The role of Bone in the acute stress respond

I’m increasingly receiving requests for help with various periodontal conditions. People are often frightened and worried about gum recession — yet, in fact, this is the least of their problems.

When I tell them this, their faces show surprise.

The gum doesn’t float in the air or in the wind; it’s firmly attached to the jawbone and the roots of the teeth. Therefore, gum recession means that the underlying bone has receded — the gum simply follows the bone.

Here arises an essential question, one that dental medicine still doesn’t have a clear and definitive answer to: why does the bone resorb?

We can suspect many factors — infectious, inflammatory, poor hygiene, dental crowding that exerts uneven pressure on the ligaments (leading to their and the bone’s wear), comorbidities, and others. Yet often, these factors are not active, and the bone still recedes.

For a long time, based on clinical experience, I had suspicions — but you know how it is: until you see clear, black-and-white evidence, they remain personal observations or speculations.

Recently, however, an important step forward has been made toward understanding!

Detailed research began in the 1990s, with concrete results emerging only around 2017, and clearer certainties toward the end of 2019.

I can’t cover all the materials studied, so below is a very brief conclusion:

🔗 https://scitechdaily.com/your-bones-secrete-a-stress-hormone-causing-fight-or-flight-response/

Let’s recall a few things about bone.

Bone is a hybrid tissue, a composite material made up of:

Organic matrix — mainly type I collagen, resembling strong ropes that provide flexibility.

Inorganic matrix — hydroxyapatite crystals (Ca₁₀(PO₄)₆(OH)₂), which give hardness and strength.

To bond these two components firmly, bridge molecules are needed. The key “manager” protein is osteocalcin. Working alongside it are osteopontin, bone morphogenetic proteins, proteoglycans, fibronectin, and tenascin C.

How is osteocalcin produced?

It’s synthesized by osteoblasts, the bone-forming cells.

After synthesis, osteocalcin is carboxylated with the help of vitamin K — an essential step that allows it to bind calcium with high affinity.

The binding mechanism is as follows:

Collagen forms a fibrous network in the bone matrix on which hydroxyapatite crystals (rich in calcium and phosphate) are deposited.

Osteocalcin, with its negatively charged carboxylated sites, binds strongly to the positively charged calcium ions on the crystal surface.

At the same time, another region of osteocalcin interacts with collagen — thus anchoring the crystal to the organic molecule.

Osteocalcin acts as a molecular anchor — one end attaches to mineral crystals through calcium, the other to collagen, resulting in solid yet flexible bone capable of absorbing shocks without fracturing easily.

What happens if osteocalcin is missing or not carboxylated?

Minerals no longer bind efficiently to collagen, leading to more porous, fragile bone. This can be seen, for example, in vitamin K deficiency, when osteocalcin remains undercarboxylated or uncarboxylated — weakening calcium bonds and increasing fracture risk.

In short, osteocalcin has two roles:

A structural role, long known — acting as a “molecular adhesive” that contributes to bone’s mechanical strength, as described above.

A hormonal role, discovered more recently.

A portion of osteocalcin is released into the bloodstream in its bioactive form, involved in stress response (it inhibits parasympathetic tone and supports sympathetic tone), regulates glucose and insulin metabolism, and supports muscle function, memory, and male fertility.

But what happens when osteocalcin is more active than it should be?

What happens when stressors are no longer occasional — not a predator or a survival need — but daily: your boss, emails, deadlines, partner, neighbor, coworker, financial worries, constant pressure?

When you’re exposed for more than an hour, a day, or a week to this kind of stress and your body must repeatedly activate the acute stress response?

Then certain endocrine-metabolic mechanisms deteriorate, requiring special attention to restore adaptive balance.

Studies show that women report stress and anxiety symptoms more frequently than men — partly due to hormonal profile, a coping style more oriented toward relationships, and partly due to multiple roles and social pressures.

After age 40, especially in women, a form of periodontal disease or osteoporosis may appear. The issue isn’t necessarily peri-menopause, or low protein or calcium intake — but that osteoblasts release osteocalcin as a mediator of the acute stress response, not just as a marker of bone formation.

It has even been observed that even in the absence of glucocorticoids and catecholamines (e.g., in adrenalectomized animals), osteocalcin can maintain a normal adaptive stress response due to high blood levels.

Osteocalcin evolved to respond to acute stress (escaping predators, intense effort), where it doesn’t have time to damage bone.

But if this mechanism is triggered frequently or chronically (through continuous sympathetic and cortisol activation), bone will suffer — both from reduced vascular perfusion (via constant activation of alpha-sympathetic receptors in arterioles) and from the depletion of its essential molecular “glue.”

As a result, bone enters a net resorption process, leading to bone mass loss and increased osteoporosis risk.

I’ve presented an extremely simplified mechanism — in reality, the neuroendocrine axes can cascade into numerous other peripheral imbalances as the body struggles to cope with chronic stress.

Alongside dental treatments, it’s clear that a multidisciplinary approach is needed.

I encourage you to invest time in understanding the connection between your physiology and your psyche — between your organic reactions and the way you live.

There are no universal recipes or solutions, no simple algorithms that work for everyone, no dictionary of causes or remedies — because we are all unique.

If you’re facing any form of periodontal disease, whether early or advanced (note that “periodontosis” is a popular term that doesn’t necessarily reflect the actual state of the supporting tissues), I warmly invite you to learn more about the mechanisms behind it — and about yourself.

This way, you’ll increase your chances of close monitoring and halting the progression of the condition.