RUIN?

[Guest guest]

Hi to everyone on this list.

I will be the one to demonstrate my ignorance (it'll RUIN me!). When I first

read the acronym RUIN, my first response was WTF. But then I realized I must

just be un-informed on this condition. Then I did a search of Google for ruin,

and radial ulnar ischemic necrosis, and found basically nothing. Then I

searched on VIN and found alot of references, and a whole lot of radiology

folder references, but nothing that could be considered a true reference from a

refereed journal or textbook. So let me ask a couple of questions:

1 - Is there any real reference that accurately describes this condition?

2 - Has this condition actually been biopsied and had true histologic evidence

of ischemic necrosis? Or is this radiographic diagnosis only?

3 - Why is this condition not mentioned in any of the surgery, medicine, sports

medicine, orthopedic, or rehab books I have checked in? (The only description I

found for RUIN was back in a 2008 post on VIN by a radiologist - Post Below)

4 - If this is not a histologically confirmed disease entity, then how do we

differentiate it from inflammatory, infectious, neoplastic, traumatic or

biomechanically stress related? Does not the need for treatment, the treatment

choice and the success of treatment depend on the diagnosis? I wonder if this

is one of those disease entities that can have various different causes for the

same

If this is a true disease entity and verified by histologic evidence, can

someone point me to it? If it is, then I freely admit to being un-knowledgeable

and thanks for the knowledge.

Mark B. Parchman, DVM, DACVS, CVA, CCRT (I actually finally finished!)

Bend Veterinary Specialists

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" The interosseous ligament joins the radius to the ulna at about the junction of

the proximal third and distal two thirds. There is an interosseous membrane that

extends between the two bones proximally and distally. The interosseous muscle

is on the palmar aspect of the metacarpals(tarsals) and originate from the

proxmial MC and insert by way of a branched tendon onto the proxial P1.

RUIN is a form of enthesiopathy. There are several types of reaction that occur

at the entheses. For example, we may just see an enthesiophyte at the enthesis

of (say) the cruciate ligament. We recognize this as a bony production

radiographically. There may be surrounding sclerosis, but there is no lytic

component. Another type of change is RUIN. So, RUIN=enthesiopathy. With this

type of enthesiopathy, we see a lytic component. Using histopathologic

examination, the lytic area is either filled with cartilage (forms in low oxygen

tension)or an avascular, acellular mesenchyme. We (at least " I " ) don't know what

drives the different manifestations. With a more acute enthesitis, there may be

a purely vascular response at the enthesis. The region may have a fuzzy,

ill-defined lucency. I think that many of these end up having an enthesiophyte.

We all know that enthesiophytes may be present without causing clincal symptoms.

Remember that we are not imaging what makes the animal hurt....we are imaging a

process. Thus, not all enthesiopathies are painful. The same is true of RUIN.

Some are painful, some are not. In my experience, those that have purely bony

production (and some of these are quite voluminous as we have seen here on VIN)

tend not to be painful. Those that have the lytic component may or may not be

painful. When trying to rationalize why these animals are painful (turining up

the imaginoscope), I suspect that they are painful because of an increase in

intramedullary pressure. Bone is extremely sensitive to increases in

intramedullary pressure. For example, as part of our panosteitis research, we

would take Michele trephine biopsies of active panosteitis lesions, then the

next day, the animals were no longer painful. What we did, of course, was to

release the intramedullary pressure caused by the inflamm

ation. If there is active inflammation at a RUIN site (remember we cannot see

the inflammation radiographically), the animal may be painful. Most of the time,

NSAID therapy and rest is all that is required, but those recalcitrant cases

need to be curetted surgically. This seems to be successful in the vast majority

of cases at this stage. Is this a repetative strain injury? I really don't know

for sure. This has never been shown with a controlled study, but my sense is

that it probably is.

I see this radiographic change in almost all breed types. Little

chondrodystrophic breeds may have it and may be lame, but, of course, they

almost always have elbow incongruity and I suspect that this may cause loading

on this ligament. The large breed dogs (Labs, GSD, etc) are more active and have

a heavier body on an immature skeleton. It seems intuitive that this could be a

factor in developing the disease.

The elbow is a complex joint. The more I learn about it, the more that I realize

what I don't know. The interosseous ligament is just " down stream " from the

elbow. I think that diseases and mechanics that affect the elbow also affect the

ligament. "