Dr. Pardeep Kumar Sharma, M.D. (Ayurveda) · Sukhayu Ayurved Hospital, Jaipur · Updated September 2026

Almost every patient who writes to me about avascular necrosis asks the same question in the same shape: is it reversible or not? They want a yes or a no, because that is what they have been given everywhere else — a no from one side, a yes from the other, and no explanation from either.

The honest answer is that the question, as asked, cannot be answered. Not because the answer is being withheld, but because "reversal" is not one event. It is a word that covers at least four different things happening inside a hip, each with its own biology and its own speed. Some of those things genuinely reverse. One of them does not reverse for anybody, by any method. A patient who does not know which is which cannot judge any claim made to them — including mine.

So this page does not begin with an answer. It begins by taking the question apart.

"Reversal" is four separate things, and they do not move together

When a report says avascular necrosis, it is describing a sequence, not a single lesion. Blood supply to the femoral head is compromised. Bone cells in the supplied territory die. The marrow around that territory becomes inflamed and waterlogged. The body walls off the dead zone with a reactive rim, which is what shows up as sclerosis. And finally, if enough of the weight-bearing dome loses its structural competence, the surface fractures beneath the cartilage and the head loses its round contour.

Ask about reversal of each of these separately and you get four different answers.

Marrow oedema is the most reversible. This is worth understanding precisely, because it is the finding most often quoted and most often misread. When pathologists have examined the marrow-oedema zone around an osteonecrotic lesion, what they have found is serous exudate, patchy interstitial bleeding and mild fibrosis — not an extension of the dead bone itself. The oedema is a live, fluid, inflammatory response sitting beside the necrosis. That is why it can resolve, and why its resolution is a real radiological event rather than a claim about resurrecting dead tissue. It is also the finding most closely tied to the pain the patient actually feels.

Blood supply can improve. The femoral head depends on terminal retinacular vessels with very little collateral backup, which is precisely what makes it vulnerable. Circulation at that level is a physiological state, and physiological states respond to treatment.

Sclerotic change can regress, because the reactive interface is a response to the lesion rather than the lesion itself, and responses recede when what provoked them recedes.

Structural contour does not come back. Once the weight-bearing dome of the femoral head has fractured and flattened, no medicine and no therapy restores that shape. Not Ayurvedic treatment. Not core decompression. Not grafting. That is the honest floor under everything else on this page, and any practitioner of any system who tells a collapsed hip otherwise should be treated with suspicion.

This is why "is AVN reversible" has no single answer. In one patient, three of those four things are still in play. In another, the fourth has already happened and the conversation is a different one entirely.

The stage decides the answer, and most patients have never been told their stage

The line that matters more than any other in avascular necrosis is not early versus late. It is before collapse versus after collapse. Every staging system in use draws it — Ficat–Arlet, ARCO, Steinberg — and they draw it in slightly different places, which is exactly why a grade number quoted without its system is close to meaningless. A "Grade 3" in one system is not a "Grade 3" in another.

Before collapse, the situation is biological. Dead bone is present, but the architecture is intact and the tissue around it is alive and responsive. Radiological regression in this window is not an Ayurvedic idea; it is documented in the orthopaedic literature under non-surgical treatment too. In one prospective series of pre-collapse hips treated with extracorporeal shock wave therapy, the lesion regressed in roughly 43 per cent of hips and marrow oedema resolved significantly on follow-up imaging, without any surgical intervention. The point is not the therapy used. The point is that a pre-collapse osteonecrotic hip is capable of moving backwards on imaging.

After collapse, the situation is mechanical. A mechanical problem does not respond to a physiological treatment, whichever system is offering it. Treatment after collapse is still worth doing — pain, mobility, the opposite hip, and the rate of further deterioration are all real targets — but it is no longer a conversation about reversal, and I do not conduct it as one.

If you do not currently know your stage and your staging system, that is the first thing to establish, before you evaluate any treatment offer at all. We have set out what each stage means and what is realistically available at each one in a separate piece on AVN of the hip and knee: stages and recovery.

Waiting is a decision, and it has a cost

Many patients are sent home with a version of "wait and watch, and when it collapses we will replace it." That is presented as the neutral, conservative option. It is not neutral.

Pooled natural-history data on untreated osteonecrotic hips has reported that the femoral head is preserved in only a minority of cases — on the order of 13 to 35 per cent depending on the series. In other words, in most untreated hips, the disease proceeds to the one change that nothing reverses. Waiting spends the window in which the reversible components are still reversible.

This is also not an argument that surgery is wrong. It is not. Core decompression has reported overall clinical success in the region of two-thirds of cases, which is a real result, and there are hips that need replacement and should have it. What it is an argument against is the idea that the interval before surgery is empty time in which nothing can be attempted. We have written separately on why "wait for collapse, then replace" is not the only path, and on what joint replacement does and does not solve in avascular necrosis.

Why the classical name changes the treatment, not just the vocabulary

In the classical literature, this presentation corresponds to Gambhīra Vātarakta — the deep-seated variety of Vātarakta, as distinguished from the superficial (uttāna) form that stays in skin and superficial tissue. The correlation is not mine alone; it is the correlation used in the published Ayurvedic case-report literature on osteonecrosis of the femoral head.

The distinction is worth more than a label. Vātarakta places the disturbance in rakta — in the blood and the vessels carrying it — driven by vitiated Vāta. Gambhīra places it deep, in the tissues beneath, rather than at the surface. Read together, the classical name says the problem is a vascular problem striking a deep structure, which is exactly what avascular necrosis is at the level of the terminal vessels supplying the femoral head.

That reading has a practical consequence. It directs treatment at the blood channel rather than at the joint surface. A patient whose hip hurts naturally expects treatment aimed at the hip. The classical reading says otherwise: work on the raktavaha srotas, and the joint follows. This is the difference between treating where the pain is and treating where the disease is, and it is the single most consequential decision in the whole protocol. The mechanistic argument is set out at greater length in reversing osteonecrosis with Ayurveda: a scientific approach.

Where these cases come from, and one that is documented

The risk factors are well established: prolonged corticosteroid exposure, alcohol, trauma and post-surgical injury to the vessels, sickle cell disease, and a substantial idiopathic group. Steroid exposure remains the single most common non-traumatic cause worldwide, which is why we have a standing page on what to know before taking steroids.

The post-COVID cohort deserves separate mention, because it changed who walks into the OPD. A pooled review of published post-COVID AVN cases — seventeen studies, over two hundred patients and more than three hundred hips — reported a mean interval of roughly four months from infection to diagnosis, a mean cumulative corticosteroid exposure above one gram in prednisolone-equivalent terms, a mean age in the early forties, and, importantly, most patients presenting already at the middle stages. That last detail is the one that matters clinically. A forty-year-old with four months of hip pain after a steroid course is not too early to investigate. They are often already at the stage where the window is closing.

One more diagnostic point, because it costs patients months. Avascular necrosis of the hip frequently presents as pain in the groin, buttock and thigh — and is regularly assumed by the patient, and sometimes treated, as sciatica. It is a completely different condition with a completely different cause. Thigh pain that does not follow a nerve distribution and worsens on weight-bearing and internal rotation deserves a hip MRI, not a lumbar one. Similarly, early AVN of the knee is routinely reported as osteoarthritis.

A documented case

A serving soldier in his thirties, a volleyball player, a lifelong teetotaller with no steroid history, developed left hip pain he attributed to the game. Because he had no alcohol history, avascular necrosis was not considered; he was treated for muscular pain. The pain worsened, he began to limp, and a man who had played regularly for years reached the point where walking a hundred metres was difficult. At a higher military facility, MRI identified avascular necrosis of the left hip. He was offered core decompression by one surgeon and total hip replacement by another. He declined both and came to Sukhayu Ayurved.

On comparison MRI after treatment, the reporting radiologist recorded:

Complete resolution of the bone marrow oedema
No extension of disease to the opposite hip
Complete resolution of the sclerotic changes
Restaging from Grade III to Grade II [CONFIRM: staging system used — Ficat–Arlet / ARCO / Steinberg; pre- and post-scan dates; reporting centre]

Two things should be said about that list plainly. The first three findings are changes in the live, responsive components described at the top of this page — oedema, reactive sclerosis, and the behaviour of the contralateral hip — and they are exactly the components that are capable of moving. The fourth, the change in grade, is what the comparison report recorded; it is one patient's imaging, read by a radiologist, and it is not a rate, a percentage, or a promise to the next patient. The full record of this case, with imaging, is published separately as a case study of AVN hip reversal from stage 3 to stage 2.

What this case does not establish is that every hip does this. What it does establish is that the outcome is possible, which is the only thing a single documented case can ever establish — and the only thing this page claims.

What the treatment actually is, and what it costs in time

Two arms, run together, not in sequence.

Internal medicines, directed at the blood channel rather than at the joint. The formulary is built around rakta-śodhana — clearing and correcting the blood — with supporting preparations for the inflammatory component and for the integrity of the joint structure while healing proceeds. Classical Mañjiṣṭhādi Kaṣāyam sits in this group for its action on rakta. Our own preparations, developed over fifteen years of clinical use at Sukhayu and manufactured in a GMP-certified pharmacy, are used alongside it. These are prescription preparations selected per patient; the combinations differ by stage, by constitution and by cause, and none of them is appropriate for self-medication. What each does, and why, is set out on the Ayurvedic medicines used in avascular necrosis page, and our position on manufacturing standards on how our medicines are made.

Panchakarma, with Basti as the principal procedure, performed classically. Basti is not a detox event here. It is a route — the principal route by which aggravated Vāta is addressed, and the reason it is described in the texts as the foremost of the therapies. Why that is so is explained in Basti Chikitsa: the king of Panchakarma.

And then the part that most pages leave out. In the case above, Panchakarma ran across four admissions — the first of sixteen days, the subsequent three of eight days each — and internal medicines continued for close to two years. That is the real shape of this treatment. Anyone offering avascular necrosis a three-week package and a discharge is describing something other than what this disease requires. We do not sell packages. We treat diagnoses — the protocol is built to the patient, as set out in how we treat.

Discuss your case

If you have an MRI report, that is the place to start — the stage and the system it was read under determine everything discussed above. You can send it for review through an online consultation, or contact the hospital directly. If you want to understand the reasoning behind how this hospital works before that, start with why Sukhayu Ayurved.

Reversal of Avascular Necrosis with Ayurveda