Pharmacology · patient case with 4 questions

Bisphosphonates and a Diastema

Patient: 67-year-old female

Chief Complaint: “I've always hated the gap between my front teeth. Can it be closed?”

Background: Osteoporosis, on oral alendronate for four years. Tooth #8 was root treated eight years ago.

Medications: Alendronate 70 mg weekly, calcium, vitamin D

Vital Signs: BP 134/78 mmHg · HR 70 bpm · RR 16 · T 98.4°F

Findings: A 2.5 mm midline diastema between #8 and #9. Tooth #8 is root treated with an intact but discoloured crown; #9 is vital and unrestored. Periodontium is healthy with no bone loss.

Question 1

What is the most appropriate way to close the diastema?

  1. Crowns on both #8 and #9
  2. Veneers on both #8 and #9
  3. Extract #8 and place an implant
  4. Orthodontic space closure
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Correct answer: A. Crowns on both #8 and #9

  • A. CORRECT for this specific tooth combination. Tooth #8 is ROOT TREATED with a discoloured crown, and a root-treated anterior tooth that needs both shade correction and width increase is better served by full coverage — it protects the weakened tooth, masks the intrinsic discoloration reliably and gives predictable control of the emergence profile. Matching #9 with a crown gives a symmetrical, predictable aesthetic result across the midline.
  • B. A veneer on #8 must bond to a root-treated, discoloured, possibly dehydrated substrate and may not fully mask it. Veneers would be the more conservative choice if BOTH teeth were vital and undiscoloured, which is the usual answer — but that is not this case.
  • C. Extraction and implant placement is exactly what should be AVOIDED. Elective bone surgery in a patient on four years of a nitrogen-containing bisphosphonate is the trigger for MRONJ. There is no indication to remove a restorable tooth.
  • D. Orthodontics is genuinely the most conservative option and is worth raising with the patient. It is not what the recall item was testing, and in a 67-year-old with a fixed aesthetic complaint and an already-compromised #8 it is often declined.

Note: ⚑ The bisphosphonate is the hinge of this case: it does not change how you restore the teeth, but it firmly excludes any option involving extraction or implant surgery. Note that the exam wants you to recognise the constraint, not to over-treat.

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Question 2

Apart from bisphosphonates, which drug class is most associated with medication-related osteonecrosis of the jaw?

  1. Antihypertensives
  2. Antibiotics
  3. Antiangiogenic agents
  4. Antihistamines
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Correct answer: C. Antiangiogenic agents

  • A. Antihypertensives have no association with osteonecrosis of the jaw.
  • B. Antibiotics are part of MRONJ MANAGEMENT, not its cause.
  • C. CORRECT. ANTIANGIOGENIC agents are the other major MRONJ class. Bevacizumab (a VEGF monoclonal antibody) and the tyrosine kinase inhibitors sunitinib and sorafenib block new vessel formation, and bone that cannot revascularise cannot heal after injury. Denosumab, a RANKL inhibitor, is the third major agent — antiresorptive like the bisphosphonates but through a different mechanism.
  • D. Antihistamines have no association with MRONJ.

Note: Full MRONJ drug list worth knowing: nitrogen-containing bisphosphonates (alendronate, zoledronate, pamidronate), denosumab, and the antiangiogenics (bevacizumab, sunitinib, sorafenib). Risk rises steeply with IV oncology dosing, duration over four years, corticosteroid co-therapy, diabetes and smoking.

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Question 3

Bisphosphonates exert their effect primarily on which cell?

  1. Osteoclasts
  2. Fibroblasts
  3. Odontoblasts
  4. Osteoblasts
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Correct answer: A. Osteoclasts

  • A. CORRECT. Bisphosphonates bind avidly to hydroxyapatite and are taken up by OSTEOCLASTS during bone resorption. Nitrogen-containing bisphosphonates then inhibit farnesyl pyrophosphate synthase in the mevalonate pathway, which prevents prenylation of the small GTPases the osteoclast needs to maintain its ruffled border and cytoskeleton. The osteoclast loses function and undergoes apoptosis. Resorption falls, bone density rises — and remodelling is suppressed, which is why the jaws, with their high turnover, become vulnerable.
  • B. Fibroblasts produce connective tissue matrix and are not the target.
  • C. Odontoblasts form dentine and are unrelated.
  • D. Osteoblasts build bone. They are affected indirectly through the coupling of resorption and formation, but they are not the target. Anabolic agents such as teriparatide act on the osteoblast lineage.

Note: Bisphosphonates have a half-life in bone measured in YEARS — often more than ten. This is why stopping the drug before an extraction ('drug holiday') has limited and debated benefit, and why the exposure history matters more than current use.

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Question 4

Where does MRONJ most commonly occur?

  1. Posterior mandible
  2. Mandibular condyle
  3. Posterior maxilla
  4. Anterior maxilla
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Correct answer: A. Posterior mandible

  • A. CORRECT. The POSTERIOR MANDIBLE, particularly the mylohyoid ridge and lingual aspect, is the commonest site — roughly two-thirds of cases occur in the mandible. The reasons are anatomical: thin overlying mucosa over sharp bony prominences that ulcerate easily, a relatively poorer blood supply than the maxilla, and the fact that this is where extractions and denture trauma concentrate.
  • B. The condyle is not a site of MRONJ; it is not exposed to the oral environment.
  • C. The posterior maxilla accounts for most of the remaining third of cases — less common than the mandible but not rare.
  • D. The anterior maxilla has a rich blood supply from multiple sources and is an uncommon site.

Note: Staging: Stage 0 is non-specific symptoms with no exposed bone; Stage 1 is exposed necrotic bone, asymptomatic, no infection; Stage 2 adds pain and infection; Stage 3 extends beyond the alveolus with pathological fracture, extraoral fistula or sinus involvement. Stages 1 and 2 are managed conservatively — antimicrobial rinses, antibiotics, analgesia — with surgery reserved for Stage 3 or non-responsive disease.

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