Cell Apoptosis, Bone Remodeling Repair Cycle Process

University of Detroit School of Dentistry 1969
Published in JADA, FDJ, HDA Journal, Townsend Letter'

We were all taught that cells die by necrosis. With necrotic death, all of the cell’s innards are explosively released, creating painful inflammation. Turns out, the body is far more sophisticated than that. Cells are programmed to quietly fade and die for a variety of reasons during growth and development as well as during wound repair. With apoptotic cell suicide, the cell’s useful organelles are prepackaged for easier reclamation by associated dendritic gobbler white blood cells, creating quiet efficient reorganization of tissues.

In utero, developmental webs between human fingers quietly reorganize and disappear. Orchestrated by associated phagocytic dendritic cells, bone and skin cells disappear and melt away to allow a tooth to erupt, or to create a pimple (an infectious fenestration) or to emerge a fistulous tract. Some folks have thin and atrophic gums and bone. Others have thick, vibrant even hypertrophic bone and gums. Changes in apoptotic signaling to the tissues determine these differences.

During development, parts of the brain must die to allow rewiring for speech. Environmental toxins and excessive stress messaging from the civilized diet paradoxically compromise apoptosis of brain nerve cells programmed to die as pruning for brain development and reorganization. This compromises speech development and other socially interactive skills. Autistic children end up with larger brains.

Apoptosis signaling is naturally heightened during rapid growth, especially around the inherently stressful peak 5-7 year growth spurts (and is at apogee during tooth shedding and eruption). ‘Twelve year’ molars signal another apoptotic peak and the beginning of the next and biggest programmed stress in life, the pubertal growth spurt.

Growth spurts are known to be the best time to move teeth orthodontically. Very light consistent physiologic forces on teeth promote efficient apoptotic remodeling of bone with gentle movement of the teeth carrying and even growing bone. Excessive forces transmitted through the teeth create focal necrosis, painful inflammation with delayed movement of teeth and often less than optimal remodeling of bone.

Stress disables cellular immunity, allowing accumulation of unfavorable biofilm on still porous teeth. Streptococcus mutans is a bacterium with a unique survival strategy of living where most bacteria do not like to live, in an acid environment. Some sticky mutans varieties have lipopolysaccharide markers in their cell walls which mimic endotoxin, with its highly virulent threatening message. These small antigenic molecules can be drawn to the pulp through pores in enamel during catabolic tidal flows, alarming the dentinoblasts, our outer cellular border.

Cytokines call in phagocytic white blood cells. These dendritic immune cells congregate under the dentinoblast border. They create a ‘protective’ oxidative alkaline outflow, quickly dissolving the tooth from the inside out via liquefaction necrosis of uncontrolled inflammation. The heightened apoptotic signaling of programmed rapid growth would alter apoptosis and cause increased survival of inflammatory pulpal phagocytes with easier apoptotic death of structural ‘bordering’ dentinoblasts allowing quickly penetrating decay. Heightened apoptotic signaling creates the peaks in enamel decay seen at these ages. Pimples are exfoliating cysts based on a similar process and also peak when tooth decay peaks.

During mesodermal root development of permanent teeth, root-retained ectodermal enamel-derived epithelial cells of Hertwig are programmed to die. These neural crest cells aiding and guiding root development may not die on time if their apoptotic signaling is compromised due to stress messaging overwhelming abundance messaging. They remain alive on the root surface and become ectodermal enamel pearls.

Enamel pearls or epithelial rests are permanent internal antigenic markers waiting to become activated. Patterns of antigenic enamel epithelial cells and pearls are formed on root surfaces during growth spurts of ages 4-10. This predicts the clinical pattern of periodontal disease. Systemic bone density diminishes and stress heightens directly during the shedding of the deciduous incisors and eruption of the six year molars.

Inflammatory activation occurs later in life when cellular immunity becomes compromised and humoral immunity is upregulated, creating autoimmune periodontal destruction, with cytokines similar to rheumatoid arthritis. When these autoimmune lytic lesions break through into the mouth, they become infected with characteristic opportunistic oral bacteria.

Cellular immunity becomes disabled due to lack of reduced glutathione caused by environmental load and/or genetic predisposition, poor waking and sleep cycles, negative emotions, weak breakfast (with too little sustaining protein, carbohydrate, water, fats or minerals), too much sugar or just too many calories all at once. Dental plaque accumulation is often the first clue to failed cellular immunity. Excess mucus, sinusitis, hay fever, hives, allergies and hypersensitivities signal the compensatory upregulation of destructive humoral immunity, accompanied by uncontrolled inflammation.

Endometriosis is set up by excessive stress messaging during descent of the ovaries, leaving glandular cells still-living along developmental tracts. Fibroid activation occurs later when cellular immunity becomes compromised and humoral immunity is upregulated. In cycling females, if the egg is not fertilized, endometrial cells are programmed to apoptotically die, quickly stopping the production of progesterone, triggering timely menses. If there is too much stress messaging, these tissues live on, extending the menses and altering the monthly clock.

DNA is a scaffold of possibilities that creates species, but has no enzyme activity of its own. Molecules of RNA (as ribozymes) combine memory capability with enzyme capability giving them the ability to respond to the environment and create individuality. The RNA world is easy to ignore since it surrounds and envelops us. Ribozymes are bound to the endoplasmic reticulum as ribosomes and swim freely in the cytoplasm and extracellular fluids, appearing everywhere in highly-magnified microscopic fields like dust particles dancing with Brownian movement in sunlit air. These ever-present magical molecules of the RNA world are our primary integrators with the environment and activators of gene expression. RNA expresses itself through viruses, enzymes, DNA and ultimately our actions.

Since the beginning of time’s interaction with life there have been but two environments, abundance and lack of abundance (scarcity). The RNA world existed before the DNA world and still exists, interpreting the environment and telling our DNA what to do. With RNA messaging of abundance (richly found in sunshine, soaked seeds, nuts or grains and fermented products) the body’s structural tissues become anabolic, firm, resilient and resistant to disease. With excessive RNA perceptions of stress and scarcity (e.g. from dried or toasted seeds, nuts or grains and even worse, dehydrated or weak breakfast) the body becomes depressed, irritable, catabolic, flabby, weak and autoimmune.

When perceived stress becomes overwhelming, cells are triaged into structural and survival categories. Structural tissues (our reservoirs) are bone, teeth, skin and muscle. Preservation or survival cells are fat cells, nerve cells, taste buds and inflammatory white blood cells (our mobile neurons). When environmental stress messaging overwhelms abundance messaging to our genes, structural cells wane (are allowed to die early by apoptosis) and the body cancels cell suicide in its survival cells. Paradoxically, the already stressed or defective cells of the body (designed to eliminate themselves by undergoing apoptosis or cell suicide) are also signaled to live on to grow, potentially becoming cancerous tumors.

Smoking cigarettes and drinking lots of coffee delays onset of Parkinson’s disease (caused by toxin-induced early cell death of substantia nigra brain cells). Epidemiologically, AGEs can explain what is called the ‘Parkinsonian paradox.’ Parkinson’s symptoms result from early cell death of these brain cells that primarily produce dopamine. Classic stressors (like the toasted and burnt sugars in the tobacco, coffee and, whoops, boxed breakfast cereals – even organic) which hasten most inflammatory diseases, actually delay previous apoptotic signals induced by other toxins in Parkinson’s disease, providing a salutary effect for one person in a group of two hundred.

Excessive stress messaging comes from too little sleep, too little sunshine or weak breakfast; or from synergy of heavy metals such as mercury, lead and arsenic; or the halides bromine, chlorine and fluorine; and molds, resident yeasts, bacteria and viruses allowed due to compromised cellular immunity; organophosphates, phthalates, petrochemicals, solvents and browned or glycated sugar molecules, or even too many foods with glycoproteins that mimic an incompatible blood type. When daily anabolic repair tides are overwhelmed by catabolic flows, ensuing stress-responsive inflammatory chemistry allows ‘structural’ cells (like muscles, skin, bones, teeth and the ‘shag carpeting’ filiform papillae of the tongue) to fade and wane by undergoing apoptosis, programmed cell death.

With overwhelming metabolic stress, apoptosis is shut down in ‘survival’ cells such as fat cells, creating growing expanding flab. Stressed inflammatory ‘gobbler’ white blood cells also live on, dissolving bone and creating chronic autoimmune destruction and pain. Nerves and taste buds (such as the now visible and often inflamed ‘strawberry spots’ of the fungiform papillae near the tip and on the dorsum of the tongue) survive. The Chinese say the first sign of stress overwhelming repair is a red tip to the tongue. The red tip then progresses as waning atrophied filiform papillae create a smoother tongue with newly visible ‘strawberry spots,’ survival taste buds called fungiform papillae.

With enough balancing messages of abundance from the dualistic steroid receptors to our nuclear DNA, gene expression is changed. Now vigorous structural filiform papillae restore full pink shag carpeting to the tongue; the mouth stays free of pathogenic biofilm effortlessly; flab turns to firm; tumors shrink and defective cells quietly commit apoptotic cell suicide daily. Messaging of abundance comes from the attitude of gratitude, sunshine, rhythm, effective sleep, sustaining breakfasts, soaked seeds, nuts and grains, eggs, fresh pressed vegetable juices, and fermented foods. The beneficent steroid receptor also responds to fat-soluble vitamins A, D, Es, Ks, bile, steroid hormones, retinoids and other sun generated pigments, proanthocyadinins, resveratrol and the salvesterols, aromatic essential oils and foundationally the omega-3 and omega-6 essential fatty acids.

Author Credit:

Steven N. Green, DDS, 10261 SW 72 St., #106, Miami, FL 33173, 305-273-7779 - http://www.antiagingdentist.com

Holistic Family Dentistry Miami Florida