Fosamax – not so fast….


March 5, 2008 · from

BONE BOOSTERS? Biphosphonates BNPs NDB 2007


DR. WEEKS’ COMMENT:   I worked in the Mineral Metabolism Unit of Massachusetts General Hospital for 2 years with Dr. Bob Neer (focus: osteoporosis) and Dr. Michael Hollick (focus: vitamin D metabolism) and we looked closely at factors influencing bone health. I have NEVER prescribed Fosamax and have grave concerns about these biphosphate drugs. In a nutshell, they do seem to make bones “denser” but also, and here is the problem, they make them more BRITTLE – think about the piece of chalk your teacher use to use to write on the chalkboard until it…   snapped! 

Density alone is not healty for bones, especially if it comes at the expense of strength and flexibility.  See for bone healthy targeted nutrients including not only calcium, but more importantly, boron, silica, magesium, B6 and manganese.  And don’t forget to use those bones – get out and walk!


No trials have ever been published showing that biphosphonates do overall good long term for osteoporosis– ie reduce all-cause mortality, and reduce hip fracture, without toxicity. Biphosphonate Osteonecrosis of long bones was already published in 1995, and from 2001 in USA. So their heavy marketing, and prescription like vitamins, causing the epidemic of devastating osteonecrosis, makes the prescribers, manufacturers, dispensers and Regulators – eg the FDA -criminally liable.

Effects of continuing ALENDRONATE after 5 years of treatment:  Fracture Intervention Extension to 10yrs JAMA. 2006 Black, Cummings UCSF.  (Dr. Weeks comment:  it would be interesting to see who funded this research which now seems quite misleading)

In 1099 women re-randomized to alendronate or placebo for a further 5 years (1998-2003):   Continuing alendronate halved only recognized vertebral fracture risk (2.4% vs 5.3% for placebo); their conclusion: “women at very high risk of clinical vertebral fractures may benefit by continuing beyond 5 years”. i.e. no benefit for the far more important hip bones.

But was this a dangerous lie? the 19% Risk of nonvertebral fractures was no different (RR 1 ) between continuing and discontinuing alendronate.  “Susan Ott (JCEM Mar 2005) already questioned bisphosphonate long term safety”


Biphosphonate BPN Jaw OSTEONECROSIS ONJ  is now endemic worldwide:
1st reported in 1994 (Guanabens, Spain- leg stress #s),
2001-03 – USA 63 cases (Ruggiero 2004)
(2002-5 Pozi) Italy- 35 ;
(2003-5 (Abu-Id 2006) Germany 73 cases
2004-5 (Mavrotoki) Australia 158

By July 2006 over 3000 cases of ONJ were reputedly already reported.

“of Odvina”˜s 9 cases of spontaneous fractures on alendronate – 5 were mid-femur fractures (2 bilateral same as Toulouse). 6 had delayed or absent fracture healing.

Estrogen alone is anabolic only on bone, uterus, memory, fat – If anything it both builds inner hostility, fattening, inflammation, & wastes collagen ie muscle catabolic – thus doubles incontinence.

The only true anabolics (ie strengthen muscle, melt fat) are
* food incl vita-/minerals incl. vitamin C/D; CoQ10, carnitine,
* Insulin sensitizers – metformin; natural androgens, exercise.

Dach: “ Look at Toulouse Lautrec.. His parents were first cousins… “we are giving women Toulouse Lautrec’s bone disease- the same jaw necrosis, mid-femur fractures, failure of bone healing”,

“But women who sustain fractures on BPNs are told that the fractures are due to the underlying osteoporosis, not the drug”

The osteonecrosis problem may be 95% with iv BPNs (Urade) – orally BNPs like HRT are absorbed below 10%; but as with oral HRT, the problem may be both total dose absorbed, and total length of exposure -BPNs (given over perhaps a year iv) bind to bone for 10yrs. Fosamax is swallowed for 3-5yrs. Jones & Wilkinson’s (April 2006 NHS review of oral BPN adversity) found that adherence on oral BPNs is only around 50% by 3 years due to adversity – GIT, musculoskeletal, skin…. and when stopped, BMD is maintained for up to 2 yrs due to bound Testosterone (unlike estrogen).


Is there (as there was with tobacco, Premarin & Vioxx) a Bone Mineral Density (BMD) industry  OSTEOPOROSIS FRACTURE DECEPTION?


The chief risk factor for fractures is not BMD, osteoporosis,but immobility, falls, inco-ordination, muscular frailty = sarcopenia – which in turn limits exercise, endurance, motivation. By contrast, permanent appropriate TRT in men and T+ E2RT in women can prevent eg the up to 40% bone loss that occurs in 6 months on corticosteroids (Studd 1989), restore up to 26% of lost BMD in critical areas like Ward’s triangle ie (the hipbone’s neck); of the 6 published RCTs that have given testosterone replacement (with or without estrogen) for 1-2 years post menopause, 5 showed that testosterone gave better increase in BMD than estrogen alone. In the 6th and oldest study (Studd 1992) in women both with and without hysterectomy, adding implants of testo 75mg 6mthly to Esto 100mg 6mthly made no difference over esto alone, possibly because the of the supra-physiological esto level attained (mean ~1.9nmol/L per Studd 2006) and the followup of only 1year.

In the 7th trial of only 6 months(2005), no improvement was seen in BMD on either esto alone or on Esto + testo- but it used oral HRT; lean mass increased only on the combination- so these women would have been less prone to falls and fractures. .

On the baker’s dozen of natural supplements, we have seen bone density increasing steadily by 1% a year – slightly faster in spine than hip- over 15 years in eg a severely osteoporotic woman with chronic active rheumatoid arthritis on prednisone.

After osteonecrosis the results with hyperbaric oxygen added to the natural supplements appear useful to justify it’s use to salvage whats left ..

Hormone Replacement Therapy (HRT) AND FRACTURES:

IN the Women’s Health Initiative, the fracture rate in those with womb was 0.15%pa,
and E+P reduced this by 34% over 5.6yrs in those post hysterectomy ie longer without hormones, the fracture rate was 0.17% and E alone reduced this by 39% ie 60% still had long bone fractures.  No trials have measured fracture rate on TRT in women;
but we never see women on TRT have spontaneous limb fracture.

Only androgen improves muscle strength;HRT suppresses relative androgen levels.
so why must women go without replacement androgen?

Use of platelet-rich plasma in the management of oral biphosphonate-associated osteonecrosis of the jaw: a report of 2 cases.

J Oral Implantol. 2007;33:371-82 Lee CY,

Bisphosphonates (BP) are nonhormonal medications used in the treatment of various bone malignancies and metabolic conditions. Since 2003, there have appeared a significant and growing number of articles in the worldwide medical and dental literature describing the complication of an osteonecrosis of the jaws associated with the intravenous and, most recently, the oral form of BP medication that has been refractory to any definitive form of treatment. The authors have successfully managed 2 patients taking the oral form of BP with adjunctive treatment using platelet-rich plasma (PRP), and in one case with hyperbaric oxygen (HBO). We were able to obtain complete remission in each case, which is defined as resolution of pain and complete closure of exposed bone in the jaws. The purpose of this report is to describe a treatment protocol and the rationale for using PRP and HBO to obtain complete remission of this new pathologic condition.

Hyperbaric oxygen treatment and bisphosphonate-induced osteonecrosis of the jaw: a case series.

J Oral Maxillofac Surg. 2007 Jul;65(7):1275-6. Freiberger JJ, Padilla-Burgos R, Chhoeu AH, Kraft KH, Boneta O, Moon RE, Piantadosi CA.Duke University Medical Center, Divers Alert Network, Durham,.
PURPOSE: Bisphosphonate (BP)-associated osteonecrosis of the jaw (ONJ) is an emerging problem with few therapeutic options. Our pilot study of BP-ONJ investigated a possible role for hyperbaric oxygen (HBO(2)) therapy. PATIENTS AND METHODS: A total of 16 patients, ranging in age from 43 to 78 years, with BP-ONJ were treated with adjunctive HBO(2) between July 2003 and April 2006. Staging was based on the size and number of oral lesions. Clinical response after treatment and at distant follow-up; the odds of remission, stabilization, or relapse; and time to failure analysis were calculated. RESULTS: The median time on BP therapy before appearance of ONJ symptoms was 18 months, and that from symptom onset to HBO(2) therapy was 12 months. Fourteen of 16 patients (87.5%) improved in stage. The size and number of ONJ lesions were decreased after HBO(2) therapy (P < .001 and P = .008, respectively; Wilcoxon signed-rank test). Immediately after HBO(2) therapy, 7 of 16 patients (44%) were in remission and 8 (50%) had stabilized; however, stabilization without remission was sustained in only 2 patients. At follow-up, 10 of the patients (62.5%) were still in remission or had stabilized. The 7 patients who continued on BP treatment during HBO(2) therapy had a shorter time to failure (8.5 months; 95% confidence interval [CI] = 7.1 to 9.8) than those who discontinued the drug (20.1 months; 95% CI = 17.5 to 23.9; P = .006 by the log-rank test). Clinical response was not associated with cancer type or malignancy remission status. CONCLUSIONS: Adjunctive HBO(2) therapy may benefit patients with BP-ONJ; however, the outcome is improved with cessation of BP administration.


Osteonecrosis of the jaws due to bisphosphonate use. A review of 60 cases and treatment proposals.

Am J Otolaryngol. 2007 May-Jun;28(3):158-63.

Magopoulos C, Karakinaris G, Telioudis Z, Vahtsevanos K, Dimitrakopoulos I, Antoniadis K, Delaroudis S. Aristotle University, Thessaloniki, Greece.
PURPOSE: Bisphosphonates are compounds used in the treatment of various metabolic and malignant bone diseases. In the last two and a half years, there has been a striking increased referral of patients with exposed necrotic jawbone, mostly after several teeth extractions. The only clinical feature common in all patients was the use of bisphosphonates in the treatment of bone diseases. PATIENTS AND METHODS: We performed a retrospective multicentric study of 60 patients with necrotic bone lesions of the jaws of various extent from July 2003 to October 2005. The necrotic bone involved the maxilla (37%), the mandible (50%), or both (13%). The bisphosphonate administered was mostly zoledronate. The management of the patients included cessation of bisphosphonate therapy for more than 6 months, long-term antibiotics, hyperbaric oxygen administration in some cases, and various surgical restorative procedures. RESULTS: The implementation of the treatment protocol in 7 patients so far lead to high cure rates, whereas surgical restoration of the defect without previous cessation of bisphosphonate therapy had discouraging results.

CONCLUSIONS: Clinicians and dentists should have in mind this new complication of bisphosphonate administration to identify and treat osteonecrosis of the jaws.


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