Advanced Implantology Workgroup

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Advanced Implantology Workgroup

Page about oral implantology. Clinical cases and last trends in oral implantology.

23/08/2026

The hardest part of immediate placement is not the osteotomy. It is the case you decide not to do.

Place into a fresh socket and the buccal plate, the jumping distance and the gap graft stop being separate problems. They become one decision taken in a single appointment. Select well and the biology cooperates: clot, then woven bone laid straight onto the threads, then remodeling. Select badly and no drilling protocol rescues it.

Where is your own hard stop? Thin or fenestrated buccal plate, active suppuration, or insufficient primary stability. Which one makes you close the socket and come back later?

22/08/2026

When you place a connective tissue graft, are you adding thickness or are you giving the epithelium an instruction?

Karring, Lang and Loe reported in 1975 that gingival connective tissue transplanted without its epithelium was later covered by keratinized epithelium, while connective tissue taken from alveolar mucosa behaved differently. The tissue underneath can influence what differentiates on top.

That is the elegant part. The honest part is that a CTG also works through thickness, vascular support, wound stability, collagen architecture and flap behaviour, and none of that comes free with the graft. A tooth is also not an implant. With no periodontal ligament, the biological environment around an implant is not the same one those classic experiments described.

So the takeaway is not "graft it and it keratinizes". It is: build the surgical conditions where connective tissue biology can do its work.

Around implants, when do you still reach for an autogenous CTG instead of a substitute matrix?

21/08/2026

One exposed rough thread on the pre-crown radiograph is easy to dismiss. In Moser and colleagues' 2026 cohort of 261 implants, the 87 implants with interproximal bone loss exposing the rough surface before the definitive prosthesis showed 67.8% long-term survival versus 98.3% when the surface stayed covered, and peri-implantitis in 63.2% versus 5.2%.

Retrospective data with unequal follow-up between groups, so read it as a warning marker, not a verdict. A small amount of early remodeling is not automatically pathology.

The practical move: probe and take a standardized periapical radiograph at prosthesis delivery, record that post-remodeling baseline, and treat early rough-surface exposure as a finding to investigate rather than file away.

20/08/2026

Researchers detected gingipains from a gum-disease bacterium inside postmortem Alzheimer's brain tissue. That is a biological clue, not a causal verdict.

Dominy and colleagues (2019) reported gingipain levels tracking with tau and ubiquitin pathology. A 2025 umbrella meta-analysis found a 26% higher risk of cognitive disorders in periodontitis cohorts, at low to moderate certainty (Qadir et al., 2025).

The boundary that matters: a Mendelian-randomization study found no genetic causal signal, and a 643-participant gingipain-inhibitor trial missed both co-primary endpoints in the overall population (Hu et al., 2024; NCT03823404).

Treat periodontitis because it destroys periodontal support. Do not promise patients that periodontal treatment prevents Alzheimer's disease.

19/08/2026

Is a 6 mm implant a way around the sinus lift, or a different operation with its own entry criteria?

A 10-year randomised trial found no significant survival difference against sinus lift with longer implants (96.0 versus 100 percent, p = .24), alongside fewer surgical complications and less chair time. A 2026 pooled analysis across mixed indications pointed the other way: paired risk ratio 0.920 (confidence interval 0.857 to 0.987), favouring longer implants at ten years.

Both sets of numbers are real. What sits between them is patient selection.

That was Monday's issue of The Periospot Brew, the weekly read for clinicians who want the evidence with the caveats left in. Free, one email a week.

18/08/2026

Can the gums outside tell you anything about the membrane inside?

Before a lateral window, most of us judge the Schneiderian membrane on CBCT and hope the elevation goes clean. Aimetti and colleagues reported an association: a thick gingival phenotype came with thicker membranes, around 1.26 mm on average, and a thin phenotype with around 0.61 mm. Later CBCT work has looked at the same relationship.

Treat it as a clue, not a rule. Membrane thickness also moves with odontogenic infection, sinus health, allergies, smoking, septa and the measurement method itself. A thin phenotype is not an automatic perforation, and a thick one will not save you from one.

Still, it costs you two seconds in the pre-op exam. What does your experience say?

17/08/2026

When did you last probe around an implant that had no symptoms?

Peri-implant bone loss is usually silent. Biofilm colonizes the surface, the mucosa inflames, and the crater deepens thread by thread before anything hurts. The only stage that is reliably reversible is mucositis, and you only catch it if you probe and radiograph on a schedule instead of waiting for a complaint.

Reported prevalence swings widely depending on the case definition used, which is exactly why a fixed recall protocol beats a gut feeling.

Watch the progression, then check your own recall interval.

16/08/2026

A graft can look consolidated on the radiograph and still be mostly scaffold.

Radiopacity tells you mineral is present. It does not tell you how much of it is living bone. Most substitutes act primarily as osteoconductive scaffolds, and what happens next is host response: stable clot, vascular access, host cells depositing osteoid, woven bone bridging the scaffold, remodeling over time.

Resorption differs by material. Some particles disappear relatively quickly. Slow resorbing mineral may remain in the site for years, sometimes surrounded by bone, sometimes by connective tissue. Human biopsies commonly show new bone, marrow or connective tissue, and residual graft together. Residual particles are not automatic failure, and fast resorption is not automatic success.

So the argument worth having: how much of your result comes from the material you opened, and how much from clot stability, space maintenance and barrier choice, and defect morphology?

14/08/2026

In 1976 immediate placement was called reckless. What changed since then was not the answer, it was the question.

Willi Schulte put a ceramic implant into a fresh socket in Tübingen and it failed. The idea sat buried for two decades, until Schropp showed that extraction alone costs roughly half the ridge width in the first 12 months. The socket was already the problem.

Then the 2005 Araújo and Lindhe dog study scared the field off immediate placement, and almost nobody asked how it had been done. Juan Blanco changed the variables: flapless, narrower implant, palatal position, and the buccal loss dropped. Joseph Kan turned it into a repeatable protocol. In 2011 Araújo and Lindhe themselves showed that grafting the buccal gap helps.

The debate was never whether to place immediately. It was how.

Where do you draw your own line on immediate placement in the anterior maxilla?

13/08/2026

The nasopalatine canal is not an empty hole in the anterior maxilla. It is a neurovascular corridor.

In one CT study of severely resorbed ridges, the canal opening occupied a mean 35.6% of the area available for implant placement (Mardinger et al., 2008).

Reviews report high implant survival in selected canal-management cases, but the evidence is small and heterogeneous, and neurosensory change is a real reported outcome.

Map the shape before you plan the trajectory.

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