from 2001 to 2008, forecast forward for 7 years to 2015. – The report provides qualitative analysis of market drivers, restraints, future outlook and challenges by categories and segments. – The report also covers information on the leading market players, the competitive landscape, and the leading pipeline products and technologies. – Key topics covered include the global dental care devices M&A landscape, global market landscape in the “crowns and bridges” market and opportunity analysis of the emerging markets. – The report is built using data and information sourced from proprietary databases, primary and secondary research and in house analysis by Global Markets Direct’s team of industry experts.

Reasons to buy – Develop business strategies by understanding the trends and developments that are driving the dental devices market globally. – Design and develop your product development, marketing and sales strategies. – Exploit M&A opportunities by identifying market players with the most innovative pipeline. – Develop market-entry and market expansion strategies. – Identify key players best positioned to take advantage of the emerging market opportunities. – Exploit in-licensing and out-licensing opportunities by identifying products, most likely to ensure a robust return. – What’s the next being thing in the dental devices market landscape? – Identify, understand and capitalize. – Make more informed business decisions from the insightful and in-depth analysis of the global diabetes care devices market and the factors shaping it.

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dental device

Research and Markets(http://www.researchandmarkets.com/research/02a121/israel_dental_devi) has announced the addition of Global Markets Direct’s new report “Israel Dental Devices Investment Opportunities, Analysis and Forecasts to 2015″ to their offering (see also <http://www.newsrx.com/library/topics/Research-and-Markets.html> Research and Markets).

Summary

This report is an essential source for in-depth information and data relating to the Israeli dental devices market. It also offers detailed and comprehensive coverage of market revenue, volume, distribution and company share information; and the latest news, financial deals and pipeline products information of each of the key sub-segments of the dental devices market in Israel

Scope

The report provides dental devices information broken down into detailed categories and segments in Israel.

Total revenues, products sold, end users, and average pricing.

Market shares of all the key competitors.

Key pipeline products that are set to shape the market, broken down by sector.

Information on the top medical equipment companies in the sector in the country covering business description, strategic analysis, and financial information.

Healthcare structure, regulatory environment, approval process, pricing trends and reimbursement.

Product and brand updates, strategy changes, R&D projects, corporate expansions and contractions and regulatory changes.

Key mergers and acquisitions, partnerships, private equity investments and IPOs.

Customer, hospitals and physicians data.

Reasons to buy

Gain a strong understanding of the dental devices market in Israel.

Evaluate and compare the attractiveness of the market in the country.

Identify growth segments and opportunities in each industry sector within the country.

Evaluate the pipeline of key products that will change the sector, and identify threats and opportunities before the products are launched in the country.

Analyze the competitiveness of the market in the country and identify hotspots.

Develop strategies based on the latest product, brand, expansion and research and development news in the country.

Do deals with an understanding of how competitors are financed, and the mergers and partnerships that have shaped the market in the country.

Identify and analyze the strengths and weaknesses of the industry incumbents in the country. Key Topics Covered: 1 Executive Summary

2 Introduction

3 Definitions of the Markets Covered in the Report

4 Healthcare Sector Review

4.1 Healthcare Sector Review

4.2 Healthcare Expenditure

5 Regulation System

6 Pricing and Reimbursement

7 Distribution Structure

8 Dental Devices in Israel

9 Crowns and Bridges In Israel

10 Dental Biomaterials In Israel

11 Dental Chairs and Equipment In Israel

12 Dental Implants In Israel

13 Dental Lasers In Israel

14 Dental Radiology Equipment In Israel

15 Overview of Key Companies in Israel Dental Devices Market

16 Financial Deals Landscape

17 Appendix

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