Acute Gingival and Periodontal Conditions, Lesions of Endodontic Origin, and Avulsed Teeth
1. Explain periodontal abscesses, including the cause, signs and symptoms, and treatment.
2. Discuss lesions of endodontic origin, including the cause, signs and symptoms, and treatment.
3. Explain herpetic infections, including the cause, signs and symptoms, and treatment.
4. Discuss pericoronitis, including signs and symptoms and treatment.
5. Explain necrotizing periodontal diseases, including the causes, signs and symptoms, and treatment.
6. Discuss how to manage the avulsed tooth, including:
• Collaborate in caring for clients with common periodontal and dental emergencies.
• Educate clients about the need for immediate treatment of common periodontal and dental emergencies and the expected outcome of emergency care.
The dental hygienist is frequently in a position to identify urgent periodontal conditions in need of treatment. A major part of care provided in these situations is recognizing the disease process. In some situations, the dental hygienist provides therapeutic or palliative care; in other cases, the hygienist's responsibility lies solely with referral for care. Postponement of appropriate care can result in prolonged pain, further periodontal tissue destruction, and tooth loss.
Periodontal Abscess
A periodontal abscess is a localized accumulation of pus within the periodontal tissues.1 Periodontal abscesses are distinguished by location (i.e., either gingival or periodontal) and by the course of the disease (i.e., acute or chronic).
• A gingival abscess is a periodontal abscess that is confined to the marginal gingiva and that often occurs in previously healthy gingival areas (Figure 32-1).
• A periodontal abscess is a deeper infection associated with periodontal pockets, furcations, and bone loss (Figure 32-2).
• An acute periodontal abscess is a lesion with expressed periodontal breakdown occurring over a limited period of time and with easily detectable clinical symptoms.1 It is characterized by pain, swelling, and other symptoms that lead the client to seek urgent care (Figure 32-3).
• The chronic periodontal abscess is a long-standing infection that often is associated with a sinus tract. This opening permits drainage of the infection and a diminution of acute symptoms such as pain and swelling, thus making the abscess chronic in nature. The sinus tract, which is an abnormal channel that connects the abscess to another space or to the surface, is called a fistula1 (Figure 32-4).
Periodontal abscesses also have been classified by number as either a single abscess or multiple periodontal abscesses.
• A single abscess is caused by local factors that lead to acute or chronic symptoms.
• Multiple abscesses have been related to factors such as medically compromised systemic health, uncontrolled diabetes mellitus, and systemic antibiotic therapy for situations that are not related to oral health.1
The importance of recognizing and treating clients with periodontal abscesses cannot be overemphasized. Data show that most abscessed teeth—particularly those receiving regular periodontal maintenance—benefit from treatment and can be preserved. An interesting retrospective study of tooth loss caused by a periodontal abscess demonstrated that 55% of teeth with periodontal abscess were maintained for an average of 12.5 years (range, 5 to 29 years).1 The importance of recognizing the disease process and encouraging clients to follow through with treatment is significant to one major goal of dental hygiene practice: preserving oral health.
Microbiology of the Periodontal Abscess
All periodontal abscesses share a characteristically complex pathogenic microflora similar to that associated with periodontal diseases. In these pathogenic microflora, the preponderance of bacteria changes from approximately 75% gram-positive facultative rods and cocci associated with gingival health to one harboring approximately 74% gram-negative rods.2 These are complex mixed infections that vary from person to person and from one site of infection in the mouth to another within the same person.2
Those microbial species most associated with abscesses are listed in Box 32-1.
Characteristics and Treatment of Periodontal Abscesses
Acute Periodontal Abscess
The acute periodontal abscess is a localized accumulation of pus in the gingival wall of a periodontal pocket. It usually occurs on the lateral aspect of the tooth, and it appears edematous, red, and shiny. It may have a domelike appearance or come to a distinct point. Figure 32-3 presents an example of an acute periodontal abscess with these characteristics. Acute abscesses are frequently associated with preexisting periodontal disease. The anatomic features of periodontal pockets—pocket depth of at least 5 mm, furcation involvement, and tortuous pocket anatomy—may predispose the client to occlusion of the pocket orifice. This occlusion permits an exacerbation of infection in the pocket wall as well as pus formation. Pus can often be expressed from the pocket with gentle finger pressure (Figure 32-5).1
Abscess formation can also occur when a foreign body becomes lodged in the pocket.1 An exacerbated inflammatory reaction then occurs. If the pocket continues to drain through the orifice, it can stabilize and become a chronic infection that drains pus to relieve pressure in the tissues. Conversion to the chronic state rarely occurs when foreign objects such as peanut skins and popcorn hulls are embedded in the pocket, thus provoking the acute response.
Incomplete scaling and root planing that leaves residual calculus at the base of treated pockets has been suggested as a cause of periodontal abscesses.1 It is postulated that the pocket orifice tightens from improved gingival health, thereby leaving the calculus and associated plaque to infect the deeper pocket tissues. This perspective is a commonly held belief, but few data support it. In an analysis of 29 persons who sought treatment at a postgraduate periodontics clinic and who had been diagnosed with periodontal abscess, 18 (62%) had untreated periodontal disease, 7 (24%) were on periodontal maintenance, and only 4 (14%) reported a history of recent scaling and root planing. Of these 29 persons, 27 were diagnosed with moderate to severe periodontal disease; the other two had early periodontitis. The mean probing depths of these abscesses were quite deep (i.e., 7.3 mm; range, 3 to 13 mm), and the abscesses were mostly associated with molar teeth.3
Given the number of abscesses treated, one would expect to see a much larger proportion of clients returning shortly after scaling and root planing appointments if incomplete treatment were a major cause of acute exacerbation. In another study, four types of periodontal treatment were compared, and abscess rate was noted. Quadrants treated with supragingival scaling alone developed abscesses to a far greater extent than those treated with subgingival scaling and root planing or those treated with periodontal surgery.1 These data suggest that abscess formation is more associated with deep pockets and untreated disease than with recent scaling and root planing treatment. It is also known that residual calculus and plaque biofilm is often left in pockets after even the most thorough scaling and root planing, especially in deep pockets.1 This information highlights the following three points:
1. It is extremely difficult to remove all calculus from periodontal pockets.
2. The clinician should scale and root plane as completely as possible with the intention of removing all subgingival deposits.
3. Supragingival scaling alone is totally inadequate for periodontal treatment and may predispose periodontal clients to acute abscess formation.
Signs and Symptoms
Acute periodontal abscess may be associated with any tooth in the mouth. Abscesses appear as shiny, red, raised, and rounded masses on the gingiva or mucosa. Abscesses can point and drain through the tissue or simply drain through the pocket opening. Purulent exudate is usually apparent around the abscess opening, or it can be expressed by finger pressure. Box 32-2 lists the signs of acute periodontal abscesses.
The client also may report that the tooth “feels high,” because it may become slightly extruded as a result of swelling.1 Radiographs may be helpful for locating a preexisting area of bone loss and can suggest the origin of the abscess. However, the infection moves through the tissue in the direction of least resistance, so the external features may appear at some distance from the affected tooth.1
Treatment
Treatment consists mainly of drainage and the appropriate use of antimicrobial agents. The acute phase of the disease must be managed to alleviate pain and prevent the spread of infection. The abscess must be drained, either through the pocket opening or through an incision. Drainage through the pocket opening is less invasive; this is commonly performed by the dental hygienist. The tooth or teeth in the affected area are anesthetized and scaled. Postoperative instructions call for rest, fluid intake, and warm saltwater rinses to help reduce swelling. The client is scheduled to return in 24 to 48 hours for reevaluation of the area and to plan for required follow-up treatment (e.g., periodontal surgery to eliminate the problem area).1
The dentist often delegates the initial treatment of the acute abscess that does not require surgical intervention to the dental hygienist. However, sometimes treatment requires an incision and reflection of the tissue (i.e., surgical flap procedure) to provide access to perform the debridement. If the client is febrile or if lymphadenopathy is present, the dentist prescribes antibiotic therapy. Figure 32-6 shows an example of debridement therapy for acute periodontal abscess.
Repair potential for acute periodontal abscesses is excellent. After treatment, the gingival appearance returns to normal within 6 to 8 weeks. Bone defect repair requires approximately 9 months. Bone is lost rapidly during the acute phase; however, with immediate problem recognition and proper treatment, the lost tissue can largely be regained.1 The positive nature of clinical results from healing further emphasizes the importance of the recognition and treatment of acute abscesses by the dental hygienist.
Chronic Periodontal Abscess
A chronic periodontal abscess resembles an acute periodontal abscess in that there is an overgrowth of pathogenic organisms in a periodontal pocket that drains inflammatory exudate.2 Chronic abscesses have communication with the oral cavity, either through the opening of the pocket or through a sinus tract that permits regular drainage. The chronic periodontal abscess is usually painless, or it may causes dull, intermittent pain; however, the client may recount previous episodes of painful acute infection.1 Figure 32-7 provides examples of draining chronic periodontal abscesses.
Signs and Symptoms
The signs and symptoms of chronic periodontal abscesses are similar to those of acute periodontal abscesses; however, the pain level can be the distinguishing feature (Box 32-3). The dental hygienist must assess exudate associated with the periodontium as being indicative of possible chronic abscess to ensure that appropriate dental referral and treatment are provided.
Treatment
Treatment of chronic periodontal abscess is similar to treatment of acute periodontal abscess. Scaling (usually requiring local anesthesia in the abscess area) must be performed. The client returns within 24 to 48 hours for further diagnosis. The dentist must determine the need for more periodontal treatment to reduce pocket depth and to address other periodontal defects. Additional treatment usually includes pocket reduction periodontal surgery, but it also may include tooth extraction and more frequent periodontal maintenance visits. Some chronic periodontal abscesses are better treated initially by gaining surgical access.10 Figure 32-8 shows the surgical treatment sequence for a chronic periodontal abscess.
A, Abscess associated with tooth #3 exhibits swelling and a fistula that is not draining. The tissue is very reddened, and the patient has intermittent severe pain. B, Periodontal probe inserted to show the depth of the pocket and determine its association with the buccal furcation. C, Flap reflected to permit access for debridement. Note the extent of the bone loss and the depth of the furcation involvement. D, After debridement, the flap is sutured in place. E, Healing after 1 month shows tissue returned to normal color and consistency and no evidence of the fistula. Note the recession that occurred after surgical treatment. This client must keep the teeth clean and return for frequent periodontal maintenance visits to preserve the tooth. (Courtesy Philip R. Melnick.)
The dental hygienist plays a major role in educating the client about the condition's chronic nature. The client is informed of the likelihood of increased bone loss and future acute episodes if no further treatment is performed in addition to the need for frequent maintenance care that includes scaling, root planing, and daily plaque biofilm control. Often the discussion of the risk of rapid bone loss during acute episodes of abscess helps the client value the need to seek further care to better preserve the teeth.4
Gingival Abscess
The gingival abscess usually occurs in previously disease-free areas, and it is often related to the forceful inclusion of some foreign body into the area. Gingival abscesses are most frequently found on the marginal gingiva and not associated with deeper tissue pathology.1
Signs and Symptoms
The gingival abscess can be observed on the marginal gingiva; Box 32-4 includes a list of signs and symptoms of this condition. A pus-filled lesion that is not associated with the sulcular epithelium is often clearly seen. Figure 32-9 shows a gingival abscess in the otherwise healthy periodontium of a teenager.
Treatment
The gingival abscess must be drained and the foreign object removed by the dentist or periodontist. The acute lesion is incised and irrigated with saline solution. Sutures are not usually required. Warm saltwater rinses are recommended for postoperative therapy at home. The client must return for postoperative observation in about 24 hours, at which time the swelling should be greatly reduced and the acute tenderness subsided.
Lesions of Endodontic Origin
Lesion Types
The lesion of endodontic origin (LEO), which is the most common dental emergency,1 is also referred to as a dentoalveolar, apical, periapical, or endodontic abscess.1 Inflammatory processes in the periodontium associated with necrotic dental pulps have a clear infectious cause. In a LEO, the inflammatory processes are directed toward infectious components released from bacterial growth and bacterial disintegration in the root canal system.4 It is sometimes difficult to distinguish a LEO from an acute periodontal abscess, because the associated facial pain and tenderness to the tooth are similar. The endodontic abscess commonly results from pulpal tissue infection as a result of caries, traumatic tooth fracture, or dental procedure trauma. Pulpal infection can be spread laterally to a tooth from an adjacent infected tooth, from infected periodontium, or through the lateral canals.4
Microbiology
Most commonly, the LEO is caused by microorganisms spreading into the pulp through the dentinal tubules from a carious lesion. However, the inflammatory processes in the periodontium occurring as a result of root canal infection may not only be localized at the apex; they may also appear along the lateral aspects of the root and in furcation areas of multirooted teeth.4 This lesion type appears to be an infrequent event that does not seem to emerge at a rate that corresponds with the frequency with which lateral canals occur in the teeth.
Dissemination of the microorganisms and their toxic by-products through the enamel to the dentinal tubules can be very rapid. Although microorganisms are the most common pulpal disease cause, bacterial toxins also can initiate pulpal disease by penetrating through tubules with pores small enough to block bacteria.4 The toxins affect the odontoblastic cells and then penetrate into the pulp, thus initiating an inflammatory response. The bacterial cells also move toward the pulp by demineralizing the hard tooth structure with acids that they produce along the way. The microorganisms colonize in the pulp and produce a variety of toxins that result in pulp cell death. Bacteria and their metabolic products exit the apical foramen and can cause localized granulation tissue formation; this tissue contains lymphocytes, plasma cells, mast cells, and other immune response elements. If the irritation continues, the granulation tissue gradually replaces the normal bone and periosteum at the tooth apex and gives rise to the common radiographic appearance of the LEO: a defined radiolucency at the apex of the affected tooth called a periapical pathosis (Figure 32-10).1
Characteristics and Treatment
Periapical Abscesses
There are both acute and chronic periapical abscesses. The acute periapical abscess occurs when bacteria or toxins rapidly enter the periradicular tissues, usually from the tooth pulp chamber. The confined abscess can cause severe pain. The pain may subside as the infection spreads toward a surface or space to provide relief to the tissues. Clients typically experience pain and swelling and may have systemic symptoms of infection, including osteitis (i.e., inflammation of the bone) or cellulitis (i.e., inflammation of cellular tissue, usually occurring in the loose tissues beneath the skin, in the mucous membranes, around muscle bundles, or around organs, which can be life-threatening). The chronic periapical abscess is associated with a more gradual introduction of irritants from the root canal into the periradicular tissues. The inflammatory response is intense, but the client gets relief from an either constantly or intermittently draining sinus tract.1 These tracts usually drain into the mouth through a fistula in the bone or through the periodontal ligament, but they can also drain through the facial skin. If a sinus tract through the periodontal ligament is left untreated, it will become a true periodontal pocket.1
Signs and Symptoms
The LEO is most identifiable on radiographs as a rounded radiolucency at the apex of the tooth. Figure 32-10 shows the typical appearance. However, early during abscess formation, the radiographic changes are often not obvious. If the LEO drains through a sinus tract in the cortical bone or through the periodontal ligament, it is likely to be much less identifiable on radiographs. LEOs that drain through the periodontal ligament can resemble acute periodontal abscesses, because their symptoms are very similar: both exhibit reddened tissue, swelling, and a sinus tract opening. It is often difficult to determine if the fistula opens into the periodontal pocket or goes to the apex of the tooth (Box 32-5).
When assessing an abscess to determine its origin, it is helpful to know that 85% of tooth pain is pulpal and that 15% is periodontal. In addition, many teeth with endodontic lesions are nonvital, which is a good distinguishing clue. However, some client populations that are likely to be treated by the dental hygienist, such as those treated in the periodontal practice, are much more likely to have periodontal than pulpal abscesses. Pain may be the distinguishing feature for differentiating between periapical and periodontal abscesses. Periapical pain is characterized as sharp, severe, intermittent, and hard to localize. By contrast, periodontal pain tends to be constant, less severe, and localized.1
Treatment
Apical abscess treatment requires either endodontic treatment to remove the tooth pulp and replace it with inert material or tooth extraction. Untreated endodontic abscesses can lead to severe cases of brain abscess or fasciitis of the neck or chest wall that can be life-threatening.1 The dental hygienist has a responsibility to inform clients with untreated LEOs of the risk of delaying treatment. Clients without acute symptoms caused by abscess draining are likely to have the need for conceptualizing the disease process so that they pursue care and avoid further tissue destruction and ill effects from the infection. Table 32-1 summarizes LEO treatment strategies.
Combination Abscesses
The periodontium is a continuous unit. Pathology at the tooth's apex from infection of the root canal system can extend to the marginal tissues, and infection originating in the periodontal tissues can progress to the pulp through openings at the apex or through lateral canals. A true combination periodontal and periapical abscess is present when both of these infectious processes are present. Whatever the route or source of the infection, when both the periodontal and pulpal tissues are involved and the disease has abscess formation, the abscess is considered a combination periapical and periodontal abscess.1
Signs and Symptoms
Combination abscesses cause some combination of the signs and symptoms described separately for periapical and periodontal abscesses. They are sometimes difficult to diagnose and can result in extensive damage to the surrounding periodontium, because the intermittent nature of symptoms often causes clients to delay seeking treatment. The dentist diagnoses combination abscesses when symptoms of both pulpal and periodontal infection are identified. Figure 32-11 illustrates a combination abscess.
Treatment
The most common form of treatment for periapical and periodontal abscesses is surgical exposure of the area, including the removal of the granulation tissue.4 Combination abscesses require the treatment of both sources of infection. Both periodontal and endodontic therapies are indicated to preserve the tooth. In some cases, the periodontal tissue destruction is so severe that the tooth must be extracted even though endodontic therapy could be performed successfully.5
Herpetic Infections
More than 80 herpesviruses have been identified,6 eight of which are known human pathogens.1,7
Herpes simplex viruses (HSVs) belong to the ubiquitous Herpesviridae family of viruses, which contains HSV-1, HSV-2, varicella-zoster virus, cytomegalovirus, and Epstein-Barr virus as well as human herpesviruses and Kaposi's sarcoma–associated herpesvirus (type 8).6
Herpesvirus infection occurs worldwide, has no seasonal variation, and affects only humans naturally. The prevalence of HSV-1 infection increases gradually from childhood, reaching 60% to 95% prevalence among adults.
Primary HSV-1 infection in oral and perioral sites usually manifests as gingivostomatitis, whereas virus reactivation in the trigeminal sensory ganglion gives rise to mild cutaneous and mucocutaneous disease; this is often called recurrent herpes labialis.6,7
Primary Herpetic Gingivostomatitis
Irrespective of the viral type, HSV primarily affects the skin and mucous membranes.7 Primary herpetic gingivostomatitis (PHGS) is the most common orofacial manifestation of HSV-1 infection, and it is characterized by oral and perioral vesiculoulcerative lesions.7 Although herpetic gingivostomatitis is a self-limiting disease, affected individuals may experience severe pain and be unable to eat or drink.
The virus is spread by physical contact, but there is no documentation that it can be spread through the airborne droplet route, contaminated water, or contact with inanimate objects. Most people encounter the virus and never show signs or symptoms of primary infection.7 It is known that up to 90% of the population has antibodies to HSV-1.
PHGS typically develops after the first-time exposure of seronegative individuals or among those who have not produced an adequate antibody response during a previous infection with either of the two HSVs.6
The majority of infections are subclinical. Although PHGS typically affects children between the ages of 1 and 5 years, occasional cases of primary infection affecting adults also occur.6 Infants are passively protected through maternal immunity for the first 6 months of life. The clinical manifestations of the infection, whether from HSV-1 or HSV-2, may lead to primary oral infection; nearly all are caused by HSV-1.6,7 The majority of HSV-1–induced primary orofacial infections are subclinical and therefore unrecognized.6 Symptomatic PHGS is typically preceded or accompanied by a sensation of burning or paresthesia at the inoculation site, cervical and submandibular lymphadenopathy, fever, malaise, myalgia, appetite loss, dysphagia, and headache. The most characteristic signs at presentation are acute, generalized, marginal gingivitis, with the inflamed gingiva appearing erythematous and edematous. Most clients with primary herpetic infections never experience the secondary or recurrent forms. In healthy individuals, primary infection has an excellent prognosis, with recovery expected within 10 to 14 days.6 Nevertheless, the painful herpetic ulcers in the mouth associated with primary infection often cause a reduction in food and fluid intake, thereby creating a human need for the prevention of the health risks that accompany this disease. Nutritional deficits can be critical in children and infants. Serious dehydration is not uncommon, and this can lead to infant hospitalization.
Signs and Symptoms
Acute herpetic gingivostomatitis is recognized by a set of characteristic systemic and intraoral signs and symptoms (Box 32-6). The vesicular eruptions may occur on the skin, the vermilion border, or the oral mucous membranes. Intraorally, they may appear on any mucosal or gingival surface, the hard palate, and the alveolar mucosa or any other oral soft-tissue area.6 The discrete grayish vesicles rupture and coalesce within 24 hours to form ulcers. The ulcers have a red, elevated, “halolike” margin with a depressed yellow or gray central area. They are teeming with shedding virus. Figure 32-12 exemplifies the intraoral appearance of primary herpetic infection in a teenager. The disease is commonly associated with systemic symptoms including fever, malaise, headache, and cervical lymphadenopathy.6
The recognition of PHGS is based on knowledge of the appearance of the ulcers and the assessment of systemic manifestations. Diagnostic tests, such as culturing for herpesvirus by the client's physician, can be conducted for confirmation of the presence of the virus, but these are not routine. In addition, this is a highly infectious disease; therefore the dental hygienist, the client, and the client's parents (in the case of children), must work together to prevent the transmission of the virus to family members and other members of the oral healthcare team. Figure 32-13 shows a more unusual presentation of primary herpetic infection on the facial skin.
Treatment
The treatment of gingival inflammation and any other elective dental care should be postponed until the PHGS has run its course. The client is assessed by the dentist to obtain a definitive dental diagnosis. The management of acute herpetic gingivostomatitis is entirely supportive because of the infectious nature of the disease and the fact that it runs its course in 7 to 10 days. The client should be instructed to rest, take fluids, and make every effort to eat a nutritious diet. The client should also try to clean the teeth at home with an extra-soft toothbrush if it can be tolerated.6,7
Professional care should not be performed because of the risk of transmission of the virus to other head and neck areas of the client or to the dental hygienist and other workers. Even if the hygienist was previously exposed to the herpesvirus or has had an episode of initial infection with or without recurrent lesions, he or she can still be inoculated with the virus by an inadvertent finger puncture with an HSV-contaminated instrument. This infection could result in the development of herpetic whitlow (Figure 32-14). Herpetic whitlow is a recurrent herpetic finger lesion that can be extremely painful and debilitating. The whitlow can last many weeks longer than the usual 2-week course of herpesvirus infection in the oral tissue.1
The dental hygienist educates the client about consuming adequate fluids and soft, nutrient-dense foods; performing oral hygiene as much as possible at home; and using over-the-counter topical anesthetics and systemic nonsteroidal anti-inflammatory agents to minimize discomfort. The client can swab topical anesthetics onto the lesions for controlled local delivery. Topical anesthetics should be used cautiously with children so as not to anesthetize the throat, which can be frightening to them.
Recurrent Oral Herpes Simplex Infections
After primary infection, latent HSV reactivates periodically, migrating from the sensory ganglia to cause recurrent oral or genital herpes.6,7 Despite the high prevalence of HSV-1 in the population, only 15% to 40% of seropositive patients ever experience symptomatic mucocutaneous recurrence.1,6,7 An individual's genetic susceptibility, immune status, age, anatomic site of infection, initial dose of inoculums, and viral subtype appear to influence the frequency of recurrence. As compared with primary infections, recurrent episodes are milder and shorter in duration, with minimal systemic involvement.7
Clients often arrive for dental hygiene appointments when they have recurrent herpetic lesions. These lesions are quite common, as previously mentioned, and they do not interfere with activities of daily living, so clients are frequently unaware of the nature of the event. The typical recurrent lesion is on the lip and is referred to as herpes simplex labialis. Common names such as fever blister and cold sore reflect the public's understanding of what precipitates these recurrences. Unfortunately, these are extremely innocuous names for lesions with serious potential effects for the dental hygienist.
Signs and Symptoms
Clients often have prodromal symptoms of burning, tingling, or pain at the site where the lesion recurs (Box 32-7). Within hours of the prodromal symptoms, vesicles appear, and these become ulcerated and coalesce into a large ulcer or ulcers. The lesions heal without scarring in about 14 days, and they can recur as often as once per month. Typically lesions will recur in the same place on the vermilion border and on the skin around the face. Figure 32-15 shows an example of a recurrent herpetic lesion.
Treatment
Recurrent lesions shed vast amounts of herpesvirus. For this reason, the dental hygienist must not treat the client while the lesions are present. Sometimes this can be very disconcerting, because it requires reappointing a client who has waited months for an appointment. However, the dental hygienist is placed at great risk of inoculation, just as with primary herpetic infections. Not only are herpetic whitlow lesions a possibility, but the virus is also shed in the saliva, which means that spatter during treatment can be hazardous. Figure 32-16 shows an example of a recurrent herpetic infection of the cornea that was acquired as a result of spatter.
Herpetic lesion treatment is entirely supportive. There are some antiviral agents available by prescription (e.g., acyclovir) that the client may benefit from using. These agents can reduce the extent and duration of the recurrence. The dental hygienist should inform the client of this possibility and refer the client to the physician or dentist for further information.
It is extremely important for the client to be educated about these lesions and about his or her responsibility for preventing the spread of infection. Clients who have common recurrences are often aware of the prodromal symptoms and should be informed to call and reschedule dental appointments until the disease runs its course.
Recurrent herpetic lesions can occur intraorally, and they usually appear on the soft palate.6 These lesions sometimes erupt after therapeutic scaling and root planing, when repeated palatal injections have been given to the client to achieve anesthesia. The client will either call or return for a subsequent appointment, and the typical oral ulcers will be evident in the area in which the injections were given. Figure 32-17 is an example of recurrent palatal herpes subsequent to periodontal therapy in the maxillary arch. This situation requires the same management as other herpetic episodes. The client should not be treated until the lesions have healed, and the client must be educated about the situation.
Recurrent intraoral herpetic lesions can almost always be easily distinguished from the more commonly occurring aphthous ulcers. Reviewing the client history for recent trauma or illness may be helpful, but either lesion can result. The more distinguishing characteristic is that recurrent herpetic lesions almost always occur on the gingiva or the hard palate, and aphthous ulcers almost always appear on the movable mucosa.
Pericoronitis
Pericoronitis is soft-tissue inflammation associated with a partially erupted tooth. It may be acute, subacute, or chronic in nature.8 The most commonly affected tooth is the mandibular third molar, but maxillary third molars and other teeth that are the most distal in the arch have been associated with the disease. The tissue flap that either completely or partly covers the associated tooth is called an operculum. The space between the tissue flap and the tooth is an ideal location for food debris to collect and bacteria to grow. As bacteria increasingly infect the area, the tissue responds by becoming extremely inflamed and painful.8 There is constant inflammation in the area, so it is always considered subacute or chronically infected, even if the acute symptoms are not present.8
Acute pericoronitis involves an extremely high degree of inflammation in the local area. As inflammation increases, the tissue swells, and this can interfere with the complete closing of the jaws. This interference can lead to added trauma, increased inflammation, and severe pain. The tissue becomes quite red, suppuration is evident, and the pain can radiate to the throat and ear.
This disease is a common problem associated with young adults, and it has been considered to be a serious problem for military personnel, most of whom are in the 17- to 26-year-old age group. In fact, 20% of dental emergencies reported by the military during World War II and 16% of those from the Vietnam conflict were acute pericoronitis.1 Figure 32-18 shows an example of acute pericoronitis.
Signs and Symptoms
Oral areas that have an operculum are predisposed to pericoronitis and typically exhibit chronic signs of the disease, increased redness, and some exudate (Box 32-8).
The tissue may be so swollen that it interferes with mastication, and it is easily traumatized during eating. The infection can extend very deeply into the tissues and cause peritonsillar abscess formation, cellulitis, and Ludwig's angina.5 These signs are rare sequelae, but they emphasize the importance of recognition and lesion treatment.
A review of military studies documents the extent of symptoms associated with pericoronitis. In a military study of 359 recruits, pain, swelling, and redness were present in every instance. Purulent exudate was reported in half of the cases, few patients bled on palpation, and no individual in that population had a fever. In addition, two thirds of 25 cases in the naval population reported previous episodes of pericoronitis, which suggests that pericoronitis is often a recurrent problem.8
Treatment
A number of considerations are involved when treating pericoronitis, including the severity of the case, whether it is a recurrence, and possible systemic complications. The dentist may ask the dental hygienist to participate in the care of the client with pericoronitis, which requires multiple visits.
Initial dental management is aimed at treating symptoms with the goal of making the client more comfortable. The infected area is debrided, usually by gentle flushing with warm water or dilute hydrogen peroxide delivered in a disposable irrigating syringe with a blunt needle. Topical anesthetic is applied first. Much tissue manipulation may not be possible, but the tissue needs to be lifted away from the tooth to permit as much debridement as is tolerable at the first treatment appointment.1 After this initial debridement, the client is instructed to rest at home, use warm saltwater rinses, and drink fluids to avoid dehydration. The dentist may prescribe antibiotics if the client is febrile or if there is cervical lymphadenopathy. The client is asked to return the next day. At the second visit, the area is irrigated again and instrumented if possible, and more thorough homecare is initiated. A marked improvement is usually observed at the second appointment.
After the acute condition has resolved, the client is assessed by the dentist to determine further treatment. Dental treatment may include the extraction of the offending third molar or operculum removal to produce a more normal gingival contour if the tooth is to be retained.9
The presence of any operculum is assessed and viewed with suspicion. There is almost always some amount of inflammation present, and the potential for acute exacerbations is likely. The dental hygienist informs clients about the potential issues associated with the condition to permit them to understand the situation and take responsibility for their oral health.
Necrotizing Periodontal Diseases
Acute necrotizing ulcerative gingivitis has been reported widely, and it is not uncommon in developing countries.10 Classical diagnostic features include ulceration and necrosis of the interdental papillae, pain, and spontaneous gingival bleeding. Necrotizing ulcerative periodontal diseases are clinically recognizable diseases that are distinct from chronic periodontitis. Until 1999, the condition was most commonly called acute necrotizing ulcerative gingivitis or just necrotizing ulcerative gingivitis. However, the disease is often associated with attachment loss, which makes the term gingivitis inaccurate, so the disease is now referred to as necrotizing ulcerative periodontitis. It is not certain whether the conditions involving attachment loss are separate diseases from those confined to the gingiva, so the consensus is to use the more general disease name of necrotizing periodontal diseases.
Necrotizing ulcerative periodontal diseases are opportunistic gingival infections that are associated with lifestyle risk factors (e.g., stress, tobacco use) as well as with systemic conditions (e.g., blood dyscrasias, acquired immunodeficiency syndrome, Down syndrome).10
The disease was first described by Vincent during the late nineteenth century, and it was so common among troops fighting in trenches in Europe during World War I that the name trench mouth was adopted. It was primarily seen in young adult individuals, and it was thought to be communicable.10 However, the disease is not communicable, infectious, or spread through direct contact. Necrotizing ulcerative periodontal diseases are recognized to be recurrent diseases with complex bacteriology consisting of a large proportion of spirochetes and gram-negative organisms. The consistent presence of specific bacteria, fusobacteria, and spirochetes has suggested that the cause could be explained in microbiologic terms. These organisms invade the tissue, which causes the characteristic appearance of the disease. Other contributory factors implicated include poor oral hygiene, mouth breathing, smoking, stress, sepsis, malnutrition, and systemic diseases, including hormonal imbalance and alterations in lymphocyte and neutrophil function.10
Signs and Symptoms
Necrotizing ulcerative periodontal diseases have specific clinical characteristics that distinguish them from other forms of acute oral infections. The clinical appearance of the disease is one of cratered or “punched-out” papillae, very reddened gingivae, and pain. There is often a collection of debris, dead cells, and bacteria on the gingival surface that appears gray and that is referred to as the pseudomembrane. The gingival lesions may be localized to specific areas or generalized throughout the mouth, and they progressively destroy the gingiva and the underlying periodontal structures. Clients frequently exhibit an extremely offensive and fetid breath odor that can be smelled anywhere in a room that is occupied by the client. They may also complain of a thick or pasty texture to the saliva. In addition, the acute lesions can be extensive and cover parts of the face, as is seen in developing countries in association with malnutrition. Figure 32-19 shows the clinical oral features of necrotizing ulcerative periodontitis.
The three most reliable criteria for recognizing the disease are as follows:
Other symptoms have been recognized as being strongly associated with the disease (Box 32-9).
Stress is often related to both the initial occurrence and recurrence of this disease. The role of the psychologic factors involved with stress is not well understood, but it has been postulated that changes in the immune system that occur at stressful times predispose certain individuals to an exuberant bacterial response that results in necrotizing ulcerative disease.
Treatment
The course of a single episode of necrotizing ulcerative periodontitis is usually short but painful. Clients come to the oral care setting most often as a result of the associated pain. Because of the cyclic and recurring nature of the disease, treatment focuses on microbial control through mechanical debridement by both the client and the clinician. It also requires consultation with the client's physician because of possible predisposing systemic factors, such as human immunodeficiency virus infection.6 Treatment should progress daily during the acute phase of the disease, because the pain often inhibits thorough cleaning by the client or the dental hygienist at one time. Treatment includes periodontal debridement with ultrasonic scalers, plaque biofilm control, and 0.12% chlorhexidine rinses twice daily. The dentist may prescribe a systemic antibiotic if fever and lymphadenopathy are present. The recommended treatment sequence is described in Table 32-2.
TABLE 32-2
Treatment Regimen for Necrotizing Ulcerative Periodontitis
Given the signs and symptoms, most clients with necrotizing periodontal diseases have unmet human needs in the areas of freedom from head and neck pain, skin and mucous membrane integrity of the head and neck, and conceptualization and problem solving. Client health and oral health and well-being are the keys to the successful treatment of these diseases. Clients must be knowledgeable about the roles of stress, bacteria, and nutrition in the disease process and encouraged to take control of their oral health and lifestyle behaviors. Suggestions to identify stress-management techniques and to improve nutrition are necessary components of dental hygiene care (see Chapters 35 and 41).
Avulsed Tooth
Prevalence
The avulsion of permanent teeth is the most serious of all dental injuries. The avulsed tooth is one that is separated from the alveolar bone by trauma.11 Although avulsion is not strictly a periodontal emergency, it does involve traumatized teeth that can be replanted successfully if managed properly. The prognosis depends on the measures taken at the scene of the trauma or immediately after avulsion. In some cases, the dental hygienist may be the first person in the dental profession to meet the patient. In this situation, the dental hygienist may have the opportunity to help the parent of a small child or a student or adult participating in athletic activities to preserve an avulsed tooth through quick action.
Traumas to the oral region occur frequently and comprise 5% of all injuries for which people seek treatment. Among preschool children, the figure is as high as 18% of all injuries. Avulsion is the most common dental injury to children who are less than 15 years old. The situation occurs in as many as 1 in every 200 American children, which results in approximately 2 million occurrences per year. Among all facial injuries, dental injuries are the most common; avulsions occur with 1% to 16% of all dental injuries.12 Replantation is the treatment of choice, but this cannot always be carried out immediately. To meet the client's need for a biologically sound and functional dentition, it is incumbent on the dental hygienist to respond to this dental emergency. However, the dental hygienist should take responsibility to inform parents, children, students, and adults who are participating in athletic activities to use mouth protectors to prevent oral injuries. In addition, information should be given to teachers and coaches about the risk of oral injuries during certain sports activities. Furthermore, replantation should not be performed when primary teeth have been avulsed because of the risk of injury to the underlying permanent tooth germ.11,12
An appropriate treatment plan after an injury is important for a good prognosis. Guidelines are useful for dental hygienists, dentists, and other healthcare professionals to use to deliver the best care possible in an efficient manner. The International Association of Dental Traumatology has developed a consensus statement in response to the dental literature and group discussions. Lost time and improper handling of the avulsed tooth can substantially reduce the long-term success of replantation. Moreover, the dental hygienist should inform parents, teachers, and coaches about the procedure; increased awareness can improve the opportunity for successful tooth replantation when injuries that cause avulsed teeth occur.
Good healing after an injury to the teeth and oral tissues depends, in part, on good oral hygiene. Patients should be advised about how best to care for teeth that have received treatment after injury. Brushing with a soft brush and rinsing with 0.12% chlorhexidine are beneficial to prevent the accumulation of plaque and debris.
The procedure for constructing a custom-made athletic mouth protector is described in Procedure 37-7 of Chapter 37. Athletic mouth protectors are highly recommended to prevent tooth avulsion.
Treatment
The dental hygienist might be present at a sporting event or another venue when a tooth is traumatically avulsed, or he or she may have a child who experiences a traumatically avulsed tooth. The avulsed tooth is quickly separated from the alveolus after a fall or a strike of some kind. Typically a layer of periodontal ligament cells remains on the cemental surface of the avulsed tooth and on the bone in the socket because of the very fast occurrence of the trauma. The successful treatment of avulsed teeth by replantation is dependent on rejoining intact periodontal ligament cells covering the tooth's cementum with those that remain in the socket.
The object of this emergency treatment is to promote periodontal ligament healing after the tooth is replanted in the socket. To maximize the chances of healing, the tooth must be handled only by the crown to prevent damage to the remaining periodontal ligament cells. It is essential that the avulsed tooth not dry out and that it not be debrided in any way. As little as 1 hour of dry storage before replantation negatively affects the procedure success rate.11,12
The ideal place to store and transport the avulsed tooth is in the socket, if it can be gently placed and held there while the client is taken to an oral healthcare setting or a hospital emergency department. The socket provides the most nutritious environment for the cells of the periodontal ligament, thereby increasing their survival rate. If it is not possible to replace the tooth temporarily in the socket as a result of other injuries associated with the trauma or emotional upset, physiologic saline is a safe alternative. Unfortunately this substance may not be handy. Milk is also a good medium, because it has physiologic osmolality and relatively few bacteria. Saliva has more bacteria than milk, but the use of milk is a good way to keep the tooth moist. However, the client may be too upset or too young to hold the tooth in the mouth. Warm saltwater can prevent dehydration, but it cannot keep the cells alive for long. Air drying or wrapping the tooth in gauze or other materials, even for a short time, is contraindicated, because such a procedure will kill the periodontal ligament cells.11,12 Alternatives may have to be thought through quickly and a decision made during a stressful situation to avoid the dehydration and death of cells. The options for the storage and transportation of the avulsed tooth are highlighted in Table 32-3. Box 32-10 discusses the documentation of an avulsed tooth.
TABLE 32-3
Storage of Avulsed Teeth During Transportation for Treatment
| Choice | Transportation Medium |
| First | Replace in socket. |
| Second | Store in physiologic saline. |
| Third | Store in cold, fresh milk. |
| Fourth | Place in the individual's mouth, either under the tongue or in the cheek. |
| Fifth | Store in warm saltwater. |
| Sixth | Store in tap water. |
At the emergency treatment facility, the tooth is removed from its transport medium, gently rinsed, replanted in the socket after the blood clot is removed, and splinted into place. A 5- to 7-day course of systemic antibiotics typically used for dental infections is prescribed. Endodontic procedures need to be performed at a later time (i.e., about 2 weeks after replantation) to avoid inflammatory root resorption.12 The protocol for the management of the avulsed tooth is presented in Procedure 32-1. A comparative summary of the conditions presented in this chapter can be found in Table 32-4.
Procedure 32-1 Emergency Management of the Avulsed Tooth
| EQUIPMENT | |
| STEPS | RATIONALE |
|
4. Place the tooth in the socket or in the transport medium (see Table 32-3). |
|
TABLE 32-4
Summary Comparison of Acute Gingival and Periodontal Conditions, Lesions of Endodontic Origin, and Avulsed Teeth
| Cause | Risk Factors | Signs and Symptoms | Prevention and Management |
| Acute Periodontal Abscess | |||
| Periodontal pathogens | |||
| Chronic Periodontal Abscess | |||
| Periodontal pathogens | |||
| Gingival Abscess | |||
| Foreign object | |||
| Lesion of Endodontic Origin | |||
| Caries Periodontal disease Tooth fracture Traumatic dental procedures |
|||
| Combined Periodontal Abscess | |||
| Caries Periodontal disease Tooth fracture Traumatic dental procedures |
|||
| Acute Herpetic Gingivostomatitis | |||
| Herpes simplex virus | |||
| Recurrent Herpetic Lesions | |||
| Herpes simplex virus | |||
| Acute Pericoronitis | |||
| Bacterial plaque | |||
| Necrotizing Ulcerative Periodontitis | |||
| Pathogenic bacteria | |||
| Avulsed Tooth | |||
| Trauma |
Preservation of tooth in appropriate transport medium (see Table 32-3) Immediate transport to treatment facility for replantation of tooth |
||
Client Education Tips
• Educate clients about disease transmission and lifestyle influences, particularly those related to the herpesvirus and necrotizing periodontal diseases.
• Educate clients with painful oral infections to consume adequate fluids and nutrient-dense foods, to perform oral hygiene, and to use over-the-counter topical anesthetics to control their discomfort.
• Review methods to prevent the transmission of an active herpetic infection.
• Teach clients with a history of recurrent herpetic infection to cancel dental appointments when an active oral lesion is present.
• Review methods and treatment to prevent the recurrence of pericoronitis and necrotizing periodontal diseases.
• Teach parents, teachers, and coaches about avulsed teeth and their management to improve the probability of successful tooth replantation.
• Teach clients who are at risk for tooth avulsion about the need for a mouth protector.
Legal, Ethical, and Safety Issues
• Dental hygienists have a legal responsibility to recognize emergency conditions, to make appropriate referrals, and to treat those conditions within the scope of dental hygiene practice.
• Dental hygienists have an ethical responsibility to educate clients about the significance of their diseases and the potential for recurrence and the infection of others.
• Dental hygienists have a responsibility to educate and refer clients in cases of dental trauma and to prevent oral injuries when possible.
• Dental hygienists must consider their own personal safety from infectious diseases when treating clients with acute infectious conditions, such as primary herpetic gingivostomatitis or herpes labialis.
Key Concepts
• Periodontal abscess is a treatable and often preventable disease process.
• A lesion of endodontic origin is a serious infection that requires consultation and referral for immediate treatment. Left untreated, a lesion of endodontic origin could develop into a brain abscess or fasciitis of the neck or chest wall, which can be life-threatening.
• Periodontal abscesses have a pathogenic microflora similar to that associated with periodontal diseases.
• Incomplete subgingival scaling and root planing has been suggested as a cause of periodontal abscesses; however, there are few data to support this assumption.
• Abscesses can point and drain through the tissue or simply drain through the periodontal pocket opening.
• Infection moves through tissue along the pathway of least resistance; therefore clinical features of the infection may appear at a distance from the affected tooth.
• Pain may be the key feature for distinguishing between periapical and periodontal abscesses. Periapical pain is sharp, severe, intermittent, and hard to localize; periodontal pain is constant, less severe, and localized.
• Primary and recurrent herpetic infections are serious but self-limiting conditions that require the postponement of elective dental hygiene and dental treatment. Dental hygiene care should not be performed on a client with a herpetic infection because of the risk of transmission of the virus to the dental hygienist and other workers.
• Pericoronitis at any stage is a serious infection that requires referral and definitive treatment.
• Necrotizing periodontal diseases are complex processes that benefit from the dental hygiene process of care.
• Mouth protectors and their fabrication are significant to comprehensive dental hygiene care.
• Avulsion is the most common dental injury among children who are less than 15 years old. The dental hygienist has a role in the management of avulsed teeth as possibly the most knowledgeable person at the traumatic injury scene.
• The ideal place to store and transport an avulsed tooth is in the victim's tooth socket; if this is not possible, physiologic saline is one alternative.
Critical Thinking Exercises
1. A 30-year-old client who has not been treated for several years arrives for a dental hygiene appointment. The client wants to have his “teeth cleaned today” but informs you about some pain and sensitivity in the lower right quadrant and a tooth that feels “high” in that same area. The pain is intermittent but “very bothersome.” After taking the client's medical and pharmacologic histories, you determine that he is in good general health with no systemic illnesses, and he is taking no medications. Your intraoral findings indicate that the client has redness and swelling on the buccal surface of tooth #30. The gingival architecture appears normal, and there is no sinus tract, but pus can be elicited from the site by gentle finger pressure.
A What condition is most likely causing the client's symptoms?
B. What is the most likely treatment for the condition?
C What dental hygiene diagnosis should be addressed first for this client?
2. A 20-year-old client comes to the dental office complaining of severe pain in her mouth. You determine that the client has no systemic illnesses, and you examine the oral tissues. The oral findings are extreme redness and swollen gingiva throughout the mouth and small, grayish ulcers on the gingiva and mucosa in several areas.
A What condition is most likely causing the client's symptoms?
B What is the most likely treatment for the condition?
C What dental hygiene diagnosis should be addressed first for this client?
3. A client comes to the dental office without an appointment complaining of exquisite pain in her jaw. In fact, the client can hardly open her mouth. A review of the client's medical and pharmacologic histories shows that the client is in good general health and takes no medications. Intraoral findings reveal extremely reddened and swollen gingiva on the mandibular right posterior area. The client complains of a bad taste in her mouth and says that the condition “comes and goes” but that this is the worst pain she has experienced. The client has many large amalgam restorations and appears to have a partially submerged molar in the quadrant.
A What is the most likely emergency condition?
B How should the dental hygiene component of the overall dental treatment begin?
C What dental hygiene diagnosis should be addressed first for this client?
4. A 45-year-old client arrives at the dental office without an appointment and complains of severe pain. You seat the client and determine that she is in good general health, has no systemic illnesses, and is taking no medications. Intraoral examination reveals a large, pointed fistula on the buccal surface of tooth #3, about one third of the way toward the tooth apex. The client has been treated for periodontal disease in the past, including in some areas that required periodontal surgery, and she has many teeth that have been restored with amalgam and composite restorations. There is a large mesial-occlusal-distal amalgam with a lingual extension on tooth #3. The radiograph you just took shows no obvious apical pathology.
A What condition is most likely causing the client's symptoms?
B What should the dental hygiene component of overall dental treatment that day include?
C What dental hygiene diagnosis should be addressed first for this client?
5. A client arrives for his 4-month continued-care appointment. He is very excited to be leaving tomorrow for a 6-month stay in Europe, and he is anxious to have his dental hygiene maintenance care before he leaves. You notice a round, crusted lesion on his lower lip that is 6 mm in diameter, with some vesicles on the edge. He relates to you that he has never had such a sore before and that it was hurting a few days ago but is fine now. He requests that you cover the lesion with petroleum jelly so that it will not crack while you are treating him.