Do Bone Spurs Grow Back After Surgical Removal?

Bone spurs can and frequently do grow back after surgical removal, though the likelihood depends heavily on where the spur was, why it formed, and whether the underlying mechanical or inflammatory triggers persist. In the cervical spine, for instance, one study found that every patient in a cohort with diffuse idiopathic skeletal hyperostosis redeveloped osteophytes after surgery, at a rate of roughly one millimeter per year. The picture is more encouraging in other joints, but recurrence is a well-documented reality across nearly every body region where bone spurs are surgically removed.

Why Bone Spurs Form in the First Place

A bone spur is not a random growth. It is bone tissue that forms in response to stress, friction, or inflammation at a particular spot. When a tendon, ligament, or fascial band pulls repeatedly on a bony attachment, the bone remodels itself to distribute that mechanical load more evenly. Research on spur formation at fascial attachments describes this as a physiological bone response to tensile stresses rather than a disease process in itself.¹ In osteoarthritis, the process is slightly different: cartilage loss changes the way force moves through a joint, and the bone at the margins responds by building outward. Osteoblasts within these spurs produce inflammatory molecules that can further accelerate the cycle, especially when abnormal mechanical stress continues.²

This matters for recurrence because surgery removes the spur but typically does not eliminate the mechanical or inflammatory environment that built it. If the same forces keep acting on the same spot, the bone has every reason to respond the same way again.

How Often Do They Come Back?

Recurrence rates vary enormously by location and by the condition driving the spur. The evidence is clearest in a few well-studied areas.

Cervical Spine

Patients with diffuse idiopathic skeletal hyperostosis (DISH), a condition that causes widespread bony overgrowth along the spine, face among the highest recurrence rates documented. In a study following patients who had anterior cervical osteophytes removed to relieve swallowing difficulty, all patients redeveloped osteophytic formation, growing at an average of about one millimeter per year after surgery.³ That does not mean every patient needed another operation. Many regrown spurs remain small enough to be asymptomatic for years or indefinitely. But the biology of DISH is systemically overactive, which makes local recurrence almost inevitable.

For cervical spurs not driven by DISH, the picture is somewhat better. A review of anterior cervical osteophyte resection found that adding spinal fusion to the procedure and using intraoperative navigation to ensure complete removal helped reduce the chance of recurrence.⁴ Fusing the vertebrae eliminates the movement that drives new spur growth at that segment, which is one of the few surgical strategies that directly addresses the mechanical cause.

Shoulder

Subacromial decompression, where a surgeon shaves down bone on the underside of the acromion to create more room for the rotator cuff, is one of the most commonly performed orthopedic procedures. When patients continue to have pain afterward and go in for revision surgery, a residual or recurrent acromial spur turns up frequently. In one retrospective study of 36 revision decompression cases, a residual prominent bone or acromial spur was found in over half of the patients.⁵ An important nuance here is that “residual” and “recurrent” can be hard to distinguish. Some of these spurs were never fully removed in the first place, while others genuinely regrew. Both outcomes lead to the same clinical problem for the patient, and revision surgery in that study was more successful when performed arthroscopically.

After distal clavicle excision, a procedure done at the far end of the collarbone for arthritis at the acromioclavicular joint, bony regrowth around the resected area has been identified as a possible source of returning symptoms.⁶ Whether this represents true regeneration or capsular tightening with secondary bone response remains debated, but clinically it produces familiar pain and stiffness.

Ankle

Bony impingement in the ankle, where spurs along the front of the tibia or talus limit motion and cause pain, is commonly treated arthroscopically. In a study examining complex ankle bony impingement combined with chronic instability, tibial-side recurrence was found in nine cases, with talar-side recurrence in three of those as well.⁷ Chronic instability itself may be a major driver here: when the joint is loose and moves abnormally, the repeated microtrauma stimulates new bone to form at the impingement site. Addressing the instability at the same time as the spur removal appears to be important for reducing recurrence.

The Biology Behind Regrowth

Removing a bone spur leaves behind a bed of tissue that retains the cellular machinery to build bone. Research on heterotopic ossification, where bone forms in soft tissue after injury or surgery, found that surgical excision leads to re-emergence of mesenchymal stem cell populations at the excision site. The new bone that forms appears to be created from scratch by these cells rather than simply extending from bone that was left behind.⁸ In other words, even a technically perfect removal that leaves no residual spur behind can be followed by genuine de novo bone formation at the same site.

A separate line of research has shown that once inflammation and structural damage trigger spur formation, the process becomes somewhat self-sustaining. In animal models of inflammatory arthritis, blocking two of the body’s major inflammatory signaling molecules (TNF-alpha and RANKL) did not stop bony spurs from forming. The spurs depended on proliferation of the periosteum, the membrane that surrounds bone, and this proliferation was not controlled by the usual inflammatory pathways that anti-inflammatory drugs target.⁹ This finding helps explain why patients taking anti-inflammatory medications or even biologic drugs for arthritis still develop spurs. The process, once initiated by damage and inflammation, runs on a parallel track that current systemic therapies do not easily shut down.

A dramatic example of this regenerative capacity comes from spinal surgery in children. A case report documented complete regrowth of a diastematomyelic bone septum, a congenital midline bone spur that divides the spinal cord, in a teenager after the spur had been removed years earlier. The authors attributed the regrowth to persistence of residual mesenchymal cells left behind during the original operation.¹⁰ That case led to the recommendation that surgeons remove not just the bony spur but also the surrounding tissue sleeve, to eliminate as much of the regenerative cell population as possible.

Incomplete Removal Versus True Regrowth

When a patient’s symptoms return after bone spur surgery, clinicians face a diagnostic question: did the spur grow back, or was it never fully removed? Both scenarios happen. In the shoulder revision study mentioned earlier, more than half of patients had residual bone at the revision procedure, and it is often impossible to determine whether a small remnant was left at the first surgery or whether new bone formed around a clean surgical margin.⁵ For the patient, the distinction is somewhat academic. But it matters for surgical planning, because incomplete removal suggests a technical problem that can be corrected with a more thorough second procedure, while true regrowth suggests the underlying biology needs to be addressed simultaneously.

Intraoperative navigation and imaging have become tools to improve completeness of the initial removal. In cervical spine surgery, surgeons now use navigation systems to verify they have removed the entire osteophyte without breaching into the disc space or cortical bone.⁴ The idea is straightforward: if you can confirm the spur is completely gone before closing, you eliminate one major cause of early symptom recurrence. True biologic regrowth over months or years is a separate challenge.

What Reduces the Odds of Recurrence

No intervention guarantees a bone spur will never come back, but several strategies tilt the odds.

Addressing instability: In the ankle, repairing ligaments to restore joint stability at the same time as removing the spur reduces the abnormal motion that prompted the original growth.
Spinal fusion: Fusing the vertebral segment where a cervical spur was removed eliminates the movement at that level, taking away the mechanical stimulus for regrowth.
Complete tissue removal: In congenital spurs like diastematomyelia, removing the surrounding tissue sleeve along with the bone reduces the pool of mesenchymal cells available to rebuild.
Weight management: Obesity is linked to larger and more symptomatic heel spurs. A study comparing patients with plantar fasciitis and heel spurs to controls found that a BMI above 30 roughly tripled the odds of symptomatic spurs, and the spurs themselves were larger in heavier patients.¹¹ Reducing mechanical load through weight loss may slow recurrence in weight-bearing locations.

In preclinical research, locally delivered anti-inflammatory agents have shown promise. A study using controlled-release celecoxib (a common anti-inflammatory drug) delivered directly to an osteoarthritic joint in an animal model reduced the formation of osteophytes, bone cysts, and loose bodies while also reducing synovial inflammation.¹² Whether this translates to a practical post-surgical strategy for preventing regrowth in humans is still unknown, but it highlights the potential for targeted drug delivery to interrupt the spur-forming cycle at the source.

When Revision Surgery Is Needed

A regrown spur does not automatically require another operation. Many recurrences are small, asymptomatic, or manageable with physical therapy and anti-inflammatory medication. The decision to reoperate depends on whether the spur is causing functional problems: difficulty swallowing in the case of cervical spurs, impingement pain in the shoulder, or restricted range of motion in the ankle.

Revision surgery outcomes vary. In the shoulder, arthroscopic revision decompression produced satisfaction in the vast majority of patients studied, while open revision had a lower satisfaction rate, though the two groups differed in other ways that may have influenced results.⁵ For revision surgery on insertional Achilles tendinopathy, which can involve heel spur re-excision along with tendon repair, functional scores improved substantially from pre-operative levels at an average follow-up of about four and a half years, though only about a third to two-fifths of patients reached scores comparable to a healthy reference population.¹³ Revision surgery works, in other words, but expectations should be calibrated: not everyone returns to pain-free baseline.

One practical takeaway from the literature is that dense scar tissue, not just recurrent bone, contributes to persistent symptoms after spur removal. In shoulder revision cases, thick fibrous adhesions beneath the acromion were present in every patient studied.⁵ Scar tissue restricts motion and can mimic the symptoms of a recurrent spur, which is why imaging before revision is important to distinguish between the two.

The Role of Systemic Conditions

Certain conditions make recurrence far more likely than others. DISH, already discussed, essentially programs the body to lay down new bone along the spine and at entheses (the spots where tendons and ligaments attach to bone). Patients with DISH who undergo spur removal should expect regrowth and plan for monitoring rather than hoping for permanent resolution.³

Inflammatory arthritis conditions, including rheumatoid arthritis and spondyloarthritis, create an environment where bone remodeling at joint margins is ongoing. As the animal model research showed, even potent blockade of major inflammatory pathways does not prevent spur formation once structural joint damage has occurred.⁹ This does not mean biologic therapies are useless; they control the disease in many other important ways. But patients on these medications should not assume their bone spurs will stop forming as a result.

Osteoarthritis, the most common reason people develop bone spurs in the first place, is a progressive condition. Removing an osteophyte from an arthritic knee or hip treats a consequence of joint degeneration without halting the degeneration itself. If the cartilage continues to wear, the biomechanical signals that drove the original spur remain active. In joints with advanced arthritis, eventual joint replacement often becomes the definitive solution, not because it removes spurs specifically, but because it replaces the entire damaged surface and eliminates the bone-on-bone mechanics that produce them.

Heel Spurs and Plantar Fasciitis

Heel spurs occupy a slightly unusual place in this conversation because their relationship to pain is controversial. Many people have calcaneal (heel bone) spurs visible on X-ray and experience no symptoms at all. When heel pain does occur, it is often attributed more to plantar fasciitis, the inflammation of the thick band of tissue on the sole of the foot, than to the spur itself. The spur is a marker of chronic tension at the fascial attachment rather than the direct cause of pain in most cases.

This distinction matters for the recurrence question. Surgical removal of a heel spur without addressing the plantar fascia tension rarely resolves symptoms on its own, and the spur may regrow if the fascia continues pulling on the calcaneus. The association between obesity and symptomatic heel spurs is relevant here: heavier individuals place more load on the plantar fascia with every step, and that chronic overload feeds both fascial inflammation and spur formation.¹¹ For this reason, heel spur surgery is typically reserved for cases that have failed extensive conservative treatment, including stretching, orthotics, injections, and weight management. When surgery is performed, it usually involves partial release of the plantar fascia alongside spur removal, which changes the mechanical environment enough to reduce the recurrence stimulus.

Even then, recurrence of some degree of calcification at the calcaneal attachment is not uncommon, though clinically significant regrowth that causes renewed pain is less frequent than in the cervical spine or ankle. The chronic, low-grade nature of the mechanical stress in the heel means the spur-forming stimulus never entirely disappears in people who are on their feet regularly, but it also means the regrowth tends to be slow and often clinically silent.

1
PubMed. Bone spurs: mechanism of production of different shapes based on observations in Dupuytren’s diathesis
2
PubMed. Osteoblasts derived from osteophytes produce interleukin-6, interleukin-8, and matrix metalloproteinase-13 in osteoarthritis
3
PubMed Central. Postsurgical recurrence of osteophytes causing dysphagia in patients with diffuse idiopathic skeletal hyperostosis
4
PubMed Central. Anterior Cervical Osteophyte Resection for Treatment of Dysphagia
5
PubMed. Comparison of arthroscopic and open revision decompression for failed anterior acromioplasty
6
PubMed Central. Bony Regrowth and New Spur Formation as Possible Causes of Failed Distal Clavicle Excision—Mid-Term Outcomes after Revision Surgery in a Matched-Pair Analysis
7
PubMed Central. Surgical Management of Complex Ankle Bony Impingement Combined With Chronic Ankle Instability
8
PubMed. Surgical Excision of Heterotopic Ossification Leads to Re-Emergence of Mesenchymal Stem Cell Populations Responsible for Recurrence
9
PubMed. Tumor necrosis factor alpha and RANKL blockade cannot halt bony spur formation in experimental inflammatory arthritis
10
Journal of Neurosurgery. Regrowth of diastematomyelic bone spur after extradural resection
11
SAGE Journals / Foot & Ankle Orthopaedics. Association of Obesity and Plantar Fasciitis in Patients With Plantar Heel Spurs
12
PubMed Central. Controlled release of celecoxib inhibits inflammation, bone cysts and osteophyte formation in a preclinical model of osteoarthritis
13
PubMed Central. Outcomes of Revision surgery for surgically treated insertional Achilles tendinopathy