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03/09/2026

Can a bad bite cost an athlete power?

Seven young elite rowers completed a power test with and without a temporary artificial bite disturbance. With the disturbance, measured muscular power fell 17.7 percent (Leroux et al., 2018). Seven subjects, one session.

There is also a published case of a professional basketball player whose jaw symptoms and recurrent low back pain interrupted training. She improved after a combined splint and physiotherapy program (Baldini et al., 2012). One patient, no control group.

Then the story stops being tidy. Fifty young runners with and without malocclusion showed no meaningful difference in estimated maximal aerobic capacity (El Ouali et al., 2023). A 2026 review of 13 trials and 335 athletes found positive effects for some variables, neutral effects for others, and no universal benefit from bite aligning mouthguards (Cichelli et al., 2026).

The clinical takeaway is narrow. Treat pain, dysfunction, chewing limitation, trauma risk and interrupted training. Those are real reasons to intervene. Do not promise that braces or a splint will manufacture a medal.

Protect the athlete's teeth. Do not sell the podium.


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02/09/2026

The socket is closed. What did you close it with?

After an extraction, most of the attention goes to the graft inside the socket. The soft tissue over it gets treated as a lid.

Stimmelmayr and colleagues described another way in 2010. Fill the socket with a xenograft. Then prepare a supraperiosteal tunnel labial and palatal to the socket, and use a combination graft: the connective tissue portion slides into those tunnels, the epithelialized portion seals the opening.

The point of the tunnel is contact. It thickens the buccal soft tissue and increases the contact between the graft and the receptor site instead of leaving the graft sitting on the socket rim.

Honest limits. This was published as a described technique, not as a comparative trial. It does not stop buccal plate remodeling, and it does not answer whether this socket needed grafting in the first place. What it changes is the soft tissue you have to work with months later.

Closing a socket and preserving a ridge are two different goals.



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01/09/2026

Can you place an immediate implant in this molar socket? The answer sits in the septum.

Smith and Tarnow (2013) sorted molar extraction sockets into three types, based on where the implant actually finds its stability.

Type A. The coronal portion of the implant is completely contained within the interradicular septum.

Type B. The implant is stabilized but not completely contained by the septal bone. A gap remains between the implant and the inner socket walls.

Type C. No septal bone is available for stabilization. A wide diameter implant has to engage the inner socket walls, or bone apical to the socket, to be stable.

The classification does not tell you whether to place. It tells you where your primary stability is coming from, and how much of it depends on bone you should already have measured on the CBCT before the tooth comes out.

Type C is the one that quietly changes the plan.



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30/08/2026

Why perforate healthy cortical bone before you graft on top of it?

In this anterior maxilla the plate is decorticated on purpose, right before the guided bone regeneration. The reason is access: open marrow spaces let vessels and progenitor cells reach the graft from the bone underneath, and not only from the periosteum above.

The mechanism is plausible and the step costs seconds. What it buys you in measurable bone volume at reentry is less settled in humans than the routine suggests, and the comparative clinical studies are few.

So perforate for a reason you can say out loud, and do not expect it to rescue a graft that has no space or no primary closure.



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Is periodontitis caused by one bacterium?Porphyromonas gingivalis became the famous name because of the keystone-pathoge...
28/08/2026

Is periodontitis caused by one bacterium?

Porphyromonas gingivalis became the famous name because of the keystone-pathogen hypothesis: an organism present in low abundance can help tip the host-microbe balance and push a biofilm toward dysbiosis (Hajishengallis et al., 2012).

The Honest Truth is that P. gingivalis does not act alone. The red complex described by Socransky in 1998 gave us a useful map, and the oral microbiome catalogued since then is far wider than three names (Dewhirst et al., 2010). Periodontal destruction is built by a microbial community, the host inflammatory response, individual susceptibility, time, and clinical behavior.

That changes what you are treating. Not one culprit to eliminate, but an ecosystem to disrupt and then keep disrupted.

The pocket is an ecosystem. Treat it like one.

References: Socransky et al., 1998; Dewhirst et al., 2010; Hajishengallis et al., 2012; Hajishengallis and Lamont, 2012 and 2021.


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Are you probing the pocket, or the crown contour?In a 2026 cross-sectional study of 61 patients and 83 implants, mean pr...
27/08/2026

Are you probing the pocket, or the crown contour?

In a 2026 cross-sectional study of 61 patients and 83 implants, mean probing depth increased by 0.887 mm after the prosthesis was removed.

Maximum probing depth without the prosthesis showed better diagnostic accuracy for peri-implantitis. But the story is not simply that crown off is better. When probing depth was combined with bleeding or suppuration, diagnostic performance did not differ significantly between examinations with and without the prosthesis.

The measurement gap was larger around anterior implants, concave emergence profiles, and implants with peri-implantitis.

This was a single center study on implants restored with removable prostheses. It does not justify routine crown removal.

Practical takeaway: treat probing as a measurement through a prosthetic access corridor. Chart six sites, use light force, record bleeding or suppuration, compare with baseline and radiographs, and document when contour limits access. Remove the prosthesis only when that uncertainty could change the decision.

References: Xu et al., 2026; Renvert et al., 2018; Yi et al., 2020.



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26/08/2026

A socket can heal and the ridge can still lose its shape. Those are not the same result.

After an extraction, clot, vessels, osteoblasts and woven bone gradually fill the socket. At the same time the walls model and remodel, and the thin facial wall is usually the one that pays for it.

That is why three outcomes get confused. Vital bone percentage in a biopsy is a histologic result. Change in the external ridge contour is a dimensional result. Whether you can still place and restore an implant is a clinical result. They are related, but they are not interchangeable.

A 2026 randomized trial compared four grafted non-molar groups at 18 to 20 weeks. Vital bone percentages differed, yet within those groups the percentage in the sampled core was not significantly associated with changes in ridge width or facial and lingual height (Foster et al., 2026).

Across the wider evidence, alveolar ridge preservation can reduce dimensional loss. It does not freeze the ridge, guarantee more vital bone, or promise that later augmentation will be unnecessary (Atieh et al., 2021; Canullo et al., 2022; Fok and Jin, 2024).

So the question after an extraction is not only whether the socket healed. It is whether the architecture fits what you plan to do next.


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25/08/2026

Two classic studies on immediate implants are quoted to defend opposite habits. Read the methods and the disagreement mostly disappears.

Araujo 2006 and Blanco 2008 are both dog studies on implants placed straight into fresh extraction sockets. They are not interchangeable. The implants sit differently in relation to the buccal wall, the diameters are not the same, and the flap handling differs. Change where the implant sits and whether you raise a flap, and you have changed the biology you are measuring.

What both models keep showing is the uncomfortable part. The buccal bundle bone belongs to the tooth, and it remodels once the tooth is gone. Placing an implant in the socket on the same day does not switch that off.

What surgical decisions can still influence is how much buccal plate is standing when healing is finished. That is a different claim, and a much smaller one, than saying immediate placement preserves the ridge.

These are animal models. They explain mechanism. They do not hand you a survival rate for the patient in your chair.

So before you cite a paper to justify a protocol, check that the surgery in the paper is the surgery you are actually performing.



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24/08/2026

Can periodontitis in a parent leave a trace in a child's gut?

A 2026 study compared 80 parents and children across four groups. Parents with periodontitis showed distinct faecal microbial profiles, and related patterns appeared in their children. Both groups also had higher urinary claudin-2, a marker used in intestinal barrier research (Paz et al., 2026).

Earlier work had already reported different oral microbial communities in children of parents with periodontitis. But families share far more than genes: diet, environment, hygiene routines, physical contact and access to care all shape how similar two microbiomes look.

Here is the honest boundary. This was a small cross-sectional study with 20 participants per group. It did not show strain-level transmission, it did not show direction, it did not show intestinal disease or future risk, and it did not test whether treating the parent changes anything in the child.

So treat it as a family-level signal, not a diagnosis. It is a good reason to talk about periodontal health as something that lives in a household, not only in one mouth.



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