The hard tissues of the oral cavity include the bones of the maxilla and mandible, hard palate, and teeth (occupying almost 20% of the total surface of the mouth) (Figure 45.1).

The entire oral cavity is lined by a wet mucous membrane consisting of an epithelium and connective tissue named as the lamina propria. Based on the histology of the tissue, the mucosa is divided into three types³:

The tooth proper consists of enamel, dentin, and pulp. Enamel is 96% inorganic composing of hydroxyapatite crystals and is acellular. This nonvital and insensitive tissue cannot be repaired or regenerated but allows ion exchange between the enamel and saliva. Dentin forms the bulk of the tooth and supports the enamel. It is highly mineralized and made up of odontoblasts, harbors open nerve endings, and is capable of regeneration and/or repair (sclerotic or secondary dentin). Pulp is a specialized connective tissue present in a chamber underlying the dentin. It consists of collagen, noncollagenous protein, glycoproteins, enzymes, growth factors, and phospholipids.

The other supporting structures of the tooth include alveolar bone, periodontal ligament, and the cementum. Cementum covers the root dentin, and periodontal ligament fibers help anchor the tooth to the alveolar bone of maxilla and mandible.

The different habitats in human oral cavity, hard and soft tissues shedding, and nonshedding surfaces can harbor over 600 known diverse bacterial species.⁴ Despite the anatomical complexity and diversity of oral microorganisms, the oral cavity’s innate immune response helps maintain the integrity of oral epithelium.⁵ The various innate immune factors present include the following:

Salivary immunoglobulin IgA aggregates oral cariogenic bacteria like Streptococcus mutans and prevents its attachment on the tooth surface. Constituents like bicarbonates, phosphates, and urea help maintain the pH of the oral cavity, whereas calcium, phosphate, and various proteins can modulate demineralization and remineralization of enamel.

In the human body, the oral cavity and the gastrointestinal tract are the only two dynamic microenvironments, where the attachment of microflora is site specific and the bacterial load changes over time depending on the time of the day, diet intake, and overall health status. Microorganisms from the oral cavity have been shown to cause a number of oral infectious diseases, including caries (tooth decay), periodontitis (gum disease), endodontic (root canal) infections, alveolar osteitis (dry socket), and tonsillitis. Moreover, when oral bacteria enters systemic circulation, they can cause conditions like cardiovascular disease,¹⁹ stroke,²⁰ preterm low-birth-weight babies,²¹ diabetes,²² and pneumonia.⁴

At birth, a neonate’s oral cavity is exposed to diverse microorganisms of the outside world and the establishment of the oral microflora begins. The initial microbial colonization depends on the type of delivery (vaginal or cesarean), diet (breastfed or formula-fed), and contact with parents and medical staff. Within the first 24 hours, gram-positive cocci such as Streptococcus and Staphylococcus species are the most common organisms. As the first tooth (lower central incisors at the age of 6-9 months) erupts in the oral cavity, the cariogenic bacteria S mutans is found to have the greatest affinity to the nonshedding tooth surface and fights for a niche on the tooth.²³ The diversity of bacteria and their interdependencies for nutrition and niche leads to a complex consortium of microorganisms known as a biofilm. The biofilm continues to grow and harbor organisms like streptococci, Actinomyces, Haemophilus, Neisseria, Fusobacterium, and Prevotella. Children’s oral microbiota can vary throughout the development of teeth, mixed or permanent dentition, diet and lifestyle changes, and hormonal changes associated with growth and puberty. The progression and maturation of biofilms can continue until adulthood. Different bacterial species within the biofilm interact by various cell signaling mechanisms and contribute to ecologic stability by differentiation and maturation of the host mucosa and immune system. Normal resident microflora can keep pathogenic bacteria out by maintaining basic pH around the tooth surface, thereby preventing the invasion and growth of pathogens. Saliva and GCF provide nutrients (salivary amylase breaks down starch) for microbial growth and also contain (lactoferrin, lactoperoxidase, mucins, cystatins, etc) antimicrobial activities, thereby stabilizing the microbial community.

Tooth surface is never dry (in physiologic conditions) and gets covered by a thin proteinaceous layer called the acquired enamel pellicle (AEP).²⁴ This 100 to 1000 nm thick film is attached to the enamel surface due to selective physical forces and plays an important role in determining the fate of an oral microbiome.²⁵ Selective oral streptococci have the ability to attach to this pellicle as initial colonizers and occupy sites at the tooth surface and selective oral sites such as the tongue and buccal epithelium.²⁶ Once established, these colonizers provide attachment sites for secondary and tertiary colonizers leading to a complex ecosystem of symbiotic microbial communities—the dental biofilm known as “plaque.” The communities stabilize and live with a simple cross-feeding model in harmony with the host until the balance is tipped offleading to dysbiosis. The modifiable factor of dysbiosis can range from being a change in the salivary flow, lifestyle changes (like inclusion of more sugar in the diet), poor oral hygiene, or an underlying disease. Dysbiosis leads to a shift in the microflora, such as from aerobic to anaerobic and aciduric bacteria. The predominance of aciduric bacteria around the tooth surface causes the dissolution of mineral salts from enamel leading to one of the most common dental diseases of the world—dental caries. Based on the location and depth of lesion, the dental caries can be on the enamel, root, or reach deep into the pulp. Enamel and dentin caries is caused by S mutans and Lactobacillus species. Initial enamel caries is referred to as “white spot lesions” and can be reversed if the bacterial growth is arrested and symbiosis of oral microorganisms is achieved. But if the carious lesion reaches deeper tissues, it can even lead to irreversible pulpitis rendering the tooth nonvital. Because bacteria are site specific, certain bacteria like Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia, etc, can target the supporting structures of the tooth leading to periodontitis and gingivitis.²⁷ Periodontal disease is a chronic bacterial infection characterized by persistent inflammation, connective tissue breakdown, and alveolar bone destruction. With advancing gingivitis and periodontitis, Actinomyces and other anaerobic species can
gain entry to the exposed root surfaces causing root caries. As long as bacteria are present on the hard tissue and do not enter the systemic circulation, the best mode of treatment is to excavate the carious lesion with a suitable dental bur and restore the structure and function of the tooth by restorations like the use of an amalgam or composite. In cases of extensive decay extending to the pulp, root canal treatment or extraction is required.

In cases of gingivitis and periodontitis, excessive microbial load and the oral epithelium’s innate immune responses can lead to inflammation and tissue breakdown. Hence, supragingival and subgingival debridement of the tissue (such as scaling and root planing) targeted toward the reduction of plaque and microflora can help revert disease states to health. Untreated pulpal or periodontal pathology may progress to the neighboring soft tissues, causing cellulitis and osteomyelitis if bone is infected. The host’s local defense factors, regional anatomy, microbial load, and bacterial virulence will determine the extent of the damage. Because dental diseases are multifactorial, the presence of bacteria and the host tissue response along with predisposing factors like immunocompromised state, malnutrition, smoking, and poor oral hygiene can lead to severe destructive orofacial lesions like cancrum oris. Figure 45.2 shows the progression of bacterial infections in the mouth.

For dental-related infections, the advantage of reducing microbial load by caries excavation and scaling and root planing should be utilized before resorting to antibiotics. In today’s era of increased antibiotic resistance and improved culture sensitivity testing, the identification of the associated bacteria is of utmost importance. Dentist should be encouraged to prescribe antibiotics only if necessary. Patient compliance, nutrition support, and medical care including analgesics, antipyretics, and anti-inflammatory drugs constitute the proper management of every infection.

The overall goal of managing bacterial infections is to reduce the microbial burden and eliminate the modifying factors that lead to the dysbiosis of oral microflora.
Depending on the severity of infection and presence of local factors, the treatment will range from a minor change in brushing habits or type of brush/toothpaste to mechanical debridement of factors by a dental professional. Figure 45.3 shows an example of pre- and postscaling leading to reduction in the local factors and inflammation. Table 45.1 summarizes the various treatment options for common bacterial infections of the oral cavity.

Oral health can be maintained at home with mechanical and chemical methods, lifestyle changes (if need be), and regular visit to the dentist.²⁸ The mechanical methods include tooth brushing and flossing. Some of the various factors affecting mechanical method include the type of brush (manual versus powered; soft, medium, hard bristled), frequency of brushing, brushing technique, type of toothpaste, and the type of floss.²⁹,³⁰,³¹ Poor patient compliance is a major factor in reducing the effectiveness of mechanical plaque control. Hence, chemical methods, mouthrinses, and chewing gums are based as an adjunct to tooth brushing and flossing. Several clinical studies have been conducted on the efficacy of mouthrinses as an antiplaque agent.³² Based on the studies, an ideal mouthrinse should be tolerated well by the hard and soft tissues (pH regulated) and maintain bacterial homeostasis, thereby reducing dental plaque and caries occurrence. Most of the available mouthrinses contain a biocide, which according to the European commission, is defined as “an active chemical molecule to control the growth of or kill bacteria in a biocidal product.”³³

Biocides range from naturally occurring to synthetic compounds and are used in various personal care products due to their broad-spectrum antimicrobial activity.³⁴ Systemic antibiotics and biocide differ in their mode of action, availability, and susceptibility to resistance. Direct biocide delivery and availability in the form of mountrinses, skin ointments, gels, etc, will limit systemic side effects, if any, and their multiple target sites on microorganisms make them less susceptible to the development of resistance.³⁵ Moreover, higher concentrations of biocides than that required to inhibit microorganisms also contribute to their effectiveness, lack of resistance development, and concerns on the development of opportunistic flora.Combination of biocides in oral health care have been shown to reduce certain adverse effects like staining or irritation while maintaining the positive effect of antibacterial properties intact. For instance, a combination of chlorhexidine (CHX) + hydrogen peroxide (H₂O₂) is superior to CHX alone, and it minimizes extrinsic tooth discoloration (especially in pits and fissures) without affecting the plaque-inhibiting efficacy of CHX. Other examples include the use of 5% to 10% of polyvinylpyrrolidone (PVP) with 0.06% CHX (for slow release overtime) to reduce the staining of tongue and teeth compared to when 0.06% CHX is used alone³⁶ and a combination of CHX and sodium hypochlorite (NaOCl) has been suggested to demonstrate enhanced antibacterial activity.³⁷

More recent advances have been made in the field of dental materials where antimicrobial agents are added to the increase the longevity of the restoration and help reduce the microbial load. Most of the studies indicate antimicrobial effect in laboratory studies, and more evidence is required clinically.³⁸ But meta-analysis of a 6-month clinical trial on mouthrinses with CHX, essential oils, or cetylpyridinium chloride (CPC) concluded that essential oils and CHX are superior to CPC in their antiplaque and anti-gingivitis potential.³⁸ Their effects are maximized when used as an adjunctive therapy with toothbrushing.³⁹,⁴⁰ Multiple clinical studies ranging from a period of 6 months to 3 years show the antiplaque and antigingivitis effect of biocides used worldwide.