CLINICAL REVIEW Recognition and Management of …jabfm.org/content/23/3/285.full.pdf · Topics reviewed include the sequelae of dental caries, periodontal disease, and trauma. Prevention

CLINICAL REVIEW

Recognition and Management of Common AcuteConditions of the Oral Cavity Resulting From ToothDecay, Periodontal Disease, and Trauma: AnUpdate for the Family PhysicianPaul C. Edwards, MSc, DDS, and Preetha Kanjirath, BDS, MDS

This article presents an overview of common and/or significant diseases of the oral cavity that the familyphysician is likely to encounter, with an emphasis on pathogenesis, recognition, complications, andmanagement. Topics reviewed include the sequelae of dental caries, periodontal disease, and trauma.Prevention and early intervention strategies are emphasized. Recent updates and practical issues for thefamily physician are highlighted. (J Am Board Fam Med 2010;23:285–294.)

Keywords: Dental Decay, Otolaryngology, Periodontal Diseases

The oral cavity is a distinctive region of the bodythat, as a result of being exposed to the harsh oralenvironment, is subject to a distinctive set of con-ditions and diseases, many of which are unique tothis area. Furthermore, the effect of disease in theoral cavity can have significant impact on the over-all health of the individual.

Dental Caries and Tooth PainThe teeth are 32 highly specialized hard tissue unitsthat each consist of 3 functional units. First, thevisible crown portion, which is exposed to the oralenvironment and is composed of an outer layer ofinorganic, heavily mineralized tissue (enamel) over-lying a somewhat softer collagen-containing calci-fied substance (dentin) that resembles bone in itsratio of organic to inorganic composition. Sec-ondly, the root portion, which anchors the tooth tothe surrounding alveolar bone by means of a dense,

fibrous connective tissue attachment (periodontalligament). Finally, a central pulp complex that iscomposed of neurovascular and loose, fibrous con-nective tissue.

Dental caries, or tooth decay, is one of the mostprevalent chronic diseases affecting modern soci-ety. These are also known colloquially as cavities,reflecting the cavitation that occurs in more ad-vanced lesions. Once viewed as a disease of children(Figure 1), it seems that, because a greater percent-age of the adult population are retaining theirteeth, adults are now developing new carious le-sions at the same incidence rate as children.1

Among some methamphetamine abusers, a patternof rampant carious destruction is noted, a conditiontermed “meth mouth”2 (Figure 2). There is also anexponential increase in risk of developing cariesamong patients who take multiple medications thatpredispose to xerostomia. Among the aging popu-lation, caries are commonly seen on the root sur-face of the teeth, where the gums have receded(Figure 3).

Caries develop through a complex interaction inwhich transmissible cariogenic oral microflora, pri-marily Streptococcus mutans and lactobacilli, metab-olize fermentable dietary carbohydrates, resultingin lactic acid production.3 The resultant drop in pHat the tooth surface results in dissolution of themineral component of the enamel. This process is

This article was externally peer reviewed.Submitted 3 February 2009; revised 30 November 2009;

accepted 4 December 2009.From the Department of Periodontics and Oral Medicine,

Faculty of Dentistry, University of Michigan, Ann Arbor.Funding: none.Conflict of interest: none declared.Corresponding author: Paul C. Edwards, MSc, DDS, De-

partment of Periodontics and Oral Medicine, Faculty ofDentistry, University of Michigan, 1011 N University Ave-nue, Ann Arbor, MI 48109-1078 (E-mail: [email protected].)

doi: 10.3122/jabfm.2010.03.090023 Common Acute Conditions of the Oral Cavity 285

a dynamic one, in which demineralization is coun-tered by remineralization through the bufferingcapacity of the saliva.4 Progression of caries resultswhen the rate of demineralization exceeds theremineralization rate. Clinically, caries start in thedeep pits on the biting surfaces of the posteriorteeth or on the smooth surfaces of the teeth (Figure4). Although often visible to the naked eye as a softarea of surface cavitation, ranging from white (re-flecting early demineralization) to brown or blackin color, the caries process can also occur beneathan intact layer of surface enamel or between 2adjacent teeth, making early visual recognition ex-tremely difficult without the assistance of radio-graphs (Figure 5).

Although the caries process in the heavily min-eralized enamel layer of the tooth is primarily aphysicochemical process, the underlying dentin isconnected to the highly innervated pulp tissue at

the center of the tooth through small-diameterdentinal tubules. When caries penetrate throughthe full thickness of the enamel to reach the under-lying dentin, patients will typically exhibit momen-tary tooth pain on exposure to cold and/or osmoticagents such as sugar. This process, termed reversiblepulpitis, is not an acute emergency and can typicallybe treated by conservative mechanical removal ofthe decay and placement of a dental restoration (a“filling”) to replace the lost tooth structure, pro-vided that this treatment is initiated in a reasonabletime frame (typically several weeks). A similar typeof pain can be elicited in patients who have gingival

Figure 1. Rampant caries in a child. (Photographcourtesy of Dr. Ana Veira.)

Figure 2. Rampant caries in a methamphetamine user.

Figure 3. Root caries may be difficult to detectclinically because they are frequently hidden by thegingiva. (Photograph courtesy of Dr. EduardoBresciani.)

Figure 4. Caries commonly start in the deep grooves(pits and fissures) located on the biting surface of themolar teeth. In this case, a small surface openinghides extensive subsurface decay. (Photographcourtesy of Dr. Eduardo Bresciani.)

286 JABFM May–June 2010 Vol. 23 No. 3 http://www.jabfm.org

recession, resulting from either excessively roughtooth brushing habits or as a result of periodontaldisease. The exposed root surface, especially whencoupled with toothbrush-related removal of theprotective cementum, results in momentary toothpain on exposure to cold and/or osmotic agentssuch as sugar. The degree of sensitivity can bereduced by instructing the patient to change theirbrushing technique and use less force while brush-ing, incorporating a vertical brushing stroke insteadof a “back and forth” horizontal brushing motion,coupled with long-term use of specially formulatedtoothpaste for “sensitive” teeth. These toothpastescontain salts such as potassium nitrate or potassiumoxalate that seal the exposed dentinal tubulesand/or modulate nerve transmission. Dentist-ap-plied agents such as fluoride varnishes and thinlayers of bonded resin can provide more rapid res-olution of symptoms.

If caries go untreated, severe dental pain thateither persists after removal of the inciting stimulusor occurs spontaneously will typically result. Thiscondition, termed irreversible pulpitis, results in se-vere pain that may last for hours or days if un-treated. Patients with irreversible pulpitis will typ-ically present on an urgent basis in acute distresswith minimal physical reserves after being unableto obtain any relief for an extended period of time.The pain is typically generalized, involving the areaof several teeth, and may even be referred to theopposing jaw, often making precise identification ofthe offending tooth by the patient or provider dif-ficult. Patients should be offered palliative treat-ment for pain. Although nonsteroidal anti-inflam-

matory agents (eg, ibuprofen 600 to 800 mg every4 to 6 hours) may be beneficial in cases of mild tomoderate pain, in more severe cases acetamino-phen-narcotic combinations (eg, Tylenol #3, Per-cocet, or Vicodin) are typically required. Althoughantibiotics are often inappropriately prescribed,they are not indicated at this stage. Instead, it isimportant to refer the patient to a dental provider.Definitive treatment involves either surgical extrac-tion of the involved tooth or, if the decision is madeto try to preserve the tooth, mechanical extirpationof the pulpal tissue (a pulpectomy; the first step inroot canal treatment).

Eventually, if untreated, pulpal necrosis will de-velop as a result of prolonged inflammation withinthe confined space of the pulp cavity. This condi-tion, termed acute apical periodontitis, is character-ized by severe pain located to the affected tooth.The pain is aggravated by pressure (eg, touch orbiting). As with irreversible pulpitis, treatment in-volves prompt root canal therapy or extraction ofthe tooth. Because the pain is the result of necroticpulp tissue and not an infectious process, antibiotictherapy is not indicated.5,6 However, in the pres-ence of underlying medical conditions that com-promise host resistance, such as poorly controlleddiabetes or among patients taking high-dose corti-costeroids, antibiotic therapy, as described belowfor an acute apical abscess, should be considered.

In many cases, depending on the host’s immuneresponse, bacterial load, and virulence, inflamma-tion may spread beyond the apical area of the tooth,resulting in an acute apical abscess. This is evidentclinically by the presence of an intraoral swelling,typically located within the buccal vestibule apicalto the tooth root. This situation is ideally managedby a dentist through removal of the tooth or extir-pation of the necrotic pulp tissue and/or incisionand drainage of any fluctuant abscess. If immediatedental management cannot be arranged, empiricalbroad-spectrum antibiotic coverage should be con-sidered, especially if the patient has any underlyingmedical conditions that could reduce bacterial re-sistance (eg, diabetes, inability to sleep because ofsevere dental pain, alcoholism, etc).

Dental infections are typically caused by normaloral flora. During the first 3 days of the process,facultative Gram-positive oral streptococci pre-dominate. The antibiotic of choice during this earlyperiod is penicillin VK 500 mg by mouth every 6hours for 7 days.7,8 Amoxicillin—500 mg every 8

Figure 5. This radiograph shows interproximal cariouslesions that would have been difficult to detect byclinical examination alone.


hours—is an acceptable alternative. If the swellinghas been present for more than 3 days or is unre-sponsive to penicillin therapy, metronidazole (250to 500 mg by mouth every 6 hours) may be added.9

For a patient who is allergic to penicillin, clinda-mycin 300 mg by mouth every 6 hours for 7 days isrecommended.9

This infection has the potential to develop into atrue medical emergency if not treated promptly andaggressively. Cellulitis, characterized by painfulswelling, regional lymphadenopathy, and in manycases fever, may rapidly develop if the infection isallowed to spread into the surrounding fascialplanes. Serious complications can include compro-mised breathing (Ludwig angina) for infections ofmandibular origin and orbital or cavernous sinusinvolvement for maxillary infections. Althoughrare, death can occur, especially among healthyyoung adults.10 Any sign of fascial plane involve-ment necessitates immediate referral to an oral andmaxillofacial surgeon or a hospital dental depart-ment. If any signs of respiratory difficulty are ap-parent, the patient should be referred directly tothe nearest emergency department.

Fortunately, in most cases, the necrotic toothfollows a less fulminant clinical course, progressinginstead to a chronic low-grade inflammatory pro-cess involving the apical supporting bone. Degra-dation products from bacteria and necrotic pulptissue lead to chronic bone destruction and theformation of a mass of chronically inflamed gran-ulation tissue within the jaw, termed chronic apicalperiodontitis. In long-standing lesions, mediators ofinflammation may trigger a proliferation of dor-mant epithelial cells in the area of the root apex,resulting in the formation of a periapical cyst. Clin-ically, the involved teeth are usually asymptomatic,although a slight increase in mobility and milddiscomfort may be elicited by tapping on the bitingsurface of the tooth. An area of bone resorption istypically noted around the apex of the tooth rootfollowing radiographic examination.

Definitive treatment involves extraction of thecausative tooth with conservative curettage of anyremaining lining from the cyst cavity. When suffi-cient tooth structure remains to allow for restora-tion of the tooth, endodontic treatment can beattempted.11 Failure to treat these lesions will leadto continued bone destruction and eventual perfo-ration of the cortical plates of bone. In exceedinglyrare cases, the epithelial lining can undergo malig-

nant transformation.12 More commonly, thischronic process will continue with only sporadicmild symptoms until it is recognized by the pa-tient’s dentist. In many cases, the patient will even-tually develop an acute exacerbation of chronicapical periodontitis, which clinically resembles anacute apical abscess. Typically, the patient will re-port waking up in the morning with a prominentswelling and in severe pain resulting from tissueexpansion. Treatment involves empirical antibiotictherapy as previously described until the patientcan be definitively treated.

Diseases of the Structures That Support theTeethThe periodontal complex (Figure 6) consists of thegingiva; cementum (an acellular, bone-like hardtissue that covers the tooth root); the periodontalligament (a vascular connective tissue that envelopsthe tooth and connects it to the jaws,13 forming ahammock-like structure); and the alveolar bone. Inthe periodontally healthy adult, the masticatorymucosa covers the alveolar bone and the tooth rootjust coronal to the cementoenamel junction.

Periodontitis refers to a complex process involv-ing the periodontal supporting structures and re-sults from breakdown of the connective tissue andthe supporting alveolar bone in response to inflam-mation after bacterial colonization. Gram-negativebacteria such as actinobacillus actinomycetemcomitans,porphyromonas gingivalis, and spirochetes14 are themost common microbial agents implicated in peri-odontitis. Within the adherent plaque, these bac-

Figure 6. Pictorial representation of the componentsof a normal periodontium with healthy tissues.(Diagram courtesy of Chris Jung.)


teria stimulate the production of inflammatory cellmediators (including interleukins, tumor necrosisfactor �, prostaglandin E2 and matrix metallopro-teinases), which in turn reduce the production ofnew collagen fibers resulting in tissue destruc-tion.15 Although the host inflammatory response tosuperficial bacterial colonization (“plaque”) is anessential component to the development of peri-odontal disease, this response is modified by bothlocal and systemic factors. Local etiologic factorsinclude calculus (calcified plaque deposits along theroots of teeth), deep gingival pockets around theteeth that make removal of bacterial deposits by thepatient through routine home care more difficult,less than ideal spacing between teeth, xerostomia,and trauma from occlusion. Systemic factors thatmay predispose an individual to periodontal break-down include congenital conditions such as Downsyndrome and Papillon-Lefevre syndrome16,17 andacquired conditions such as diabetes.14 Althoughdefinitive evidence is lacking at this point, there isa growing body of research that suggests that thepresence of chronic inflammation from periodontaldisease may exacerbate the progression of systemicconditions such as diabetes18 and cardiovasculardisease19,20 and may be associated with an increasedrisk of preterm labor.21,22

From the aspect of patient management, early-stage periodontitis is a chronic condition that usu-ally presents with few overt visual signs of diseaseactivity other than increased bleeding when brush-ing. It often involves only a few teeth at a time. Bythe time the degree of attachment loss has pro-

gressed to the point of tooth mobility, the pros-pects of a favorable outcome (ie, long-term toothpreservation) are guarded.

As periodontal disease progresses, the loss ofsupporting tissues between the tooth root and al-veolar bone leads to the creation of defects knownas periodontal pockets (Figure 7). Proliferation ofmixed anaerobic bacteria within a periodontalpocket may lead to a localized purulent inflamma-tion termed a periodontal abscess, which is character-ized by suppuration from the periodontal pocketaccompanied by pain, tenderness, swelling, andtooth mobility (Figure 8). Periodontal abscesses aretypically noted in otherwise healthy patients withuntreated periodontal disease.23 Patients with a re-duced ability to combat infection as a result ofunderlying systemic diseases such as diabetes are ata higher risk of developing periodontal abscesses.Periodontal abscesses can also result from the in-troduction of a foreign body into the periodontalpocket (eg, a popcorn husk) or from mechanicalinjury to the periodontal lining after routine dentalscaling.

Clinically, the differential diagnosis of a local-ized abscess involving a single tooth also includesthe acute apical abscess from a necrotic tooth (seeabove for details). Periodontal abscesses typicallyare characterized by mild to moderate pain,whereas abscesses of pulpal origin are associatedwith a greater degree of pain. Reaching a definitivediagnosis is not easily accomplished in a familyphysician’s office. A definitive diagnosis is accom-plished by demonstrating suppuration from theperiodontal pocket in the presence of a vital tooth.Initial management of a periodontal abscess will

Figure 7. Schematic representation of periodontaldisease showing tissue destruction and alveolar boneloss. (Diagram courtesy of Chris Jung.)

Figure 8. Periodontal abscesses involving 2neighboring teeth, resulting in draining fistuloustracts.


depend on the severity of the infection and involvesboth pain management and local intervention rang-ing from incision and drainage to extraction of thetooth. Systemic antibiotics are reserved for rarecases involving cellulitis and systemic symptoms.Definitive management requires referral to a den-tist for treatment of the underlying periodontaldisease, which typically involves the mechanical re-moval of calcified deposits (calculus) through pro-cesses known as scaling and root planing, and, incertain cases, systemic or locally applied antibiotics.

Necrotizing ulcerative gingivitis, also known as“trench mouth,” is an acute inflammatory condi-tion of the gums caused by anaerobic bacteria (pri-marily treponema, selenomonas, fusobacterium,and prevotella intermedia). This condition typicallypresents in young adults under stress in whom hostdefenses are compromised by poor nutrition andpoor oral hygiene. Clinically, the gingival tissue isdenuded with punched out, crater-like areas of ne-crosis and blunting of the interdental papilla. Thiscondition is accompanied by pain, fetid odor, andsystemic symptoms of fever, malaise, and cervicallymphadenopathy.

Patients should be prescribed penicillin VK 500mg orally every 6 hours for 7 days.24 In patientswith a penicillin allergy, erythromycin 500 mg ormetronidazole 500 mg twice daily for 7 days isrecommended. Home care involves gentle cleans-ing of the involved areas using frequent rinses ofchlorhexidine gluconate and salt water. Referral toa dental practitioner for debridement and definitiveperiodontal therapy is recommended. An exceed-ingly rare but severe presentation of this condition,termed noma (from the Greek numein, meaning “todevour”), in which the area of necrosis extends pastthe gingival margins, may occur in patients withadvanced acquired immune deficiency syndrome orwho are otherwise severely immunocompromisedor malnourished.

Pericoronitis is an acute gingival condition char-acterized by inflammation around the tissue of apartially erupting tooth. This typically occurs inyoung adults. The pathogenesis of this condition isanalogous to the periodontal abscess. Entrapmentof debris between the tissue overlying the partiallyerupted tooth (the operculum) and the tooth per-mits the growth and spread of anaerobic bacteria(Figure 9).25 The inflamed operculum is often sec-ondarily traumatized by the opposing tooth, fur-ther aggravating the situation.

Pericoronitis is accompanied by pain radiatingto the ipsilateral ear and throat. Severe cases maybe accompanied by fever, malaise, lymphadenopa-thy, and trismus. Clinically, a partially eruptedthird molar covered on the distal aspect by ery-thema and inflamed gingiva with associated swell-ing and/or purulence is noted. If untreated, infec-tion can progress to the submandibular andsublingual spaces. If any evidence of airway com-promise is noted, immediate referral for emergencyairway management and drainage are indicated.Fortunately, this outcome is rare.

Management options include surgical removalof the operculum or irrigation with 2% chlorhexi-dine gluconate and debridement of the tissues. Thepatient can also be instructed to irrigate under theoperculum with warm salt water or 0.12% chlo-rhexidine. Antibiotic therapy with penicillin VK isrecommended. Definitive treatment involves re-moval of the partially erupted third molars.

Nonodontogenic Mimickers of Dental PainThe vast majority of symptoms experienced withinthe oral cavity are related to the conditions dis-cussed above (Figure 10). However, the clinicianmust always consider the possibility of pain of non-dental origin when assessing the patient’s chiefcomplaint. The most common cause of referredpain to the posterior maxillary teeth is maxillarysinusitis. Typically, the pain is of mild to moderateintensity, and usually involves 2 to 3 posterior max-

Figure 9. Early pericoronitis associated with partiallyerupted third molar. Note the soft tissue coverage overthe distal portion of the third molar (operculum). Inthis case, the gingiva was slightly erythematous. Noassociated swelling was noted, however, purulentexudate was expressible from the pocket. Also note thecaries on the partially erupted third molar.(Photograph courtesy of Dr. Pilar Hita-Iglesias.)


illary molar teeth. The patient will report increasedpain when bending over or if asked to firmly pressdown on their feet. Other common conditions thatmay present as oral pain that can be mistaken forpain of dental origin include temporomandibularjoint disorders and aphthous ulcers. Rare mimick-ers of dental pain include referred myocardial pain,atypical facial pain syndromes, and maxillary sinusmalignancies.

Dental TraumaDental trauma is extremely common, with an esti-mated 10% to 16% of children exhibiting evidenceof damage to the permanent incisor teeth by age15.26 Dental trauma is particularly common in the6- to 12-year-old age group. Depending on theangle and the magnitude of force, trauma mayresult in injuries ranging from fracture of the crownto concussive, intrusive-, or extrusive-type injuriesto the tooth to outright fractures of the alveolarprocess or the jaws. Fortunately, the root is sup-ported by a fibrous periodontal ligament, renderingit able to absorb mild to moderate forces. This mayin part account for the observation that the mostcommon permanent injury among teeth subjectedto trauma is the fracture of an incisal portion of thecrown.26

Although all types of injury to the maxillofacialcomplex require prompt evaluation by a dentist, itis essential that all patients with avulsive injuries ofpermanent teeth be treated immediately. Studieshave shown that if the tooth is reimplanted within

60 minutes, the success rate of reimplantation isdramatically improved.27 The ideal situation is ifthe patient or a caregiver can reimplant the tooth atthe time of injury, providing the tooth or sockethave not been visibly soiled. If not, the goal ofmanaging such a scenario is to keep the cells of theperiodontal ligament viable by keeping them moistuntil the tooth can be reimplanted. The ideal stor-age/transport medium is Hanks balanced salt solu-tion, which is available commercially in a kit formas “Save-A-Tooth” (Phoenix-Lazerus, Inc., Potts-town, PA). Other good options include placing thetooth in milk or having the patient keep the toothin the mouth, positioned against the cheek. Storagein plain water or saline is to be avoided, although itis still preferable to desiccation. When the patientarrives at the practitioner’s office, the tooth shouldbe reimplanted immediately with minimal manip-ulation of the root tissues. If necessary (for exam-ple, if the tooth root was visibly soiled), the toothand socket can be rinsed carefully with a cell-pre-serving media. Once the tooth has been reinserted,the clinician should carefully compress the alveolarbone around the socket with moderate finger pres-sure and arrange for immediate referral to a dentist.Depending on how long the tooth has been out ofthe socket and the degree of closure of the rootapex, the dentist will decide on the need for addi-tional tooth preparation before reimplantation.The dentist will then stabilize the tooth to theneighboring teeth using a bonded splint. The pa-tient should be evaluated for concussive injuries to

Figure 10. Differential diagnosis of common causes of dental pain. Additional clinical information and treatmentrecommendations are provided in the text.

Mild-Moderate Pain Severe Pain

Reversible PulpitisPeriodontal Abscess vs Pericoronitis

Triggered by cold or sugar? Resolves after stimulus removed?

No

Pain to biting or pressure?

Spontaneous?Localized gingival swelling?

Irreversible PulpitisAcute Apical

AbscessAcute

Apical Periodontitis

No Yes

Yes

Swelling?


the brain and fractures of the facial bones and/ormandible. The patient should also be assessed forthe need for tetanus prophylaxis, especially if thevaccination status of the patient is unclear or if thetooth has come into contact with soil.28 The Amer-ican Academy of Endodontics28 recommends thatpatients with a reimplanted tooth be placed ondoxycycline (adult dosage of 100 mg twice a day)for 7 days. As an alternative, if staining of develop-ing teeth is a concern, penicillin VK (adult dosage:1 to 2 g immediately, then 500 mg four times perday) is an option. Based on the “dry time” and thedegree of closure of the root apex, the patient’sdentist will decide whether endodontic therapy isalso required. Primary teeth should not be reim-planted because of the risk of damage to the un-derlying developing permanent tooth. If in doubtas to whether a tooth is a primary tooth (someprimary teeth are typically present up to 12 to 14years of age), the physician should reimplant it ifpossible and arrange for immediate dental assess-ment.

Prevention of Oral DiseasesAs with most conditions, prevention and early rec-ognition/treatment offer the greatest potential toreduce the incidence and severity of dental disease.From the family physician’s vantage point, a num-ber of observations are offered:

● Reduced salivary flow, a common side effect ofmany drugs, is associated with a loss of bufferingactivity and hence an increased risk of caries andmucosal infections. Common xerostomia-induc-ing drugs include anticholinergics, antidepres-sants, antipsychotics, diuretics, antihypertensives,antihistamines, narcotics, and anxiolytics.29 Thisis a significant problem among the older popula-tion, especially in view of the trend toward morepatients keeping their teeth. This should be takeninto account when prescribing for patients in thispopulation, especially when contemplating polyp-harmacy. When the use of alternative drugs is notfeasible, cholinergic agents such as pilocarpine (5mg three times daily) or cevimeline (30 mg threetimes daily) may be considered. A number of com-mercially available saliva substitutes are availableover the counter. Many patients with severe xero-stomia experience relief from carrying a bottle ofwater with them to sip as needed. Home applica-

tion of gels and/or rinses containing fluoride shouldbe considered for patients in this group (please seenumber 6, below). As for all high-risk patients,increased dental vigilance is needed.

● Many orally administered medications containhigh concentrations of sweetening agents tomake them more palatable. In vulnerable pediat-ric populations with underlying chronic condi-tions, prolonged exposure to these agents canresult in a significant increase in caries develop-ment.30

● Because cariogenic oral microflora can be verti-cally transmitted to a child through the mother’ssaliva, management of active caries in women ofchildbearing age, pregnant women, mothers, andcaretakers of young children should be encour-aged.31

● Routine dental examinations and radiographicevaluations of the teeth should be strongly en-couraged because these are crucial to the earlydetection and treatment of carious lesions thatmay not be evident on a clinical examination.

● Management of chronic periodontal infectionwill reduce systemic spread of bacterial endotox-ins and inflammatory mediators, thus potentiallyreducing their negative impact on chronic diseaseconditions.

● The risk of developing caries can be reduced byoral hygiene practices such as brushing and floss-ing, which reduce the tooth surface biofilm, anddietary counseling to reduce the frequency ofsugar consumption. In patients unable to flosseffectively, one short-term study demonstratedthat daily oral irrigation with a dental water jetcombined with brushing may be as effective asbrushing and flossing at reducing gingival bleed-ing, inflammation, and plaque accumulation.32

Exposure of enamel to trace quantities of fluorideion (�1 ppm) results in the formation of fluori-dated hydroxyapatite crystals that demonstrateincreased resistance to acid dissolution. Theoverall magnitude of caries reduction averages25%, whether delivered professionally, self-ad-ministered through toothpaste, or by communitywater fluoridation.1 Fluoride brush-on gels witha neutral pH (eg, Prevident 1.1% brush-on gel,Colgate Professional) are preferred over acidu-lated gels for daily, at-home therapy. Weekly useof a 0.2% neutral sodium fluoride gel should alsobe considered for use by high-risk individuals.


● Pit and fissure sealants (resinous material that isplaced into the deep crevices on the biting sur-faces of the molar teeth without the need fordrilling, creating a barrier to the entry of bacte-ria) are effective at preventing caries on thesetooth surfaces, especially in patients at a high riskfor caries. This caries protection ranges fromclose to 100% protection in ideal situations, inwhich long-term retention of the sealant is main-tained with periodic re-examination and reappli-cation where needed,33 to 75% in “real world”situations.34 Because close to 90% of all cavitiesinvolving the permanent teeth of school-age chil-dren occur on the occlusal surfaces of the molars,the application of sealants can play a significantrole in reducing the caries rate, especially amongchildren with a history of high caries rate in theprimary dentition. Therefore, parents of childrenwith newly erupting molar teeth (approximately6 to 7 and 11 to 12 years of age) should beencouraged to visit their primary dental care pro-vider for assessment of whether sealants are in-dicated.

● The lifetime direct financial cost for treatment ofa single tooth lost to trauma as a child or teenagereasily runs into the $10,000� range. The use ofcustom mouth guards should be encouraged forall patients performing any type of physical ac-tivity in which accidental trauma to the jaws is apossibility. This includes not just high-impactsports such as boxing, hockey, and football, butalso physical sports such as soccer, baseball, andbasketball that traditionally are viewed as beingless aggressive. A recent meta-analysis concludedthat wearing a mouthguard during sports-relatedactivities reduced the risk of an orofacial injuryby 1.6 to 1.9 times.35 However, the evidence as towhether mouthguards protect against concussiveinjuries was inconclusive. Although not as effec-tive and not as comfortable to wear as custommouth guards, over-the-counter products are anacceptable, lower-cost alternative.

References1. Griffin SO, Regnier E, Griffin PM, Huntley V. Ef-

fectiveness of fluoride in preventing caries in adults.J Dent Res 2007;86:410–5.

2. Shaner JW, Kimmes N, Saini T, Edwards PC. Methmouth: rampant caries in methamphetamine abusers.AIDS Patient Care STDS 2006;20:4–8.

3. Loesche WJ. Role of Streptococcus mutans in humandental decay. Microbiol Rev 1986;50:353–80.

4. Selwitz RH, Ismail AI, Pitts NB. Dental caries. Lan-cet 2007;369:51–9.

5. Nagle D, Reader A, Beck M, Weaver J. Effect ofsystemic penicillin on pain in untreated irreversiblepulpitis. Oral Surg Oral Med Oral Pathol Oral Ra-diol Endod 2000;90:636–40.

6. Keenan JV, Farman AG, Fedorowicz Z, Newton JT.A Cochrane systematic review finds no evidence tosupport the use of antibiotics for pain relief in irre-versible pulpitis. J Endod 2006;32:87–92.

7. Sweeney LC, Dave J, Chambers PA, Heritage J.Antibiotic resistance in general dental practice: acause for concern? J Antimicrob Chemother 2004;53:567–76.

8. Warnke PH, Becker ST, Springer IN, et al. Penicil-lin compared with other advanced broad spectrumantibiotics regarding antibacterial activity againstoral pathogens isolated from odontogenic abscesses.J Craniomaxillofac Surg 2008;36:462–7.

9. Ellison SJ. The role of phenoxymethylpenicillin,amoxicillin, metronidazole and clindamycin in themanagement of acute dentoalveolar abscesses: a re-view. Br Dent J 2009;206:357–62.

10. Otto M. Boy’s death fuels drives to fund dental aid topoor. Washington Post. March 3, 2007;B01.

11. Caliskan MK. Prognosis of large cyst-like periapicallesions following nonsurgical root canal treatment: aclinical review. Int Endod J 2004;37:408–16.

12. Whitlock RI, Jones JH. Squamous cell carcinoma ofthe jaw arising in a simple cyst. Oral Surg Oral MedOral Pathol 1967;24:530–6.

13. McCulloch CA, Lekie P, Mc Kee MD. Role ofphysical forces in regulating the form and function ofthe periodontal ligament. Periodontol 2000 2000;24:56–72.

14. Consensus report. Periodontal diseases: pathogene-sis and microbial factors. Ann Periodontol 1996;1:926–32.

15. Page RC. The pathobiology of periodontal diseasesmay affect systemic diseases; inversion of a paradigm.Ann Periodontol 1998;3:108–20.

16. Kinane DF. Blood and lymphoreticular disorders.Periodontol 2000 1999;21:84–93.

17. Kinane DF. Periodontitis modified by systemic fac-tors. Ann Periodontol 1999;4:54–64.

18. Taylor GW, Borgnakke WS. Periodontal diseaseassociation with diabetes, glycemic control and com-plications. Oral Dis 2008;14:204–5.

19. Beck J, Eke P, Heiss G, et al. Periodontal disease andcoronary heart disease: a reappraisal of the exposure.Circulation 2005;112:19–24.

20. Beck J, Garcia R, Heiss G, Vokonas PS, OffenbacherS. Periodontal disease and cardiovascular disease. JPeriodont 1996;67:1123–37.

21. Bobetsis YA, Barros SP, Offenbacher S. Exploringthe relationship between periodontal disease and


pregnancy complications. J Am Dent Assoc 2006;137(Suppl):7S–13S.

22. Scannapieco FA, Bush RB, Paju S. Periodontal dis-ease as a risk factor for adverse pregnancy outcomes.A systematic review. Ann Periodontol 2003;8:70–8.

23. Herrera D, Roldan S, Mariano S. The periodontalabscess; a review. J Clin Periodontol 2000;27:377–86.

24. Wade AB, Blake GC, Mirza KB. Effectiveness ofmetronidazole in treating the acute phase of ulcer-ative gingivitis. Dent Pract 1966;16:440–4.

25. Maloney J, Stassen LF. The relationship betweenpericoronitis, wisdom teeth, putative periodontalpathogens and the host response. J Am Dent Assoc2008;54:134–7.

26. Chadwick BL, White DA, Morris AJ, Pitts NB.Non-carious tooth conditions in children in the UK,2003. Br Dent J 2006;200:379–84.

27. Blomlof L, Andersson L, Lindskog S, HedstromKG, Hammarstrom L. Periodontal healing of re-planted monkey teeth prevented from drying. ActaOdontol Scand 1983;41:117–23.

28. American Association of Endodontists. Recom-mended guidelines of the American Association ofEndodontists for the treatment of traumatic dentalinjuries. Chicago, IL: American Association of End-odontists; 2003.

29. Moore PA, Guggenheimer J. Medication-inducedhyposalivation: etiology, diagnosis, and treatment.Compend Contin Educ Dent 2008:29:50–5.

30. Bigeard L. The role of medication and sugars inpediatric dental populations. Dent Clin North Am2000:44;443–56.

31. Napimoga MH, Hofling JF, Klein MI, Kamiya RU,Goncalves RB. Transmission, diversity and virulencefactors of Streptococcus mutans genotypes. J Oral Sci2005;47:59–64.

32. Barnes CM, Russell CM, Reinhart RA, Payne JB,Lyle DM. Comparison of irrigation to floss as anadjunct to toothbrushing: effect on bleeding, gingi-vitis, and supragingival plaque. J Clin Dent 2005;16:71–7.

33. Bohannan H. Caries distribution and the case forsealants. J Public Health Dent 1983;33:200–4.

34. Ahovuo-Saloranta A, Hiiri A, Nordblad A, MakelaM, Worthington HV. Pit and fissure sealants forpreventing dental decay in the permanent teeth ofchildren and adolescents. Cochrane Database SystRev 2008;(4):CD001830.

35. Knapik JJ, Marshall SW, Lee RB, et al. Mouthguardsin sport activities: history, physical properties andinjury prevention effectiveness. Sports Med 2007:37;117–44.


Documents

CLINICAL REVIEW Recognition and Management of …jabfm.org/content/23/3/285.full.pdf · Topics reviewed include the sequelae of dental caries, periodontal disease, and trauma. Prevention