Dental implantology

The moment the implant is placed, a blood clot forms on its surface. Over the following days, bone cells (osteoblasts) migrate along that surface and lay down immature bone, known as woven bone. This is not solid bone yet: it is a fast biological scaffold, built in 2 to 4 weeks.

Then comes remodelling: that immature bone is progressively replaced by lamellar bone — dense and oriented along the forces of chewing. This second phase is what takes 3 to 6 months. By the end, 60 to 75% of the implant surface is in direct contact with bone, a figure known as BIC (bone-implant contact). There is no glue and no ligament: bone and titanium are fused.

This is exactly why smoking and poorly controlled diabetes are a problem: both reduce blood supply and slow osteoblast activity. It is not a matter of willpower, it is cell biology — and it is measurable.

Titanium is not chosen for its hardness but for its oxide layer. On contact with air it spontaneously forms a film of titanium dioxide (TiO₂) a few nanometres thick, chemically inert, which the body does not treat as a hostile foreign object. If that layer is scratched during placement, it reforms within milliseconds. This passivation is what makes the material biocompatible.

But two implants made of the same titanium are not equivalent: the surface micro-topography is what separates them. A smooth surface integrates slowly; a surface sandblasted then acid-etched (the SLA process), with an average roughness around 1.5 µm, multiplies the real contact area and markedly speeds up bone anchorage.

The latest generations go further with hydrophilic surfaces, stored in saline so they never touch air. Blood wets them instantly and completely, which shortens the critical healing phase from 6-8 weeks down to 3-4. That is a genuine clinical gain, not a marketing line — and it is one reason premium brands cost more.

Not all bone is the same. The reference classification (Lekholm & Zarb) describes four densities, from D1 (very dense cortical bone) to D4 (spongy, poorly mineralised bone). This is no small detail: the posterior mandible is typically D2 and solid, whereas the posterior upper jaw is often D4 and considerably more fragile.

Density determines primary stability — how firmly the implant is mechanically locked into the bone on the day of surgery, before any healing. It is measured objectively in two ways: insertion torque, expressed in newton-centimetres (Ncm), and resonance frequency analysis, which yields an ISQ value from 1 to 100.

In practice: in D4 bone the surgeon adapts the drilling protocol (under-drilling, bone condensation) to gain stability, and sometimes selects a different implant diameter or shape. This is precisely what the 3D scan lets us anticipate before you ever board the plane.

Fitting a tooth the same day is not a commercial option you tick: it is a biomechanical decision. The commonly accepted threshold is an insertion torque of at least 35 Ncm, or an ISQ above 70. Below that, the implant is left undisturbed.

The reason is specific. Until bone has fused with the implant, any micromovement above roughly 150 µm under chewing load prevents osteoblasts from attaching. Instead, the body produces fibrous tissue — a soft encapsulation. The implant holds for a few months, then loosens and is lost. This is the most common failure mechanism after over-optimistic immediate loading.

That is why a serious clinic will sometimes tell you no on the day of surgery, even though the quote mentioned immediate loading as a possibility. It is not backtracking: it is the only way to protect the ten-year result.

Between the implant and the abutment carrying the crown there is necessarily a junction — and therefore a micro-space, the microgap. Oral bacteria colonise it, and the resulting local inflammation drives bone resorption. The reference criteria (Albrektsson) tolerate up to 1.5 mm of loss in the first year, then 0.2 mm per year.

Two technical answers exist. The conical connection (Morse taper) creates a friction fit that strongly reduces bacterial leakage and micromobility. Platform switching uses an abutment narrower than the implant: the microgap is shifted inwards, away from the bone crest, which measurably preserves bone level.

One last point often left unsaid: screw-retained versus cemented crowns. A screw-retained crown is removable, which simplifies any future check or replacement. A cemented crown can be more aesthetic in some cases, but excess cement left under the gum is a recognised cause of peri-implantitis. We favour screw-retained whenever the implant axis allows — which is exactly what computer-guided surgery plans for.

An implant cannot decay, but it can lose its supporting bone. There are two stages: peri-implant mucositis, an inflammation limited to the gum and reversible; and peri-implantitis, once the inflammation reaches the bone and causes progressive bone loss. The second stage does not reverse without intervention.

Studies estimate that roughly one implant patient in five develops peri-implantitis within ten years. The risk factors are well identified: a history of periodontitis, smoking, uncontrolled diabetes, insufficient hygiene, excess cement, and a complete absence of follow-up.

Prevention is unglamorous but effective: daily interdental brushes or a water flosser, a professional check every 6 to 12 months with peri-implant probing, and a baseline radiograph kept from just after placement. Without that initial image, nobody can say years later whether the bone level has changed — which is why we systematically include it in your implant passport.