Dental plaque, caries and gingivitis

Most dental diseases are associated with microorganisms, infection and the resulting inflammatory response.

Dental plaque

Caries and gingivitis are common dental diseases and are related to the formation of dental plaque. Plaque is a soft nonmineralized deposit consisting of microorganisms in a glycoprotein matrix. It begins as a pellicle of salivary proteins adhering to the enamel surface. Oral microorganisms colonize the pellicle forming the plaque content. The varieties of plaque microorganisms play a key role in the development of dental disease. If plaque is removed or reduced through regular dental hygiene practice, the incidence of dental caries, gingivitis and periodontitis is significantly reduced. Plaque that has become mineralized is called dental calculus (tartar).

Dental caries

Dental caries or decay is probably the most universal and common of all reported dental diseases. Caries development is a time-dependent event involving a critical relationship between the host, plaque microorganisms, metabolic acid production and diet. Streptococcus mutans is generally regarded as the most cariogenic microorganism, but Lactobacillus species are also implicated in some types of carious lesion. Acid production associated with a combination of cariogenic microorganisms and a cariogenic diet including sucrose or other rapidly digestible carbohydrates furthers the progression of demineralization and the development of carious lesions. Factors that reduce saliva production can also contribute to the development of dental caries. Once caries reaches the dentinal tissues, it progresses in a more diffuse pattern.

Gingivitis (inflammation of the gingiva)

Gingivitis describes the inflammatory reaction of the gingival mucosa in close proximity to the teeth to a variety of etiologic agents including plaque microorganisms.

• •
  

  Plaque-associated gingivitis is common, particularly in people with poor oral hygiene. It is usually asymptomatic except for localized bleeding during brushing. If plaque and calculus deposits expand into the gingival crevice, the nature of the microorganisms changes to an anaerobe-dominated bacterial population and leads to more serious infections of the periodontium.

  
  
• •
  

  Acute necrotizing ulcerative gingivitis (ANUG) is an acute painful form of gingival infection associated with fusiform and spirochete organisms, with a clinical presentation very different from that of the inflammatory gingivitis of plaque. Ulcerated and highly inflamed gingival tissues are typically observed. Fever and lymphadenopathy may also be part of the acute presentation.

Management

Dental plaque, caries and gingivitis are three distinct presentations of dental disease but are uniquely linked as a focus for preventive dental medicine.

Removal of plaque and calculus (oral prophylaxis and scaling) from tooth surfaces is a major part of the overall preventive program.

Over-the-counter (OTC) mouth rinses have limited benefits in controlling plaque and calculus. Chlorhexidine gluconate oral rinse reduces plaque bacteria and gingivitis with twice daily use but must be used in conjunction with appropriate dental treatment. Its use in other oral mucosal diseases is discussed later. Dentifrices containing other antibacterial agents, including triclosan and fluoride, are also promoted for plaque control. Calculus-control toothpastes containing pyrophosphate or zinc salts are designed to prevent supragingival calculus formation and do not affect existing calculus.

Chlorhexidine gluconate is a biguanide, cationic agent with antibacterial action. The cationic portion of the molecule binds to negatively charged bacterial cell components altering cell osmotic dynamics with leakage of cellular ions. In higher concentrations, chlorhexidine is bactericidal as it causes precipitation of cellular contents. The spectrum of activity of chlorhexidine includes many Gram-positive and Gram-negative microorganisms which have been implicated in dental disease. Examples are S. mutans, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus and Campylobacter rectus . Chlorhexidine is indicated for use as adjunctive treatment to prophylaxis and scalding to reduce plaque formation and for control of gingivitis. It is administered as an oral rinse (0.12%–0.2%). Twice daily rinses (15 mL for 30 seconds and expectorated) are initiated after prophylaxis and scaling for use between dental appointments. Up to 30% of chlorhexidine is retained in the oral cavity after rinsing and is slowly released over 12 hours. The sustained action is believed to be related to binding to oral tissues, namely the hydroxyapatite of tooth enamel, the pellicle, the oral mucosa and salivary proteins. Rinsing with water, eating or drinking must be avoided for at least 30 minutes after use. Because chlorhexidine is used topically, systemic side effects are rarely noted as limited amounts will be swallowed. Repeated use of chlorhexidine rinses is associated with discoloration of teeth and alteration of taste in some patients. The discoloration is superficial and easily removed by professional tooth polishing. Chlorhexidine is contraindicated in patients with a positive history of hypersensitivity to the drug.

Treatment and prevention of dental caries includes plaque control and the use of systemic and/or topical fluorides.

Fluoride in the water supply and in a multitude of dental products has significantly reduced the incidence of dental caries in children in developed countries, but dental caries in areas where fluoride is not available remains a major dental concern. Treatment and prevention of dental caries includes removal of all carious lesions, oral hygiene to reduce dental plaque, dental sealants to cover pits and fissures in the tooth structure, cariogenic diet control and the use of systemic or topical fluorides.

The beneficial effect of fluoride in caries prevention was initially recognized in the 1930s. In many countries, multiple fluoride preparations are available for systemic or topical application to prevent dental caries. Maximum benefits accrue when fluoride use is coupled with a program of regular preventive dental care. Other uses of fluoride include a reduction in tooth sensitivity due to exposed dentinal or cemental surfaces, remineralization of incipient carious lesions, and some reduction in gingivitis. Fluoride interacts with the hydroxyapatite of enamel to produce fluorohydroxyapatite. This latter compound is less soluble in acids originating from sugar metabolism by plaque bacteria. Fluoride has also been shown to decrease the population of S. mutans and to interfere with metabolism in plaque bacteria. Fluoride can be administered as fluoride rinses, dentifrices, gels and stannous fluoride solutions, all of which are intended for topical application. Sodium fluoride tablets are also available to supplement systemic fluoride ingestion in the presence of inadequate fluoridated water supplies. Fluoride is absorbed rapidly (80%–90%) from the upper gastrointestinal (GI) tract with peak blood levels occurring in approximately 30 minutes. Fluoride is widely distributed to calcified tissues, bone and teeth, with up to 50% of the daily intake deposited in calcified tissues. Renal clearance accounts for most of the excreted dose. Systemic fluorides are generally administered with water or juice as dairy products substantially reduce fluoride absorption. Systemic fluoride should not be prescribed when the water content of fluoride exceeds 0.6 ppm. Daily sodium fluoride doses, which vary among countries, are regularly published by various dental organizations. Fluoride supplementation must take into account the total daily amount of naturally ingested fluoride from all sources, the climate (in hot climates more water is consumed) and the patient’s age, weight and physical status. Adverse effects of supplemental systemic or topical fluorides are usually limited to GI complaints and occur infrequently. However, the use of prescribed fluorides and topical home fluoride products in very young children should be supervised to avoid excessive ingestion. Side effects include nausea with or without vomiting, excessive salivation and abdominal pain. Severe toxicity, requiring medical attention, may occur with accidental ingestion of larger amounts (10–20 mg in children). Chronic ingestion of excessive fluoride can lead to the development of dental fluorosis, an unsightly staining of the teeth.

Acute dental pain

Pain as a general topic and the principles of its treatment are covered in detail in Chapter 13 . Acute pain associated with dental disease is probably the most common complaint of dental patients. Any injury to the oral tissues leads to the release of inflammatory mediators and sensitization of trigeminal afferent nerve endings by prostaglandins and bradykinin. Acute oral pain is also a symptom of many orofacial diseases including acute infection, mucosal lesions, obstructed salivary gland ducts and tissue trauma. Early carious lesions are often associated with acute transient pain that is readily alleviated by dental treatment. However, untreated carious lesions can lead to destruction of tooth structure, allowing oral microorganisms to invade pulpal tissues. Pulpal infection leads to the development of painful inflammation or to an acute periapical abscess and persistent pain. If left untreated this infection can rapidly extend from the alveolar bone into adjacent soft tissues resulting in a cellulitis. Determining the aetiology of dental pain is sometimes complicated because pain can be referred from other tissues such as the sinuses and the ears, and from the temporomandibular joint.

Management of dental pain

Management of acute orofacial pain begins with diagnosis and appropriate dental treatment. Systemically administered drugs, or local anaesthetic drugs, either alone or in combination, are most frequently used for controlling acute orofacial pain, especially before and immediately after definitive dental treatment. Opioids with a favourable oral-to-parenteral effectiveness ratio are preferred, as is the oral route of administration. Acute orofacial pain of moderate intensity or greater can be effectively managed with opioid drugs. Opioids act centrally to modify pain perception by interacting with multiple opiate receptors and mimicking endogenous opioid peptides. Sedation and euphoria often accompany opioid analgesia as an added benefit in controlling the emotional component of pain. Opioids are rarely used alone for acute dental pain and are frequently combined with aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen. Detailed discussion of these and related drugs and their use in acute pain syndromes is found in Chapter 13 . Local anaesthetic drugs with or without vasoconstrictors such as adrenaline are essential for the control of pain during dental surgery and treatment. Vasoconstrictive drugs are used in combination with local anaesthetics to prolong the duration of action by dealing absorption of the local anaesthetic drug and to reduce bleeding during soft tissue surgery. Examples of local anaesthetics/vasoconstrictors commonly used in dentistry include the following:

Amide local anaesthetics :

• •
  

  Lidocaine with and without adrenaline

  
  
• •
  

  Mepivacaine with and without levonordefrin

  
  
• •
  

  Prilocaine with and without adrenaline

  
  
• •
  

  Etidocaine with adrenaline

  
  
• •
  

  Bupivacaine with adrenaline

  
  
• •
  

  Articaine with adrenaline

Ester local anaesthetics :

• •
  

  Chloroprocaine with adrenaline

  
  
• •
  

  Tetracaine (topical only)

  
  
• •
  

  Benzocaine (topical only)

An alternative strategy for controlling postoperative dental pain has been advocated using combinations of NSAIDs and long-acting local anaesthetics. Of the latter, both etidocaine and bupivacaine provide analgesia well into the post-treatment period when the anticipated pain response is greatest. A normal dose of an NSAID is taken soon after treatment and before the return of normal oral sensations. This combination of drugs has been shown to reduce the intensity of pain in the immediate post-treatment period and reduce the need for opioid medications.

Chronic orofacial pain

Chronic orofacial pain can arise from:

• •
  

  inflammation or internal derangements of the temporomandibular joint,

  
  
• •
  

  myalgia associated with the oral and facial musculature, or

  
  
• •
  

  lesions in the central nervous system (CNS).

NSAIDs are used for the symptomatic management of pain associated with injury or inflammatory processes and opioids should be limited to longer acting drugs, used only to initiate pain control or completely avoided because of the possibility of dependence, unless the pain is due to oral cancer. Tricyclic antidepressants may be used to alleviate pain and symptoms such as depression and altered sleep patterns. The pain arising from trigeminal neuralgia responds to the anticonvulsant drugs carbamazepine and phenytoin. Centrally acting skeletal muscle relaxants methocarbamol or cyclobenzaprine are sometimes useful if myalgia or muscle spasm is present.

Adverse effects of analgesic drugs

• •
  

  The most common adverse effects of opioids are nausea, sedation and dizziness.

  
  
• •
  

  The most common adverse effect of NSAIDs is gastrointestinal irritation.

  
  
• •
  

  The most common adverse effects of local anaesthetics are usually psychogenic, such as syncope and anxiety, but they can cause arrhythmias if they become systemic.

Anxiety

A visit to the dentist can be an intimidating experience for many patients to the point some actually avoid dental care until the pain demands emergency attention. Dentists have long been portrayed as the harbingers of pain, so reinforcing the patient’s anxiety. In such patients the use of anxiolytic drugs can help.

Acute odontogenic infections

The general principles of treatment of viral and bacterial infections are described in Chapters 29, Chapters 30 , respectively. Dental caries, periodontal disease, acute periapical abscesses, salivary gland infections and many other oral infections are caused by microorganisms that are part of the normal oral flora. Other oral infections are caused by microorganisms introduced into the oral cavity by trauma ( Staphylococcus ) or other means (herpes). Separate microenvironments within the oral cavity account for the growth of aerobic and both facultative and obligate anaerobic microorganisms existing in a commensal relationship. As a result, most odontogenic bacterial infections are caused by a mix of pathogens with significant involvement of both facultative and obligate anaerobes. Aerobic streptococci and, to a lesser extent, staphylococci along with fungi (yeast) are also part of the normal oral flora and are potential pathogens.

Periodontal infections

Periodontitis (infection of the periodontium) can present in several acute or chronic forms and with different etiologies. In adults it is typically chronic with symptoms limited to an erythematous-appearing gingiva that bleeds on probing or brushing. The distinguishing feature of periodontal disease is a continuing infection of the supporting tissues of the teeth, resulting in a progressive loss of gingival attachment and alveolar bone. It is the most common cause of tooth loss in adult patients. Periodontitis often goes undetected until the patient presents bleeding gums or blood on the toothbrush, in which case the patient should be referred for dental evaluation. In the younger age group it can present as a juvenile periodontitis.

Prophylactic use of anti-infective drugs in dentistry

The prophylactic use of antibiotics in dentistry is not generally required for routine dental treatment in patients without risk factors and with a normally functioning immune system. However, selected patients with pre-existing myocardial or valvular pathology may be at risk for endocarditis secondary to a bacteraemia. Certain dental procedures, including extractions, oral and maxillofacial surgery, periodontal therapy, deep scaling and other dental procedures are associated with a transient bacteraemia that usually lasts less than 15–20 minutes. Selected oral microorganisms have been implicated as a cause of infective endocarditis in patients at risk. Advisory groups throughout the world have established guidelines for antibiotic prophylaxis for patients at risk. Amoxicillin, penicillin V potassium or another suitable alternative drug (clindamycin, a macrolide or cephalosporin) is usually recommended for prophylactic use immediately prior to the dental procedure.

There is considerable debate about the risk and benefits and drug choice for patients with joint prostheses; however, prophylaxis may be considered for patients with a compromised immune system. Recommended guidelines cannot address every patient situation, and consultation between the physician and dentist is advised. At-risk patients with poor oral hygiene, extensive caries, gingivitis or periodontitis should be placed on a dental treatment program that includes elimination and prevention of dental disease.