I'm really sorry that you are battling on so many different fronts w/ no real respite on any. I'll only echo many of the other members that as long as you are not in an immediate emergency amd can live w/ and manage the pain to tolerable levels then to get whatever tests need to be done in the immediate future and then to decide as Dahlek said on what to do and when. Like Glenntaj and Bob said I think that a skilled surgical team would offer you the best opportunity to have your situation addressed right.

Since I'm still new to the forum I probably missed this from one of your earlier posts but would bone morphogenetic protein be at all helpful to you or did it not work - sorry if I'm retracing old steps. I do hope you will get some lasting relief soon - many good thoughts to you.

Alkymst

As you all know, one of the ways I cope with the pn, and the back, is to learn as much as I can. Well, at some point I think I've learned enough, and I can go forward, and put myself in the doctor's hands. I become the "educated patient" par excellence. And it's still f**ing not enough. Bcause if I'd just looked harder, I would have learned that for several years now it's been clear that I was on a medication which would have prevented healing. And it still might, going forward.

Here's what I've learned since last night. Fosamax is really really awful. Our bones are made up of these two different cells, osteoblasts (builders) and osteoclasts (destroyers) The builders lay down minerals and the destroyers take it away. Bone is this living, breathing, evolving ecosystem that's in perfect harmony until we get older. Then the builders get more tired and can't keep up with the destroyers.

When doctors look at pictures of post-menopausal women, they often see thin bones. If you get a bone density done, they see the thinner bones more clearly. So, they recommend the lady takes Fosamax, and the next year, lo and behold, her bones are thicker and denser again on the films. Everyone is happy.

But after a year or so, she peaks out, and things don't get better. They don't get worse, but they don't get better.

At that point what has happened (and I definitely don't have the details right since I'm just trying to get the overall picture that's relevant, not necessarily biologically accurate) is that a generation of the osteo clan has died off. It's as if the osteoblasts were living in such a dense castle that there wasn't room for babies, and, besides, there were no osteclasts to do their business with and make more baby blasts and clasts.
The number of living breathing worker cells is nil.

The ecosystem is dead. The bone is dense, but it is DEAD. Like a sick woman with a facelift, an onlooker (think doctor) sees something gorgeous---FABULOUS Xrays and density scans-- but inside things are past sick, they're dead.

Into this ecosystem introduce a challenge. Say, the woman needs a tooth pulled. That leaves a hole in her jawbone, which the dentist expects will fill in with bone. Only it doesn't. It gets infected and he scrapes it out a bit more, cleans it up, and comes back adn the hole is BIGGER, not smaller. He tries to scrape and clean it up, and bone just dissolves under his instruments. Her jaw begins to turn to sawdust and basicall falls off. This is called Osteonecrosis of the Jaw. It's a happening thing. Each touch to the bone worsens the situation.

http://courses.washington.edu/bonephys/opjawON.html



Studies will show that women on Fosamax get fewer hip fractures. But other things happen. Other bones break, spontaneously. Legs break, ankles, or, THINK SILVERLADY BILLYE HERE--your foot breaks, then your leg then a vertebrae then your sacrum. And if the doctors want to put in hardware to hold things together, there's really nothing to hold the hardware in place. It all falls apart.

This link shows what has happened to Billye. It's a fulltext article, but skimmable.

http://jcem.endojournals.org/cgi/con.../3/1294?ck=nck

Now onto ME.

I've had years of traetment with Fosamax. In 1999 I was first given it for osteopenia (not even osteoporosis). My rheumi thought I was high risk given I'd been on steroids and have the bodytype for osteoporsos. My bone density improved and I was taken off. At some point I was put back on. I have no idea anymore how much I've been on it or off it, but I do know that I filled a prescription for it in Jan, 2006, prior to my Feb surgery. And I do know that it was continued through December, 2006, when I was told the surgery had failed.

Because that was when I first went to pubmed and put in every drug I'd been on and combined it with fusion to see if any influenced fusion.

There were four animal studies saying it hinderred fusion. No adult reports.
One study clearly showed it hindered fusion but the authors concluded that there was no reason to stop it for spinal fusion. (I assume there was a Merck grant much has happened. I was going to give this 6 - 9 months. The pain is worse and I'd move it up to 6 months, if there was a really good alternative offered by surgery.

But now I'm thinking this: I don't have bones inside me anymore. I have dead brick. Nothing will heal this; there are no living cells to heal me. If I get a larger surgery done, the same thing can happen.

If my worst fear is true, I will be Billye and have her life. Which has more suffering than I can imagine I can endure. She's got a shining light inside that allows her grace under pressure and pain. I really don't want to suffer like her. I can't carry it as well.

I see nothing on line that offers a solution to this problem.

The surgeon did give me one good piece of advice, which I didn't appreciate HOW GOOD on Friday. He asked me to write down the name of bone metabolism specialist and see him before surgery. I told him I didnt' need a bone guy because I dont have osteoporosis and dont' want osteoporosis drugs. But I think he understood. He said nobody really knew how bad Fosmax was until this year (getting his buddies off the hook), and I should see this guy.

I will call and see him ASAP. But omigod am I scared. I feel like not only was I hit over the head with a mallet on Friday, but that after the shock wore off, I discovered that I'd been being hit by mallets daily for years now and just didn't know it. The psychic numbness is leaving, but it's being replaced with terror.

So, yes, it's time to do more of what I do. Get information and try to learn. I hope the bone guy can see me soon. Hope he can make me less scared that what I have in me is just dead cement, ready to crumble if it's drilled into.

Please folks learn this about fosamax. Not good.

http://courses.washington.edu/bonephys/opmovies.html

This is an animation from a medical school class with a really dedicated teacher. She made a fabulous site. I'd suggest people click on the jpg for normal bone, then postmenopausal bone, then biphosphate bone. (that's fosamax) You will be started. The animations are only about 10 seconds each, but they are worth more words than I have used here.

1: Spine. 2005 Nov 15;30(22):2516-22.Click here to read Links
Alendronate inhibits spine fusion in a rat model.

Hospital for Special Surgery, New York, New York 10021, USA. huangr@hss.edu

STUDY DESIGN: A posterolateral lumbar fusion model in rats.
OBJECTIVE: To study the effects of alendronate on posterolateral lumbar fusion in rats.

SUMMARY OF BACKGROUND DATA: To our knowledge, there are no studies that show a significant inhibition of manual palpation-assessed spine fusion by alendronate.

METHODS: A total of 75 Sprague-Dawley rats underwent intertransverse fusion with 7-tailbone autograft at L4-L5. Animals received saline (control), alendronate equivalent to human dose (dose1, 5 microg/kg/day), or 10 times the human dose (dose10, 50 microg/kg/day) via subcutaneous osmotic pumps starting the day of surgery. Eight weeks after surgery, animals were euthanized, and fusion was assessed by manual palpation. Radiographic area and optical density of fusion masses were calculated. Histomorphometry was used to assess the percentage area of fusion masses occupied by bone or marrow tissues. RESULTS: Manual palpation fusion rates were lower in alendronate groups (50% and 40%, respectively) than in the control group (95%, P = 0.002). Interobserver and intraobserver kappa values were high (0.97-1.00). There were dose-dependent and statistically significant (P < 0.001) increases in fusion mass area and optical density with increasing alendronate dose. Fusion masses in dose10 animals had significantly higher percent area of bone tissue (P = 0.01) and lower percent area of marrow elements (P < 0.001) when compared to control animals.

CONCLUSIONS: Alendronate inhibits spine fusion in rats. Fusion masses in alendronate-treated animals appeared radiographically larger and denser than those in control animals despite lower fusion rates. Quantitative histomorphometry confirmed that alendronate inhibited bone graft resorption and incorporation. We recommend that patients undergoing spine arthrodesis should not take alendronate until fusion is achieved.

PMID: 16284589 [PubMed - indexed for MEDLINE]
Spine. 2005 May 15;30(10):1116-21.Click here to read Links
The influence of alendronate treatment and bone graft volume on posterior lateral spine fusion in a porcine model.
* Orthopedic Department, Institute for Experimental Clinical Research, Aarhus, Denmark. xueqingyun@hotmail.com

STUDY DESIGN: An experimental animal study with randomized, paired control design was conducted using a porcine model.

OBJECTIVES: The aim of this study was to evaluate the influence of alendronate treatment and the significance of different amounts of bone graft on posterior lateral spine fusion.

SUMMARY OF BACKGROUND DATA: Treatment with bisphosphonates inhibits osteoclast-induced bone resorption and increases bone quality and density. It has been widely used clinically for treatment of osteoporosis. Bisphosphonates have been reported to elongate the callus remodeling process during fracture healing. Bisphosphonate treatment may modify bone graft healing and the remodeling process in spine fusion. The bone resorption phase exists during the healing process. Extensive bone graft resorption could reduce the basis for new bone formation, which could be an important factor for failure of spine fusion. Furthermore, different amounts of initially applied bone graft may influence spine fusion rate and bone graft incorporation process.

METHODS: Twenty-two pigs were included in the study. Eleven pigs in the treatment group received alendronate 10 mg/day p.o. for 3 months after surgery. The other 11 pigs received no bisphosphonate and served as control group. Posterior lateral fusion with the CD Horizon system was performed on the lumbar spine using different amounts of autograft (4 g on one side and 8 g on the other side) in all animals. The fusion was evaluated using radiograph, CT scan, and histomorphometry at 3 months after operation.

RESULTS: There was no statistical difference in either fusion rate or fusion mass volume between the two groups. The fusion rate based on radiograph was 75% on the 8-g autograft side and 45% on the 4-g side (P < 0.05). The mean volume of fusion mass was 2.36 cm3 on the 4-g side and 3.29 cm3 on the 8-g side (P < 0.01). No difference was found in either trabecular bone volume or fusion rate between treatment and control groups using histologic evaluation.The treatment group showed a higher fibrous tissue volume(P < 0.05), higher proportion of woven bone structure(P < 0.001), and lower bone marrow volume (P = 0.088) in the fusion mass. Different amounts of bone graft did not change the tissue composition of the fusion mass.

CONCLUSIONS: Alendronate treatment in this study decreased fusion mass remodeling without inhibiting fusion rate. Increased amounts of autologous bone graft could improve the fusion rate in this experimental spine fusion study.

PMID: 15897823 [PubMed - indexed for MEDLINE]

: Spine J. 2004 Jan-Feb;4(1):36-43. Links
The effect of alendronate sodium on spinal fusion: a rabbit model.

Department of Orthopaedic Surgery and Rehabilitation, Walter Reed Army Medical Center, Washington, DC 20307, USA. Ronald.Lehman@NA.AMEDD.ARMY.MIL

BACKGROUND CONTEXT: Bisphosphonates affect bone remodeling and increase bone mass through the inhibition of osteoclasts. Their effect on osteoblasts, and the balance between osteoblastic and osteoclastic activity on bone turnover and healing, is not completely understood. Specifically, the effect of bisphosphonates on spinal fusion has yet to be determined. With the increasing use of bisphosphonates in the elderly population, this effect needs to be delineated.

PURPOSE: To evaluate the effect of alendronate sodium after an intertransverse process spinal fusion in a rabbit model.

STUDY DESIGN/SETTING: Randomized double-blinded in vivo study of the effect of alendronate sodium in a spinal fusion model.

METHODS: Fifty New Zealand white rabbits underwent a posterolateral L5-L6 intertransverse process arthrodesis with autogenous iliac crest bone graft. The rabbits were then randomly divided into two groups. Group I received 3 cc of saline placebo per oral gavage, and Group II received 200 micrograms (approximately 0.05 mg/kg/day) of alendronate sodium dissolved in 3 cc of saline per day for 8 weeks. Upon completion, the rabbits were sacrificed and the lumbar spines harvested, radiographed and graded for motion across the fusion site with manual palpation. Two independent pathologists then prepared and sectioned each left and right fusion mass. Three random x10 fields were examined and graded for both the cephalad and caudad ends of each section (516 fields). Fusion quality was graded using an established histological scoring scale (score 0 to 7 based on fibrous and bone content of the fusion mass).

RESULTS: Two rabbits died on the day of operation, and 48 rabbits survived the operation. Five additional rabbits died within the first 2 postoperative weeks. Thus, 43 rabbits (21 in Group I, 22 in Group II) completed the 8-week course of treatment. Grading each side separately, 26 of 42 fusion masses (62%) in Group I and 24 of 44 fusion masses (55%) in Group II had radiographic evidence of fusion (p=.76). With gross palpation, 11 of 21 motion segments (52%) in Group I versus 13 of 22 motion segments (59%) in Group II were determined to have a solid fusion (p=.76). Histologically, Group I had a higher median score (6.0; range, 0 to 7 vs. 1.0; range, 0 to 7; p<.0001) and a higher fusion rate (76% vs. 45%; p=.004) than Group II.

CONCLUSIONS: Alendronate sodium appears to inhibit or delay bone fusion in a rabbit model. Presumably, this occurs as a result of uncoupling the balanced osteoclastic and osteoblastic activity inherent to bone healing. These findings suggest that a discontinuance of alendronate sodium postoperatively during the acute fusion period may be warranted.

PMID: 14749192 [PubMed - indexed for MEDLINE]

evidence is mounting I guess on these drugs. You know, Liza, that bone
necrosis occurs with them too? That is the dark underside that is coming to
light.
http://annonc.oxfordjournals.org/cgi...full/16/7/1207
http://www.cancerpage.com/news/article.asp?id=8122

I am worried that this may occur in non chemo patients at a slower rate, and
with time more will show up with negative results from these drugs!

--what might the dietary/supplement/exercise options be, to minimize bone loss and see if we can wake up some of the cells?

Can you put together a weight-bearing exercise program of any kind? What will your sinews/muscles tolerate? (Light weights/high reps?)

And (I'm sure Mrs. D will have suggestions here)--what kind of calcium/magnesium/Vitamin D3 regimen would optimize your bone condition?

BTW, I certainly empathize with your situation, and absolutely want you to avoid the kind of bone breakdown that Billye is suffering, but you're wrong about one thing. You also carry off these situations with grace. Maybe wry, sarcastic grace, but grace nonetheless.

delemma--danged if you do, danged if you don't take the adrenolates.
I too am/have been learning the 'hard way' about bone loss [far more than I ever could have imagined].
I fear that physicians are not as up to date on the newer cautions in the prescribing info as necessary. In my case I've been taking the adrenolates for over 10 years and a recent 're-read' of the info NOW includes the suggestion to take a 'break' at a 5-year mark. The info does not say for how long tho [I suspect 'THEY' don't know].
I am told and have read that other therapies are be available so there is hope. I will be finding out very soon tho, after more tests and a visit to the endocrinologist. I am sure that Billye is in that process of 'finding out' as well.
Every medication has the potential to help or hurt us. We usually find out after a precious price has been paid.
Liza Jane, I emphasize with your concerns and fears. Your concerns are far, far greater than mine. Below is a link on thyroid activity and how it can relate to other issues and conditions, particularly medications and supplements:
http://www.powerofprevention.com/thyroid/links.php
It seems that the whole endocrine system is linked to bone development and retention. The more I learn, I understand some, and am amazed by how complicated we humans are!
As I find out more, I'll post resouce sites.
For now have a couple of these: - j

I'm so glad you brought that up didn't know you have been on that.
All my Drs. and Bob's Spine Dr. believe it or agreed on something,
which is a miracle in itself, no Fosamax. Well all of them to many
serious side effects. Fosamax is very bad for people with certain
heart conditions. And not everybody knows they have the heart
problem. It was so odd to hear this from 4 different Drs. They all
reccomended high does of calcium,vitamin D and Magnisium also
a lot of green leafy vegetables.

The Spine Dr. said a lot of people see these ad's on TV and think or
lead to believe these are miracles. Yes they say the side effects at a
fast pace at the end. He really feels they can do damage.This does
bother me,1 don't thing i've ever heard 4 Drs. agree on the same thing.

You are a very brave lady,You do your homeword and in retun we benefit
from it. Thank you so much.. Sue