Your screening form could be missing five drug classes that can destroy the jawbone. Here’s how you can ensure you don’t miss them. 

The Bisphosphonate Blind Spot

Most implant clinicians have a bisphosphonate protocol down pat: 

Ask about alendronate. Check the duration of therapy. Consider CTX testing. Perhaps request a drug holiday.

You’re doing everything right. Except you’re screening for one pathway to osteonecrosis while missing five others.

Here’s what nobody tells you: bisphosphonates represent just one mechanism of drug-induced osteonecrosis of the jaw. The condition we should actually be calling DIONJ—Drug-Induced Osteonecrosis of the Jaw—has expanded well beyond its original medication associations.

And if your screening form only asks about bisphosphonates, you’re missing patients at significant risk.

Let me show you what’s changed and what you need to be screening for.

Why DIONJ Rather Than MRONJ?

The terminology evolution tells you everything about how our understanding has expanded.

BRONJ (Bisphosphonate-Related ONJ) was the original term, reflecting early identification with bisphosphonate use. Made sense at the time—that’s what we knew.

MRONJ (Medication-Related ONJ) expanded recognition to include denosumab and other antiresorptives. (Getting warmer.)

DIONJ (Drug-Induced ONJ) encompasses all pharmacological agents affecting jaw bone biology. This is the accurate term for current understanding.

The shift from BRONJ to MRONJ to DIONJ isn’t just semantic pedantry—it reflects a fundamental expansion of risk factors that changes how we should screen every implant patient.

The Five Additional Drug Classes (That Aren’t on Your Form)

Right. Let’s get into what you’re actually screening for.

Class 1: Antiangiogenic Agents

These are typically prescribed for metastatic cancer, particularly colorectal, lung, and renal cell carcinoma. Your patient might not volunteer this information unless you ask the right questions.

Examples:
Bevacizumab (Avastin), sunitinib, sorafenib

Mechanism:
VEGF inhibition—blocking vascular endothelial growth factor signalling. Here’s why that matters: VEGF is essential for angiogenesis during wound healing. Block the signalling, compromise the healing.

Jaw impact:
Without adequate angiogenesis, post-surgical bone healing is severely compromised. The tissue can’t rebuild the vascular network it needs.

Risk level: 

High when actively on therapy

Class 2: Tyrosine Kinase Inhibitors (TKIs)

These are commonly prescribed for chronic myeloid leukaemia and gastrointestinal stromal tumours. Again, not information that typically comes up when you ask “Are you on bisphosphonates?”

Examples:
Imatinib (Gleevec), dasatinib, nilotinib

Mechanism:
Targeted inhibition of specific cellular pathways, including those affecting bone metabolism. TKIs don’t just affect cancer cells—they affect normal cellular signalling, including in bone.

Jaw impact:
Multiple pathways of bone metabolism get disrupted. The specifics vary by agent, but the outcome is compromised bone healing and remodelling.

Risk level:
Moderate to high, depending on specific agent and duration

Class 3: Corticosteroids

Long-term steroid use is incredibly common—asthma, COPD, inflammatory bowel disease, rheumatoid arthritis, organ transplant patients. These patients are everywhere in general practice.

Examples:
Prednisone, prednisolone, dexamethasone

Mechanism:
Broad immunosuppression and effects on bone metabolism. Steroids affect virtually every aspect of bone biology—cell proliferation, differentiation, and mineralisation.

Jaw impact:
Suppressed bone formation, impaired healing, increased infection risk.

Critical note:
Corticosteroids invalidate CTX bone turnover testing. This is crucial. A patient on long-term steroids can have a “normal” CTX reading that provides completely false reassurance. The test is meaningless in this population.

Risk level:
Dose and duration dependent, but significant with long-term use

Class 4: mTOR Inhibitors

Typically prescribed for renal cell carcinoma and as immunosuppression in transplant patients. Often used in combination with other agents, which compounds risk.

Examples:
Everolimus (Afinitor), temsirolimus

Mechanism:
Inhibition of the mechanistic target of rapamycin, affecting cell proliferation and survival. mTOR is a critical regulator of cell growth and metabolism.

Jaw impact:
Impaired cellular response to surgical trauma, compromised healing cascade.

Risk level:
Moderate, but additive with other immunosuppressive agents

Class 5: Radiopharmaceuticals

Used specifically for bone metastases from prostate cancer. If your patient has been treated for metastatic prostate cancer, this should trigger immediate inquiry.

Examples:
Radium-223 (Xofigo)

Mechanism:
Delivering targeted radiation to bone tissue. The drug mimics calcium and deposits in areas of high bone turnover—which is exactly where metastases tend to form.

Jaw impact:
Similar considerations to head and neck radiation therapy. The jawbone receives ongoing radiation exposure that compromises its healing capacity and infection resistance.

Risk level:
High

CTX Testing: What It Can and Can’t Tell You

CTX (C-terminal telopeptide) testing measures bone turnover markers. It’s a useful tool when used correctly. But it has significant limitations that can provide false reassurance if you’re not aware of them.

Validity Conditions (When CTX Actually Works)

CTX is only valid when all of these conditions are met:

Miss any of these, and the result is unreliable.

Interpreting Results

CTX below 100 pg/mL indicates severely suppressed bone turnover with high DIONJ risk. This is your red flag.

Critical limitation: CTX is invalid in patients on steroids, methotrexate, or with active cancer. A “normal” result in these populations provides false reassurance. You’re getting a number, but the number doesn’t mean what you think it means.

This matters because many of the patients on the five drug classes above will also be on steroids or have active cancer—exactly the populations where CTX is unreliable.

So what do you do? You rely on the drug history itself, not the biochemical marker. If the patient is on high-risk medications, treat them as high-risk regardless of CTX.

The Screening Form Revolution

Here’s the practical implementation that changes everything.

Current Approach (Inadequate)

“Are you on bisphosphonates?”

This question captures one drug class out of six. You’re screening for 17% of the risk.

Better Approach (Comprehensive)

“Are you taking any medications that affect your bones, blood vessels, or immune system?”

This opens the conversation to the full spectrum of relevant medications.

Specific Probes

Follow up with targeted questions:

These questions capture the clinical scenarios where high-risk medications are prescribed.

Implementation in Practice

Update your medical history form. Train your reception staff on which responses trigger clinical review. Create a protocol for patients who screen positive.

This isn’t complicated. It’s just comprehensive.

The Question You Need to Answer

DIONJ risk assessment must extend beyond bisphosphonates.

Five additional drug classes affect jaw bone biology in ways that compromise surgical outcomes: antiangiogenics, tyrosine kinase inhibitors, corticosteroids, mTOR inhibitors, and radiopharmaceuticals.

Each class has distinct mechanisms, but all share the capacity to impair bone healing and increase osteonecrosis risk.

So here’s the question: How many of these drug classes appear on your current screening form?

If the answer is “none” or “just bisphosphonates,” you’re screening for historical understanding, not current evidence.

At the Academy iof Implant Excellence, we teach the biology behind the protocols. Understanding DIONJ pathophysiology across all relevant drug classes is one example of the depth that changes practice. Not because it’s complicated, but because most training providers are still teaching BRONJ protocols from 2010.

And once you understand the full scope of drug-induced osteonecrosis risk, you can’t go back to asking only about alendronate.

Ready to Understand the Biology Behind the Protocols?

The Academy of Implant Excellence teaches system-agnostic, biology-first implant training. From single implants to full-arch mastery. 80+ hours of depth that covers the invisible 10% where complications happen.

Because protocols work until they don’t.

Explore Academy Training →

References

  1. Marx RE. Oral and Maxillofacial Pathology. In: Hupp JR et al. Contemporary Oral and Maxillofacial Surgery. 7th ed. Elsevier, 2024.

  2. Ruggiero SL et al. AAOMS Position Paper on MRONJ—2022 Update. J Oral Maxillofac Surg. 2022.

  3. Resnik RR, Misch CE. Misch’s Avoiding Complications in Oral Implantology. Elsevier, 2018.

Your implants are ageing. Right now. In the drawer.

Every Implant Has a Birthday

The day it was manufactured, sterilised, and sealed in packaging. From that moment, a biological clock starts ticking.

And here’s what nobody tells you: this clock measures the progressive degradation of surface bioactivity—hydrocarbon contamination from just sitting in the atmosphere. So, by the time an implant reaches your surgical tray, weeks or months after manufacture, it’s no longer biologically fresh.

The phenomenon is called biological ageing, and understanding it fundamentally changes how you think about implant success and failure.

More importantly, there’s a protocol that reverses it: photofunctionalisation.

Let me show you the mechanism, the evidence, and the clinical protocol that can transform outcomes in your practice.

What They Don’t Teach You

Traditional implant education focuses on what you control: surgical technique, bone quality assessment, primary stability, loading protocols, and prosthetic design.

These matter. (Obviously.) But they don’t tell the whole story.

What conventional training overlooks—and I mean completely overlooks—is that the implant itself is a biological variable. The surface that contacts bone isn’t static. It changes over time, and not for the better.

Most courses teach surface roughness as if it’s the only thing that matters. You learn about SLA, anodisation, and micro-topography for osteoblast attachment—all important stuff.

What you don’t learn is that these carefully engineered surfaces start degrading the moment they’re exposed to air.

I spent years placing implants before I understood this, genuinely wondering why some cases in “good bone” struggled, why identical techniques produced different outcomes.

I’d review everything: Did we achieve adequate primary stability? Was healing sufficient? Could there have been contamination?

All reasonable questions. All missing the point.

Because the root cause predated the surgery entirely: The implant was already compromised before I opened the package.

The Biology They Should Have Taught You

Titanium isn’t biologically inert. The oxide layer that forms on titanium surfaces, the layer responsible for biocompatibility, actively interacts with its environment.

In sterile manufacturing conditions, this surface has high surface energy and excellent hydrophilicity, perfect for blood contact, protein adsorption, and cell attachment.

Once it’s exposed to air, hydrocarbons start depositing on the surface. You can’t see it, can’t smell it, but it’s happening.

Within four weeks of manufacture, the surface properties have measurably degraded. Four weeks. That’s it.

The Ogawa Research (Or: The Data That Should Change Everything)

The research quantifying this comes primarily from Takahiro Ogawa and colleagues at UCLA. Their work demonstrated that aged titanium surfaces show:

Reduced surface energy

Increased water contact angle (loss of hydrophilicity)

Reduced osteoblast attachment by approximately 50%

Compromised bone-to-implant contact potential

The biological consequence? Significant doesn’t even cover it.

Fresh surfaces achieve BIC values that aged surfaces simply cannot match. In controlled studies, aged surfaces achieved approximately 55% BIC while photofunctionalised surfaces achieved 98.2% BIC.

Read that again. 55% versus 98.2%.

This isn’t a marginal difference—this is a fundamentally different biological response. Same implant design, same surgical technique, completely different biology.

Why This Happens

The mechanism is straightforward once you understand it. Hydrocarbons on the surface interfere with the initial protein adsorption cascade that precedes cell attachment. When blood contacts a contaminated surface, the biological signalling that recruits osteoblasts gets compromised.

The implant still integrates. Sure. But not optimally.

The surface that could have achieved near-complete bone contact settles for partial integration, and you never know what you’ve left on the table.

This explains those clinical observations that used to drive me mad: Why do some implants perform better than others in identical conditions? Why does the same surgeon see different healing patterns with the same implant system? Why do some cases in “favourable” conditions still struggle?

Surface age is one variable among many, but it’s been systematically overlooked. And that needs to change.

Clinical Implications: When Surface Conditioning Actually Matters

Understanding biological ageing reframes how you make clinical decisions. Instead of treating all implants as equivalent (which they’re not), you can stratify risk based on what you actually know.

Strong Indications for Photofunctionalisation

Compromised host situations where optimal integration is critical:

You know the patients I’m talking about: diabetic patients with HbA1c at the upper acceptable limit, history of smoking (recently quit), older patients with reduced bone density.

Any systemic factor that narrows the margin between success and failure. In these cases, every biological advantage matters.

Immediate loading protocols where rapid stability is required:

Here’s what the research shows: the characteristic ISQ dip at three weeks—that period when primary mechanical stability transitions to secondary biological stability—gets eliminated with photofunctionalised surfaces.

This means loading timelines can potentially be compressed in appropriate cases.

Immediate loading criteria expand, and the margin of safety in challenging cases increases.

Cases with marginal primary stability where you need every advantage:

Type IV bone, compromised extraction sockets, and situations where the mechanical foundation is less than ideal. You’re already on the edge—why wouldn’t you optimise the biology?

Moderate Indications

Implants stored longer than four weeks:

If you’re unsure how long an implant has been sitting in your inventory (and let’s be honest, who actually tracks this?), surface conditioning provides insurance.

Final abutment placement:

Soft tissue integration benefits from surface conditioning with argon plasma. Research from Canullo and colleagues has demonstrated benefits particularly for abutment surfaces.

The Evidence on Outcomes

Funato and colleagues demonstrated that photofunctionalised implants reach a stability plateau in 2 months compared to 4 months for untreated surfaces. The characteristic stability dip at three weeks? Gone.

So, immediate loading criteria expand, the margin of safety in challenging cases increases, and loading timelines compress in appropriate cases. All from treating the surface properly.

Important caveat—and I mean this:

Photofunctionalisation does not replace sound surgical principles. It enhances the biological response to surgery that’s already performed correctly. You can’t rescue poor surgical technique with surface treatment. Don’t even try.

The Protocol Framework

How Photofunctionalisation Works

You expose the implant surface to UV-C light at 254nm wavelength. This specific wavelength has sufficient energy to break the carbon-carbon and carbon-hydrogen bonds in hydrocarbon contaminants. The treatment removes the contamination layer and restores superhydrophilicity.

Treatment duration: Varies by device. 12–48 minutes for old school devices. Modern devices take just 60 secs. (Yes, that quick!)

Critical timing: Treatment must be performed immediately before placement. The refreshed surface will begin accumulating contaminants upon atmospheric exposure.

Clinical Decision Gates

Here’s where most courses hedge: “It depends.” Yeah. I’m not doing that.

STRONG RECOMMENDATION:

Compromised host situations

Immediate loading protocols

MODERATE RECOMMENDATION:

Implants stored > 4 weeks

Cases with low primary stability

Final abutment placement (consider argon plasma or UV-C)

Clear enough?

Practical Implementation

The workflow integration is about as straightforward as it gets.

Place the UV-C device in your surgical suite. While you’re preparing the surgical site, the implant is being treated. By the time your osteotomy is complete, the implant is ready with a freshly activated surface.

The workflow adds minimal time. The biological advantage is potentially significant. Worth it? Absolutely.

Alternative: Argon Plasma Treatment

Similar mechanism—removing organic contamination. Research from Canullo and colleagues has demonstrated benefits particularly for abutment surfaces where soft tissue integration is the priority. Another tool in the arsenal.

The Question You Need to Answer

Biological ageing is not theoretical. It’s documented, measurable, clinical, and real.

The evidence base supports surface conditioning as a method to optimise outcomes, particularly in cases where the margin for error is narrow.

The question isn’t whether your implants age. They do. Right now. In your drawer.

The question is whether you’ll continue treating all surfaces as equivalent, or whether you’ll integrate this knowledge into your clinical decision-making.

Can you skip photofunctionalisation? Sure. The 90% of straightforward cases will probably be fine.

But here’s the thing:

If you’re reading this, you’re not interested in “probably fine.” You’re interested in understanding the invisible 10%—the biological variables that separate predictable integration from cases that struggle. You want to stack every biological advantage in your patient’s favour when the margin between success and failure narrows.

That’s the difference between competence and mastery.

At the Academy, we teach the biology behind the protocols. Understanding biological ageing is one example of the depth that changes practice. Not because it’s complicated, but because most clinicians never learned it.

And once you understand it, you can’t unknow it. Excellence stops being optional.

Ready to Understand the Biology Behind the Protocols?

The Academy of Implant Excellence teaches system-agnostic, biology-first implant training. From single implants to full-arch mastery. 80+ hours of depth that covers the invisible 10% where complications happen.

Because protocols work until they don’t.

Explore Academy Training →

References

  1. Att W, Ogawa T. Biological aging of implant surfaces and their restoration with ultraviolet light treatment: a novel understanding of osseointegration. Int J Oral Maxillofac Implants. 2012;27(4):753-761.
  2. Aita H, Hori N, Takeuchi M, et al. The effect of ultraviolet functionalization of titanium on integration with bone. Biomaterials. 2009;30(6):1015-1025.
  3. Funato A, Yamada M, Ogawa T. Success rate, healing time, and implant stability of photofunctionalized dental implants. Int J Oral Maxillofac Implants. 2013;28(5):1261-1271.
  4. Ogawa T. Ultraviolet photofunctionalization of titanium implants. Int J Oral Maxillofac Implants. 2014;29(1):e95-e102.
  5. Canullo L, Tallarico M, Unique A, et al. Plasma of argon treatment of the implant surface for soft tissue integration: a pilot study. Clin Implant Dent Relat Res. 2023;25(1):117-125.
  6. Elkhidir Y, Cheng Y. Photofunctionalization of titanium implants: an alternative approach. J Dent. 2017;61:54-59.
  7. Suzuki T, Hori N, Oharai Y, et al. Ultraviolet treatment overcomes time-related degrading bioactivity of titanium. Tissue Eng Part A. 2009;15(12):3679-3688.