Oral Microbiology MCQ

Oral microbiology is the most directly dental of the basic sciences, because the two diseases dentists treat most, caries and periodontitis, are biofilm infections of the mouth's own resident flora. The key idea is ecological: the mouth carries a stable normal flora organized as dental plaque, and disease is usually a shift in that ecosystem rather than infection by an outside germ. Acidogenic species drive caries, a shift toward Gram-negative anaerobes drives periodontitis, a fusospirochetal overgrowth drives ANUG, and opportunistic Candida drives oral thrush. Because these are biofilm diseases, the foundation of treatment is mechanical disruption of the biofilm, not antibiotics.

Normal Flora and the Dental Biofilm

• The mouth is colonized by a diverse resident flora that, in balance, resists invasion by outside pathogens (colonization resistance). Disease usually reflects a shift within this flora, not a new infection.
• Plaque forms in a sequence: a salivary glycoprotein film (the acquired pellicle) coats the clean tooth within minutes, then pioneer streptococci adhere, and over days the community matures and diversifies.
• As plaque thickens, the deeper layers become anaerobic, so early Gram-positive, oxygen-tolerant colonizers give way to later Gram-negative anaerobes, especially below the gumline.
• Dental plaque is a biofilm: bacteria embedded in a self-made matrix of extracellular polysaccharide. The matrix and community structure make biofilm bacteria far more resistant to antimicrobials and host defenses than free-floating cells.

The Microbiology of Caries

• Streptococcus mutans is the principal initiator of enamel caries. It is acidogenic (makes acid from dietary sugar) and aciduric (keeps working in the acid it creates), so it both lowers and tolerates a low pH.
• S. mutans uses the enzyme glucosyltransferase to turn dietary sucrose into sticky glucans, which help the biofilm adhere firmly to enamel.
• Frequent sugar lowers plaque pH below the critical level near 5.5 and selects for acid-loving species, an ecological shift; lactobacilli are associated with the progression of established, deeper lesions.
• Root surface caries (exposed cementum and dentin in older adults) involves Actinomyces and other species and demineralizes at a higher, less acidic pH (near 6.0 to 6.7) than enamel, because root surface mineral is more soluble.

The Microbiology of Periodontal Disease

• In health, the subgingival flora is mostly Gram-positive and aerobic or facultative. Periodontitis reflects a shift (dysbiosis) toward Gram-negative, anaerobic, and motile species in the subgingival pocket.
• The red complex (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola) is strongly associated with chronic periodontitis; these are Gram-negative anaerobes that thrive in the deep pocket.
• Aggressive (including localized molar-incisor) periodontitis in younger patients is associated with Aggregatibacter actinomycetemcomitans, which produces a leukotoxin that kills neutrophils.
• The pocket is a low-oxygen, protein-rich niche, which is why anaerobic putrefaction there also generates the volatile sulfur compounds responsible for much oral malodor.

ANUG and the Necrotizing Diseases

• Acute necrotizing ulcerative gingivitis (ANUG) is a fusospirochetal overgrowth, driven mainly by Fusobacterium species and oral spirochetes.
• It presents with painful, punched-out (cratered) interdental papillae, a gray pseudomembrane, spontaneous bleeding, and a strong fetid odor.
• The classic predisposing factors are stress, smoking, poor oral hygiene, and immunocompromise (including HIV), which is why ANUG can be a sentinel sign.
• Treatment is gentle debridement, improved hygiene, and addressing the risk factors; metronidazole is added when there is systemic involvement.

Candida and Oral Fungal Infection

• Candida albicans is a normal oral commensal that causes disease only when the ecology or host defense shifts, so candidiasis is an opportunistic infection.
• Pseudomembranous candidiasis (thrush) shows creamy white plaques that wipe off to leave a red, sometimes bleeding base, which distinguishes it from non-wipeable white lesions like leukoplakia.
• Common predisposing factors are broad-spectrum antibiotics (which clear competing bacteria), inhaled or systemic corticosteroids, dentures, xerostomia (dry mouth), diabetes, infancy, and immunosuppression.
• Denture stomatitis is Candida-associated palatal erythema under a denture; angular cheilitis (cracking at the lip commissures) is often Candida with or without Staphylococcus aureus.