We are born with calcium in our teeth and bones. Osteoblasts and odontoblasts fix calcium and phosphorus, and then precipitate the product onto an organic matrix; this is the process of physiologic biomineralization involving apatite minerals. We are supposed to die with calcium in our bones and teeth, and nowhere else. However, as a result of “ageing” and disease states, typically disease states with an inflammatory component, we calcify our blood vessels and internal organs. Consider the following examples of this “pathological calcification”.
Soft tissue calcification
♦ Gall stones
♦ Pineal gland
calcification - “Brain Sand”
♣ Dysfunctional areas
in the brain ♦
Atherosclerotic arteries & veins
♣ Diseased organs
♦ Cardiac skeleton
♣ Prostate Stones
Kidney stones & PKD
Damaged cardiac valves
What do they have in common? Why does pathological calcification occur? Sure, urease producing common bacteria can alter urine pH to favor precipitation of minerals into struvite stones, but what causes the other 85% of stones that form at physiologic pH and urine mineral concentrations? What makes diseased arteries calcify? We didn’t get an explanation in medical school. Pathological calcification doesn’t have anything to do with high or low dietary calcium intake. It just occurs (??? No Explanation-Idiopathic) and we accept this; this is what our professors told us. We consider extra-osseous calcification to be inevitable, predictable, and sometimes helpful. Remember from the pre-CT days, when a shift from midline of pineal calcium was used to diagnose subdural hematoma in a head trauma patient, or when breast calcification was used as an early marker for malignancy? The research available shows us that pathological calcification, wherever you find it, is actually calcified nanobacteria in a semi-dormant state.
Ralph Lev MD, a cardiovascular surgeon by training, gave two lectures at a workshop that I attended. Dr. Lev told us that he got tired of operating on the same people over and over, so he began to look at and treat the factors underlying their recurrent atherosclerosis. This is the same guy, who as a university cardiovascular surgeon, described Lev’s disease, a condition we all learned about in medical school. Lev described a common, age related or idiopathic condition, whereby the cardiac skeleton demonstrates slowly progressive pathological calcification. The conduction system is affected, resulting in pathological bradycardia or heart block, requiring pacemaker implantation. I guess that Lev reasoned that if abnormal calcification was part of the problem, then calcium removal would be part of the solution. Lev was right. Pathological calcification is part of the problem, but why does it occur?
Nanobacterium sanguineum fixes calcium and phosphorus and converts it into carbonate apatite, the form in which these minerals are found in pathologically calcified tissue. N. sanguineum can be cultured from kidney stones, calcified arteries, and polycystic kidney tissue (which involves pathological calcification), and its antigen has been detected in dental pulp stones and calcified pineal tissue. So far, it appears that wherever we find pathological calcification, we will also find N. sanguineum. So how do we get from Nanobacterium sanguineum to pathological calcification?
Many sea creatures are small and
defenseless, but within their shell they enjoy protection from their natural
predators. The only natural
predator of N. sanguineum is the immune system of their host. Given the small
size and slow growth rate of this organism, N. sanguineum vs. immune system
wouldn’t seem to be a fair fight – it isn’t, the Nanobacteria always win!
The immune system can engulf or surround Nanobacteria, if the immune
response is aggressive enough. Even
then our defense is moot, as the Nanobacteria either kill the cell that engulfed
them, or they calcify inside the immune cell only to kill it later.
Host generated antibodies to the Nanobacterial biofilm should bind to the
individual Nanobacteria, rendering them a tasty morsel for circulating
phagocytes. Rapidly dividing
bacteria should hog all the available nutrients, crowding Nanobacteria out.
But this does not happen, because:
a) Nanobacteria shelters itself from the immune system (calcific semi-dormant defense),
b) Nanobacteria can live where other bacteria cannot (extremophilic defense.
Nanobacteria’s “extremophilic”defense will be covered later; here we will examine its “calcific” defense. The biofilm elaborated by individual Nanobacteria render them “sticky”. They bind to mammalian cells, trick the cell into endocytosing them, and then cause the now invaded cell to commit apoptosis (as occurs with tubular cells in polycystic kidney disease) – but not in all cases. Sometimes the appearance of the engulfed, vacuolized, Nanobacteria changes. Instead of a goey, surrounding biofilm, the now intracellular Nanobacterium is seen to be surrounded by spiculated material (figures 1 and 2, a Nanobacterium within a fibroblast, and fig. 3, a Nanobacterium within polycystic kidney tissue). Energy Dispersive X-Ray (EDAX – fig. 4) demonstrates this material to be carbonate apatite, the same stuff present in pathologically calcified human tissues.
This spiculated, thickened, partially calcified biofilm material provides the individual Nanobacterium with some protection against immune scavengers. What happens next has been well characterized in vitro, but presumably follows the same pathway in vivo.
Adjacent Nanobacteria bind together in a sticky web of biofilm (fig. 5). The biofilm then begins to change in character and consistency, thickening up as carbonate apatite spicules form within the biofilm goo (fig. 6, scanning, and fig. 7, transmission EM). From this peanut brittle-like mass of individual Nanobacteria cells surrounded by calcifying biofilm, an organized colony of adult Nanobacteria begins to emerge (fig. 8, transmission EM), kind of like caterpillars and butterflies.
The end result is a “stand alone” Nanobacterial colony, consisting of stuck together Nanobacterial cell bodies, surrounded by a thick, layered wall of carbonate apatite (fig. 9). This structure in and of itself is not noticed by our bodies as “foreign”, but rather as normal “calcium” that causes no alarm. White cells, antibodies, and other bacteria cannot penetrate this shell. The enclosed Nanobacteria may now grow at their own, leisurely pace, free from molestation by their natural predators. Only when the nanobacteria secrete their biofilm does our immune system notice that something is awry. Even then, the immune troops arrive to the scene of the biofilm ready to do battle…..only no one is home (they’re hiding in the calcium). The immune troops wait and nothing arrives. If the nanobacteria were there, they would enter the immune defense cells and kill them in approximately three days.
The scanning electron microscope gives us a 3-D view; the colonies appear as fuzzy rounded balls with dimples (fig. 9). Nanobacterial colonies formed in vitro (fig. 10) have a similar appearance, but with a cleft in their calcific armor, where the forming colony was attached to the beaker wall. Figure 11, a Nanobacteria colony that was cracked open, shows the laminated layers of calcium surrounding the Nanobacterial bodies, like the yolk of an egg surrounded by the white.
These structures, the layered walls that surround a Nanobacterial colony, are what make up pathological calcification. Figures 12 and 13 represent pathological calcification within dental pulp stones and kidney stones, respectively. Do they look familiar?
Microscopists use Von Kossa staining to demonstrate calcium deposition within tissue specimens. Figure 14 shows Von Kossa staining of a N. sanguineum inoculated fibroblast. Figure 15 shows a group of infected fibroblasts; notice the variable sized calcospherules, both within the cells and in the extracellular space. These correspond in size to Nanobacterial calcific shelters. Similar structures recovered from atherosclerotic arteries and kidney stones will light up with fluorescent IgG anti-Nanobacterial monoclonal antibodies.
While cell free or circulating Nanobacteria have a coccoid configuration, once in the safety of a calcific shelter the organism assumes a D-shaped morphology (fig. 16), and its growth rate slows to one division every six days. Shelter size, which can reach 2 millimeters, is a function of the number of enclosed D-shaped Nanobacteria. Shelter wall thickness can reach up to 2 microns. Shelters proliferate by budding off apatite bearing Nanobacteria (fig. 17), which can “grow up” into new calcified colonies. Shelter growth and shelter proliferation, now with the D-shaped Nanobacteria doubling only once every six days, is the process by which pathological calcification proceeds in the human body. In clusters they can reach the size of the largest kidney stones.
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