Micro & Immunology · patient case with 3 questions
Root caries in a dry mouth
Patient: Male, 70 years old
Chief Complaint: “My teeth are decaying at the gumline and my mouth is always dry.”
Background: Takes amlodipine, sertraline and oxybutynin. Generalised gingival recession following treated periodontitis.
Vital Signs: BP 136/80 mmHg · HR 70 bpm
Findings: Multiple soft, leathery lesions on the exposed root surfaces of several teeth. Unstimulated salivary flow is markedly reduced. One molar has long-standing deep occlusal caries; a section of an extracted tooth from the same mouth shows a translucent zone beneath the lesion and dark bands within the dentine.
Question 1
Which organism is most closely associated with ROOT SURFACE caries?
Show answer and explanation
Correct answer: C. Actinomyces viscosus
- A. Prevotella intermedia is likewise a periodontal organism, associated with pregnancy gingivitis and necrotising disease, and is not a caries pathogen.
- B. Porphyromonas gingivalis is a red-complex PERIODONTAL pathogen. It is asaccharolytic and proteolytic, meaning it does not ferment carbohydrate to acid at all, so it cannot drive a carious process. Its presence alongside bone loss is a distractor.
- C. CORRECT. ACTINOMYCES VISCOSUS, with Actinomyces naeslundii, is the organism classically named for ROOT SURFACE caries. These are gram-positive filamentous rods that colonise exposed cementum and dentine. The underlying reason the flora differs is worth knowing: dentine and cementum demineralise at a HIGHER critical pH — about 6.2, against 5.5 for enamel — so a less strongly acidogenic organism is sufficient to initiate a root lesion.
- D. S. mutans is the organism of CORONAL caries INITIATION — acidogenic, aciduric, and able to synthesise extracellular glucans that let it adhere to smooth enamel. It is recovered from root lesions too, but it is not the association the question is testing.
Note: mutans is the key for coronal initiation. Here it is the answer. The triad to memorise: coronal INITIATION → S. mutans; deep lesion PROGRESSION → Lactobacillus; ROOT SURFACE → Actinomyces. Note that this patient's three medications are all xerostomic, which is the actual driver of his risk.
Question 2
Each of the following is a dentine-pulp response to slowly advancing caries EXCEPT one. Which is the EXCEPTION?
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Correct answer: C. A rise in immunoglobulin concentration within the affected dentine
- A. DEAD TRACTS are genuine. They are dentinal tubules whose odontoblast processes have died, leaving them empty and filled with air. They appear BLACK in transmitted light and white in reflected light, and because they remain patent they transmit stimuli readily — which is one reason a tooth can be sensitive out of proportion to the lesion size.
- B. TERTIARY DENTINE is genuine, laid down at the pulpal surface directly beneath the lesion — REACTIONARY dentine by surviving odontoblasts responding to a mild stimulus, REPARATIVE dentine by newly differentiated odontoblast-like cells after a stronger one has killed the originals.
- C. CORRECT as the exception. Salivary immunoglobulin — secretory IgA — is produced by plasma cells in the salivary glands and acts in the SALIVA, agglutinating bacteria in the fluid phase. It is not a dentine response, it does not accumulate within the tooth as the lesion advances, and caries does not cause it to rise in the affected dentine. The other three are all genuine structural responses of the dentine-pulp complex.
- D. SCLEROTIC or TRANSLUCENT dentine is genuine and is the tooth's first line of defence. Peritubular dentine is laid down within the tubule lumen until it occludes, reducing permeability and slowing the ingress of acid and bacteria. Its presence is why a slowly advancing lesion is far less symptomatic than a rapid one.
Note: Picture the zones from the outside inward: necrotic and infected dentine, then demineralised AFFECTED dentine, then the sclerotic (translucent) zone, then dead tracts where processes have died, then tertiary dentine at the pulpal wall. Only AFFECTED dentine remineralises and may be left; INFECTED dentine must be removed. This is the basis of selective caries removal.
Question 3
Which factor does NOT act DIRECTLY on remineralisation of an early enamel lesion?
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Correct answer: D. Salivary immunoglobulin A
- A. Fluoride acts directly in two ways: it drives precipitation of FLUORAPATITE, which is markedly less soluble than hydroxyapatite, and it is incorporated into the remineralising lattice at the crystal surface. It also inhibits bacterial enolase, but the direct mineral effect is the point here.
- B. Saliva is SUPERSATURATED with calcium and phosphate with respect to hydroxyapatite, and those ions are the raw material from which the lesion is rebuilt. Their concentration is a direct determinant of how much remineralisation occurs.
- C. Buffering capacity — principally the bicarbonate system, with phosphate and protein contributing — determines how quickly plaque pH returns above the critical value after an acid challenge, and therefore how much of the day is spent in net remineralisation rather than net demineralisation.
- D. CORRECT as the exception. Secretory IgA acts on the BACTERIA, not on the mineral. It agglutinates organisms and interferes with their adhesion to the acquired pellicle, and the clumped bacteria are then washed from the mouth and swallowed. That reduces the acid challenge, so IgA influences the balance INDIRECTLY — but it contributes no mineral ion and takes no part in the redeposition itself.
Note: The direct-versus-indirect distinction is the specific twist this item adds. Saliva's full protective repertoire: lubrication, clearance, buffering, mineral supply, and an antimicrobial package of lysozyme, lactoferrin, salivary peroxidase, histatins and secretory IgA.