PubMed · 17167690
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J N de Jongh. 2006. NOFSA statement on generic bisphosphonates.. https://pubmed.ncbi.nlm.nih.gov/17167690/
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Here we describe a 47-year-old postmenopausal woman who had been taking alendronate 70 mg/week for osteoporosis. After two months of alendronate therapy, she developed hepatotoxicity, and no other etiological factors for this besides the alendronate were apparent. After the alendronate therapy was discontinued, the patient's hepatic enzyme levels slowly returned to normal. Hepatotoxicity due to alendronate therapy is a rare but possible adverse effect.
Bone compaction has been shown to increase initial implant fixation. Furthermore, bone compaction creates a peri-implant zone of autograft that exerts osteoconductive properties. We have previously shown that locally applied bisphosphonate (alendronate) at 4-week observation can preserve the autograft generated by bone compaction. We now investigate whether the increased amount of autograft, seen at 4 weeks, can increase implant osseointegration and biomechanical fixation. Porous-coated titanium implants were bilaterally inserted with bone compaction into the proximal part of tibia of 10 dogs. On the right side, local bisphosphonate was injected into the bone cavity prior to bone compaction immediately prior to implant insertion. On the left side, saline was used as control. Observation period was 12 weeks. Locally applied bisphosphonate significantly increased biomechanical implant fixation (approximately twofold), bone-to-implant contact (1.2-fold), and peri-implant bone volume fraction (2.3-fold). This study indicates that local alendronate treatment can increase early implant osseointegration and biomechanical fixation of implants inserted by use of bone compaction. Long term effects remain unknown.
Previously we showed a loss of bone and a concomitant decrease in mechanical properties in the first 21 days after flexor tendon insertion site injury and repair in a canine model. The goal of this short-term study was to suppress bone loss after insertion site repair using alendronate in an attempt to prevent the reduction in biomechanical properties. Flexor tendons of the second and fifth digits of the right forelimbs of canines were injured and repaired. Dogs received a daily oral dose of alendronate (2 mg/kg). One digit in each dog also received a local dose of alendronate in the bone tunnel at the time of surgery. The repair was evaluated for bone mineral density (BMD) and biomechanical properties and compared to data from a previous study in which no alendronate was used. Alendronate was effective in protecting the distal phalanx from resorption during tendon-to-bone healing (BMD was 94 and 104% of control for systemic alendronate and for systemic plus local alendronate, respectively). Alendronate treatment prevented much of the decrease in ultimate load that occurs in the first 21 days. Without treatment, ultimate load was 42% of control. With systemic alendronate treatment and systemic plus local alendronate treatment, ultimate load was 78 and 69% of control, respectively. Failure mode was significantly different when comparing alendronate treatment to repair alone. A lower incidence of suture pull through was found in alendronate treated dogs, suggesting less tendon degeneration. Ultimate load can be improved in association with preventing the bone loss that normally occurs during the early period following tendon-to-bone repair. These initial short-term data demonstrate the potential for a clinical treatment that could enhance tendon-to-bone healing.