Rampant caries on a full-mouth series

Correct answer: A. High

• A. CORRECT. HIGH risk is defined by ACTIVE DISEASE, not by predicted disease. Any patient with cavitated lesions in the last three years, and particularly one with multiple new lesions, is high risk regardless of the contributing factors. Here the risk indicators stack up: frequent fermentable carbohydrate exposure, inadequate plaque control, six years without professional care, and 14 active lesions.
• B. Low risk means no new lesions in three years, good hygiene, adequate fluoride exposure and low sugar frequency. None applies.
• C. There is no such category. Caries risk is classified low, moderate or high in CAMBRA and in the ADA framework, with an extreme category in some CAMBRA versions reserved for high risk PLUS severe hyposalivation — and salivary flow here is normal.
• D. Moderate risk describes a patient with risk FACTORS but without current active disease, or one lesion in the past three years. Fourteen active lesions puts this well past moderate.

Note: High risk changes management concretely: 5000 ppm prescription fluoride toothpaste, three-month recalls, bitewings every six to twelve months, chlorhexidine or xylitol adjuncts, and dietary counselling focused on FREQUENCY rather than total quantity of sugar.

Correct answer: B. Streptococcus mutans

• A. Porphyromonas gingivalis is a red-complex PERIODONTAL pathogen, an asaccharolytic anaerobe that degrades protein. It has no role in caries.
• B. CORRECT. Streptococcus mutans is the principal INITIATOR of coronal caries. It adheres to the pellicle, synthesises extracellular glucans from sucrose via glucosyltransferase to build the biofilm matrix, is strongly acidogenic, and is ACIDURIC — it keeps producing acid at pH values that suppress competing species.
• C. Actinomyces species, particularly A. viscosus and A. naeslundii, are chiefly implicated in ROOT-SURFACE caries, where cementum and dentine rather than enamel are the substrate.
• D. Lactobacilli are associated with PROGRESSION of established lesions rather than initiation. They are poor adherents to smooth enamel but thrive in the retentive environment of an open cavity, so their counts track lesion activity.

Correct answer: B. Crown lengthening

• A. The tooth is described as restorable. Extraction is premature when a predictable periodontal solution exists.
• B. CORRECT. Restoring into the biologic width — roughly 2 mm of connective tissue attachment plus junctional epithelium above the crest, needing about 3 mm total from crest to margin — produces chronic inflammation, bleeding, unpredictable recession and bone loss. CROWN LENGTHENING, by osseous resection with an apically positioned flap, re-establishes that dimension and gives a supragingival margin with adequate ferrule. Allow six to eight weeks of healing, and up to six months in the aesthetic zone, before definitive impressions.
• C. Placing a margin into the attachment guarantees persistent inflammation and eventual failure of an otherwise well-made crown.
• D. Orthodontic EXTRUSION of the affected tooth, not the adjacent teeth, is the legitimate alternative to surgical crown lengthening — particularly in the aesthetic zone where bone removal on neighbours would be costly. Extruding the neighbours achieves nothing.

Note: The two routes to a restorable margin: surgical crown lengthening, which sacrifices attachment on adjacent teeth, or forced orthodontic eruption with fibrotomy, which preserves it. Choose by aesthetic demand and crown-to-root ratio.

Correct answer: C. Calcium hydroxide

• A. Glass ionomer bonds chemically to dentine and releases fluoride, making it an excellent base and liner, but it is not the classic bridge-forming material.
• B. Zinc phosphate is a strong luting cement with a low initial pH of about 3.5, which is IRRITATING to the pulp. It requires a protective liner over deep dentine rather than providing one.
• C. CORRECT. Calcium hydroxide has a pH around 12.5. That high alkalinity produces a superficial zone of coagulation necrosis, and beneath it the released calcium and hydroxyl ions stimulate odontoblast-like cells to lay down a REPARATIVE DENTINE BRIDGE. It is also antibacterial by virtue of the same pH. The tradeoffs are poor mechanical strength and gradual dissolution, so it is always covered by a base or a bonded restoration.
• D. Zinc oxide eugenol is sedative and palliative, and eugenol has an obtundent effect on pulpal nerve endings, but it does not induce a dentine bridge. It also interferes with resin polymerisation.

Note: MTA and the newer calcium silicate cements such as Biodentine now outperform calcium hydroxide for direct pulp capping, giving more predictable bridges with less tunnel defect formation. Calcium hydroxide remains the classic exam answer for the mechanism.