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Treatment and Support of Musculoskeletal Healing

Treatment and Support of Musculoskeletal Healing
Article Summary

Renata Trister DO

An injury stimulates a sequence of events begins that begin healing. This healing process involves inflammation, repair, and remodeling. Tissue repair and wound healing are complex processes that involving interconnected, biochemical and cellular reactions, beginning with inflammation and followed by the repair and remodeling of the injured tissue. Connective tissue repair and remodeling involves chondrocyte reproduction, the formation of collagen fibers and ground substance. The healing process first involves removal of damaged tissue, then the subsequent rebuilding of healthy connective tissue. The redness, swelling, heat, and pain of inflammation are a natural part of the healing process. Prolonged or chronic inflammation, however, can slow down the healing process, causing continued loss of function. Furthermore, suppressing inflammation with drug treatment also results in delayed healing.

The inflammatory response is a critical part of tissue repair and wound healing.

When there is damage to connective tissue it is important to address the nutritional requirements for the synthesis of both the collagen fibers and the proteoglycans must be addressed when damage to connective tissue occurs. Many nutrients are involved in connective tissue repair and wound healing: glucosamine sulfate, D-glucuronic acid, amino acids, bioflavonoids, and select vitamins and minerals. In addition to nutritional support, homeopathy has been used for generations for both acute and chronic injuries.

The Inflammatory Response

Prostaglandins and related compounds are collectively known as eicosanoids. Most are produced from arachidonic acid, a 20-carbon polyunsaturated fatty acid (5,8,11,14-eicosatetraenoic acid).
The eicosanoids are considered “local hormones.” There are anti-inflammatory eicosanoids and inflammatory eicosanoids. The standard American diet promotes the production of those that are inflammatory. Fortunately, many substances inhibit inflammatory eicosanoids or promote the production of anti-inflammatory eicosanoids classic mechanism for controlling inflammation. They have specific effects on target cells close to their site of formation. They are rapidly degraded, so they are not transported to distal sites within the body. But in addition to participating in intercellular signaling, there is evidence for involvement of eicosanoids in intracellular signal cascades.
They have various roles in inflammation, fever, regulation of blood pressure, blood clotting, immune system modulation, control of reproductive processes and tissue growth, and regulation of the sleep/wake cycle.

Nutrients & Herbs That Modulate the Inflammatory Response

Omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are precursors of primarily anti-inflammatory eicosanoids. In addition, the omega-6 fatty acid, gamma-linoleic acid (GLA), also supports the production of anti-inflammatory eicosanoids.

Ginger (Zingiber officinale) and Turmeric (Curcuma longa)These herbs have long been used for acute and chronic inflammatory conditions. Studies suggest that both herbs may block activity of the enzymes cyclooxygenase and lipoxygenase. These enzymes are necessary for the production of inflammatory eicosanoids.

Cayenne Pepper (Capsicum annuum) Capsaicin, the main constituent of cayenne pepper, may play a role in inhibiting inflammatory eicosanoid synthesis by blocking cyclooxygenase activity as well. Capsaicin can reduce tissue sensitivity by selectively depleting a neuropeptide needed to transmit pain impulses to the central nervous system. Thereby changing “the perception of pain”.

Nutrients Involved in Connective Tissue Repair
Controlling inflammation is directly linked to the next phase of the healing process repair and remodeling. Following connective tissue injury, it is critical to supply the raw materials and proper nutrients that support tissue recovery and new tissue synthesis. These include:

Amino Acids Supplying amino acids may support the formation of collagen a critical connective tissue. Collagen fibers are made up of long chains of amino acids, of which one-third is glycine. Proline, hydroxyproline, and hydroxylysine are also prevalent.

Glucosamine and Chondroitin Sulfate are building materials that are vital for the synthesis of new connective tissue as well as for the healing process.

Antioxidants free radical production a major consequence of the inflammatory response—may aggravate an injury and delay or prevent adequate healing. Vitamins E and C are major antioxidants. Vitamin C is required for collagen fiber synthesis, a vital process for tissue repair and healing. Copper, zinc, and manganese further protect tissues by supporting the activity of superoxide dismutase—an enzyme that converts damaging superoxide free radicals into less harmful molecules.
Bioflavonoids see additional section below.

Muscle Mechanics, Relaxation, and Rest

Proper muscle use, joint alignment, and biomechanics during tissue remodeling are critical for preventing reduced range of motion due to scar tissue formation. In addition, injury can give rise to increased anxiety, stress, and poor sleep, resulting in prolonged and unfavorable healing.

Bioflavonoids
• Group of plant pigments that are largely responsible for colors of many fruits and flowers
• Useful in treatment and prevention of many health conditions
Four categories:
• PCO (Proanthocyanidins)
• Most potent PCOs are those bound to other PCOs
• Exist in many plants and red wine
• Commercially available sources are from grape seeds and bark from the maritime pine
• Quercetin
• serves as backbone for other flavonoids such as citrus flavonoids: rutin, quercitrin, hesperidin
• these derivatives have sugar molecules attached to the backbone
• most active of the flavonoids
• Citrus bioflavonoids
• include rutin, quercitrin, hesperidin, naringin
• standardized mixture of rutinosides known as hydroxyethylrutosides (HER)
• clinical results have been obtained in treatment of capillary permeability, easy bruising, hemorrhoids, and varicose veins
• Green Tea Polyphenols
• derived from tea plant camellia sinensis
• produced by steaming the fresh cut leaf
• polyphenol indicates presence of phenolic ring in the chemical structure
• polyphenols = flavonoids
• polyphenols in green tea: catechin, epicatechin, epicatechin gallate, epigallocatechin gallate, and proanthocyanidins
• epigallocatechin gallate = most significant active compound

Dietary Sources
• Citrus fruits
• Berries
• Onions
• Parsley
• Legumes
• Green Tea
• Red Wine
Average Daily Intake = 150-200 mg

Beneficial Effects
• referred to as “nature’s biological response modifiers” – modify body’s reaction to compounds such as allergens, viruses, and carcinogens
• powerful antioxidants by giving protection versus oxidative and free radical damage
• prevents formation of oxidized cholesterol through antioxidant effects
• greater antioxidant effects than Vitamins C, E, Selenium, and Zinc
PCOs
• increase intracellular Vitamin C levels
• decrease capillary permeability and fragility
• scavenge oxidants and free radicals
• inhibit destruction of collagen
• crosslinks collagen fibers to reinforce the natural crosslinking
• prevents free radical damage
• inhibits enzymatic cleavage of collagen by enzymes secreted by leukocytes in inflammation and microbes in infections
• prevents release and synthesis and compounds that promote inflammation and allergies (histamines, prostaglandins, leukotrienes)
• antioxidant effects are beneficial in:
• aging process
• chronic degenerative diseases (heart disease, arthritis, and cancer)
• fat and cholesterol oxidation
• antioxidants are produced by:
• inhibiting xanthine oxidase noncompetitively(oxygen free radicals)
• on the cellular level: PCOs are incorporated into the cell membranes along with the antioxidant effects offer great protection to cells against free radical damage.
Quercetin
• anti-inflammatory activity due to inhibition of initial processes of inflammation
• inhibits manufacture and release of histamine
• potent antioxidant activity and Vitamin C sparing action
• beneficial effects for diabetics
• helps prevent diabetic cataracts, and retinopathy
• enhances insulin secretion
• protects pancreatic beta cells from free radical damage
• antiviral activity
• activity vs. herpes virus type 1, parainfluenzae3, polio virus type 1, and respiratory syncytial virus
• in vivo, inhibits viral infection
• may be of some benefit in the common cold
Citrus Bioflavonoids
• antioxidant effects
• increase intracellular Vitamin C, rutin, hesperidin, and HER
• beneficial effects on capillary permeability and blood flow like PCOs
• anti-allergy and anti-inflammatory effects like quercetin
Green Tea Polyphenols
• potent antioxidant effects
• increase activity of antioxidant enzymes in the small intestines, liver, lungs, and small bowel
• inhibit formation of cancer causing compounds like nitrosamines in vitro
• suppressing activation of carcinogens
• trapping cancer causing agents
• forms of cancer that green tea prevents best:
1. cancers of GI tract (stomach, small intestine, pancreas, colon)
2. cancer of the lungs
3. estrogen related cancers (inhibits estrogen interaction with its receptor)
• consumption of green tea with meals inhibits formation of nitrosamines (nitrites combined with amino acids)

Principle Uses
PCOs
• Treatment of venous and capillary disorders
• venous insufficiency
• varicose veins
• capillary fragility
• Diabetic retinopathy and macular degeneration
• Prevention of heart disease and strokes
• Lowers blood cholesterol levels
• Shrinks size of cholesterol deposits in the artery
• Inhibits platelet aggregation and vascular constriction
Quercetin
• In vitro, helps virtually all inflammatory and allergic conditions
1. asthma
2. hay fever
3. rheumatoid arthritis
4. lupus
• Beneficial in diabetes and cancer
Citrus Bioflavonoids
• Venous insufficiency
• Improve microvascular blood flow and clinical symptoms (pain, tired legs, night cramps, and restless legs)
• Improve venous function
• Relieve hemorrhoidal signs and symptoms in pregnant women
Green Tea Polyphenols
• Used principally to prevent cancer

Available Forms
PCOs
• Grape seed extract (92%-95%) and pine bark extract (80%-85%)
• Used interchangeably, but grape seed extract is preferred
• Grape seed extract is considered more potent and more effective than pine bark extract because only grape seed extract has gallic esters of proanthocyanidins which are the most active free radical scavenging PCOs
Quercetin
• Available in powder and capsule forms
• For anti-inflammatory effects, combination of Bromelain (pineapple enzyme) may provide additional benefit by enhancing absorption of quercetin
• Amount of Bromelain should equal quercetin
Citrus Bioflavonoids
• Mixed preparations are most widely used
• Least active and quantified source of flavonoids
Green Tea Polyphenols
• Commercial preparations that have been decaffeinated and concentrated for polyphenols (60%-80%)
• 1 cup = 300-400 mg of polyphenols
Downside = this dose also contains 50-100 mg of caffeine

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Nutritional support for stress-induced dysfunction

Nutritional Support of Stress-Induced Dysfunctions

Article Summary
Renata Trister DO

Stress is a normal physical response to events that make you feel threatened. When you sense danger—whether it’s real or imagined—the body’s defenses kick into high gear in a rapid, automatic process known as the “fight-or-flight” reaction, or the stress response.

The stress response is the body’s way of protecting you. When working properly, it helps you stay focused, energetic, and alert. The stress response also helps you perform under pressure and motivate you to do your best. But when you’re constantly running in emergency mode, your mind and body suffer. You can protect yourself by recognizing the signs and symptoms of stress and taking steps to reduce its harmful effects.

The Hypothalamic-Pituitary-Adrenal (HPA) Axis

The HPA is a complex set of direct influences and feedback interactions among the hypothalamus, pituitary, and adrenal glands. It is the primary regulator of this stress response. While stress-induced changes in biochemistry may be beneficial to survival in the short term (acute stress), they present an increased risk of various health challenges in the long term (chronic stress). Research increasingly supports the critical role that stress can play in obesity, diabetes, osteoporosis, hypertension, cardiovascular disease, infectious disease, gastric ulcer, cancer, and gastrointestinal, skin, psychological, and neurologic disorders, as well as immune system dysfunctions.

Combating Stress With Herbal Adaptogens

Lifestyle changes such as stress reduction, relaxation, regular exercise, and a healthy diet can all support a healthy response to stress. Herbs referred to as “adaptogens” have been used over the centuries in traditional medicine. An adaptogen is a nontoxic substance and especially a plant extract that is used to increase the body’s ability to resist the damaging effects of stress and promote or restore normal physiological function. Adaptogens have a variety of beneficial effects, such as increasing energy and stamina, preventing fatigue, enhancing memory and concentration, and improving work performance. These are some herbal adaptogens:

Ashwagandha (Withania somnifera) – is a rejuvenating herb and one of the most vital herbs in Ayurvedic (Indian) healing medicine. It has been shown to enhance adaptability to both physical and chemical stress. For instance, mice pretreated with ashwagandha and subjected to physical stress showed increased endurance.

Holy Basil (Ocimum sanctum) is an Indian herb with a rich history of treating a variety of conditions. Treatment with holy basil has yielded increased physical endurance, and lowered the stress-induced release of adrenal hormones and cholesterol in animal studies.

Bacopa (Bacopa monnieri) creeping herb whose habitat includes wetlands and muddy shores. It is traditionally used to revitalize nerves and the mind, as well as to help strengthen the adrenals. In animal testing, bacopa has been shown to improve adaptations in sensory, motor, and motivational systems.

Cordyceps (Cordyceps sinensis) is a therapeutic fungus/mushroom found primarily at high altitudes in China and is one of the most valued medicinal fungi in Chinese medicine. Research dating back to 1843 suggests the use of cordyceps to help strengthen and rebuild the body after exhaustion and illness.

Asian Ginseng (Panax ginseng) is greatly valued as a tonic herb that acts to normalize body function and biochemistry. In traditional Chinese medicine, ginseng is used in patients who overwhelmed and exhausted.

Rhodiola (Rhodiola rosea) is traditionally used to stimulate the nervous system, decrease depression, enhance work performance, and eliminate fatigue.
Licorice (Glycyrrhiza glabra) is one of the most highly regarded in terms of treating conditions associated with diminished adrenal function.

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Chronic Inflammation

By Jon Trister MD and Renata Trister DO

Infectious and metabolic toxemias are two major causes of chronic systemic inflammation. Acute inflammation is a rapid onset process, with more conspicuous symptoms and a short duration. Chronic inflammation, however, is more insidious. It is the result of a perpetual onslaught from a variety of toxins and pathogens. It is a long lasting process that is often silent with indistinct symptoms.

Dysfunction
The Respiratory, GI, Integumentary and GU systems are the major sources of toxic metabolic, viral, bacterial and fungal entities that attack our immune system.
Endothelial dysfunction and immune dysregulation are the consequences of persistent stress from toxemia.

ESR, Uric acid, Triglycerides,LDL and their size, hs-CRP and VDR dysregulation (D-25-OH and D1.25 OH) and other are the markers of chronic inflammation and potential damage of the endothelium.
Connective tissue insufficiency, weakness of the support of the adventicial layers of the arteries are major factor leading to loss of tensegrity.
It is impossible to treat cardiovascular pathology without addressing GI system – especially Increased Intestinal permeability – “leaky gut syndrome”
Similarly, gingival, respiratory, dermatological and genitourinary pathology may lead to metabolic, infectious and toxemic stresses that cause a long lasting and pathological response – chronic inflammation.
Identifying and attenuating these factors will reduce the pathologies that lead to chronic inflammation.

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Immune system. Brief review. By Jon Trister MD

The Immune System, brief review

 To defend as form invaders  body has two immune systems:

The first defense system is an innate immune system we are born with. This is a  first defense against any foreigners-microbes, viruses, funguses. This is antigen non-specific defense mechanisms which respond to invaders immediately or within several hours after exposure to every foreigner. Cells associated with innate immune system are Macrophages, Dendritic cells and  B-lymphocytes

 The second defense system is an adaptive immune system (acquired) immunity refers to antigen-specific defense and require  several days to become protective and are designed to react with and remove a specific antigen. Adaptive immunity is the immunity one develops throughout life. Cells associated with adaptive immune system are T- and B-Lymphocytes

One of the function of the innate  immune system is an APC ( antigen presentation cells)-is an identification, isolation  of the antigen-specific protein -epitope-actual portions or fragments of an antigen that react with receptors on B-lymphocytes and T-lymphocytes, as well as with free antibody molecules) and presentation it in the from of complex : MHC I/epitope  or MHC ii/epitope on the surface of the APC ( Macrophages, Dendritic cells, B-Lymphocytes).Epitope is a fragment of the antigen which will provide adaptive immune system a specific  information about invader ( antigen).Without ability to perform this function as an APC innate immune system will be unable to “educate” adaptive immune system about structure of the antigen.

Polysaccharides antigens( 3-4 sugar residuals)  usually have many epitopes but all of the same specificity.

Proteins antigens (5-15 amino acids )usually have many epitopes of different specificities.

Immune responses are directed against many different epitopes of many different antigens of the same microbe.

The body recognizes an antigen as foreign when epitopes of that antigen bind to B-lymphocytes and T-lymphocytes by means of epitope-specific receptor molecules having a shape complementary to that of the epitope.

 

                     MHC molecules

MHC-I molecules are made by all nucleated cells in the body

MHC-I presents epitopes to T8-lymphocytes; MHC-II presents epitopes to T4-lymphocytes.

MHC-I molecules are designed to enable the body to recognize infected cells and tumor cells and destroy them with cytotoxic T-lymphocytes or CTLs.

CTLs are effector defense cells derived from naïve T8-lymphocytes.

MHC-I molecules are made by all nucleated cells in the body; bind peptide epitopes typically from endogenous antigens; present MHC-I/peptide complexes to naive T8-lymphocytes and cytotoxic T-lymphocytes CTL.

 

MHC-II molecules are made by antigen-presenting cells or APCs, such as dendritic cells, macrophages, and B-lymphocytes; bind peptide epitopes typically from exogenous antigens; and present MHC-II/peptide complexes to naive T4-lymphocytes or effector T8-lymphocytes that have a complementary shaped T-cell receptor or TCR

Exogenous antigens enter antigen-presenting macrophages, dendritic cells, and B-lymphocytes through phagocytosis, and are engulfed and placed in a phagosome where protein antigens from the microbe are degraded by proteases into a series of peptides. These peptides are then attached to MHC-II molecules that are then put on the surface of the APC.

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FAQ about Prolotherapy and PRP

Am I a candidate for Prolotherapy and PRP?

A: Many problems related to musculoskeletal conditions are can be successfully treated with Prolotherapy (Regenerative Injection Therapy):
1.Degenerative Joint Diseases (Osteoarthritis)-OA:all locations:
neck, TMJ, shoulders, scapulaes, clavicles, ribs, elbows, wrists, fingers, thoracic and lower back pain, “disc’s problems”, hips, knees, ankles, feet, toes.
2.Consequences of ligamentous, cartilagenous and tendinous injuries (with some limitations). Partial tears of tendons, muscles and ligaments can be successfully treated with combining various techniques :
Prolotherapy + PRP (Platelets Rich Plasma)
Prolotherapy + Mesenchymal stem cells + PRP
Prolotherapy + Neural prolotherapy.
3.Some form of arthritis may have infectious, allergic, autoimmune or metabolic causes. In such cases we will order special diagnostic tests to help patient in selection of appropriate treatment.
4.Patients with infected joints,non-healing wounds around joints,cancerous spread into the bones(metastasis,multiple myeloma, leukemias) ARE NOT A CANDIDATES FOR PROLOTHERPAY.
5.Elderly and debilitated patients may not respond well to prolotherapy.
6.Degree of joint damage (stage of the OA), age, weight, smoking status, nutritional status, use of certain medication (Steroids , NSAID) will negatively affect prognosis of the treatment.
6. Patients with illnesses related to medico-legal problems (Motor Vehicle and industrial Accidents) must have official pre-authorization from their insurances or Court order for treatment.
7. Other factors may play role too: anticoagulation therapy, anti-platelets therapy etc
During initial consultation we will perform detailed physical examination, review imaging tests, and available laboratory tests,will perform diagnostic musculoskeletal ultrasound in the office .
This will help us select right strategy for treatment.

How much does it cost?

A.: The initial evaluation cost depends on the complexity of the problem and how much time is needed to do the evaluation.  One hour is usually the time set aside for the first visit.  A few first visits are less complex, taking 30 minutes, while a few may require 90 minutes.  A call to the office will allow us to give an estimate of a consulation/evaluation fee.

When treatment is given during the office visit, there will be an additional charge for the treatment.  Charges vary according to the area(s) treated.

Will my insurance pay for this treatment?

A.:  Insurance companies vary a lot. Most insurances including Medicare and Medicaid DO NOT pay for this services. Some pay well for prolotherapy treatments.  Some pay part of the time and not other times.  Some companies will not pay for it at all. Please contact your insurance and ask this question . CPT code for Prolotherapy  is “ M0076 “

How many treatments will I need?

A.:  It is not possible to tell ahead of time how many treatments a patient might need before they are pain-free.  The doctor will give  an estimated range of the number of treatments that you will need, depending on the severity of your condition.

How far apart are the treatments?

A.:  Treatments are usually given at three-four weeks intervals.  There are exceptions to this, depending on other circumstances.

How soon after treatment can I work out or play sports?

A.:  If your sports or work-outs involve the area that is being treated, you will get the best results with treatment when you avoid exercising or stressing the area until 3 or 4 weeks after the last treatment.  If you must continue to exercise the treatment area, it may take a lot more treatments to get the desired result.  You may continue to re-injure it with the exercise or sports activity, preventing it from getting strong enough to protect it.

What is in the medicine that is used in the injections?

A.:  There is no cortisone used in prolotherapy.  The solution is normally a mixture of a very concentrated dextrose (glucose) with a local anesthetic like lidocaine.  A small amount of sodium morrhuate ( a water soluble form of cod liver oil) is added for extra stimulation of the healing reaction in some cases.

What is the success rate with prolotherapy?

A.:  Prolotherapy generally has about a 70% good to excellent response among the doctors across the country that keep track of their patients’ responses to treatment.  About 10% of the patients are in the poor response, or less than 50% improvement category.

Is there a guarantee that prolotherapy will work for me?

A.:  There is nothing in medicine that is guaranteed.

How do I contact the office for an appointment?

A.:  Please call our office at 508-754-9950 for an appointment.  The staff will be happy to schedule your appointment and give you further information.

What are the office hours?

A.:  Our office hours are 8:00 AM to 12:00 NOON and 1:00 PM to 5:00 PM, Monday through Friday.

What should I bring to the doctor’s office for the initial evaluation?

A.:  Please bring the completed paper work that the office sends to you and any X-ray or films of any other studies that you may have had.

What happens at the first visit?

A.:  Medical assistant will greet you, collect your paper work and take you to the examination room.  The doctor will review your paper work, ask you questions about your problem, examine you, read your X-rays and explain them to you, give you his opinion about what he believes is causing your pain or other problems, order any new studies that may be needed and make recommendations for treatment.  He will explain the treatment and answer your questions. You will be given Consent form for treatment and estimated cost. No treatment will be performed during consultative visit.

Will I need a driver?

A.:  Most of the time patients do need a driver. You will receive a treatment which may affect your ability to drive safely for 12-24 hours.

Will I need to be off work after the treatment?

A.:  Most patients do not need to be off work the day after the treatment if it is sedentary work.

What are the risks with prolotherapy?

A.:  There are risks with all treatments and medications, not just prolotherapy.  If the doctor feels that you are a candidate for prolotherapy, he will explain the risks to you and try to answer all of your questions.

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History of vitamin D

Vitamin D
Dr. Renata Trister DO

History of vitamin D

Vitamin D was categorized as a vitamin when it was discovered in 1922. It is not a true vitamin because an ongoing nutrient source is not required to sustain normal levels in the body. Vitamin D is properly classified as a secosteroid (derived from steroid) hormone precursor. A hormone is a chemical substance produced by one organ and then transported in the bloodstream to a target organ, where it causes a specific biological action.
D-metabolites: 25-D and 1,25-D
Vitamin D has several metabolites (forms). This summary is limited to two metabolites: 25-D and 1,25-D.
 
25-D (also known as calciferol, 25-hydroxycholecalciferol) increases calcium absorption in the gut and at high levels, acts as an antagonist on the Vitamin D Receptor. 25-D is produced in the liver and synthesized in the cells of the skin in reaction to sunlight. 25-D dietary sources (fish, fish oils, eggs), foods that are supplemented with vitamin D (dairy products, cereals.) and vitamin supplements.
 25-D is the major circulating form of vitamin D. It is used in the production of (1,25-D) in the kidneys.
1,25-D (also known as calcitriol or 1,25-dihydroxycholecalciferol or 1,25-dihydroxyvitamin-D3) is a potent secosteroid paracrine mediator and virtually affects all cellular activity.
1,25-D is primarily formed in the kidneys; but may also be formed skin, macrophages and other tissues.
Vitamin D dysregulation
1,25-D can 1nduce the innate immune system. Elevated levels can be found in patients with chronic conditions.
25-D can suppress the innate immune system.
Normally, production of 1,25-D is tightly controlled by the kidneys in response to a complex system of hormonal regulation. However, when nucleated cells are infected with bacterial pathogens, 1,25-D is generated by the inflammatory response. This causes the level of 1,25-D to exceed the upper limit normally controlled by the kidneys.
 
It is essential to measure both 25-D and 1,25-D to evaluate vitamin D levels and dysregulation. The low level of 25-D doesn’t directly reflects the deficiency. Low D- 25 could be a result of down regulation of its production in the liver by high 1.25 D.
Patients with Th1/Th17 inflammation often have a low level of 25-D while the level of 1,25-D is high. T helper 17 cells (Th17) are a subset of T helper cells producing interleukin 17 (IL-17) discovered in 2007. They are considered developmentally distinct from Th1 and Th2 cells and excessive amounts of the cell are thought to play a key role in autoimmune disease such as multiple sclerosis, psoriasis, autoimmune uveitis, juvenile diabetes, rheumatoid arthritis, and Crohn’s disease.

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Visual postural examination

 

Posterior and anterior tilt

Lateral Shift

Oblique tilt

Pelvic rotation

Pelvic torsion

 

Shape of Gluteus Maximus muscles:

Observe symmetry. Look at the level of gluteal folds- asymmetry indicates inhibition or weakness of the ipsilateral side, which will be lower.

Slight asymmetry indicate inhibition or weakness-look at the upper external quadrant.In this case it will be flat on palpation as the result of decreased of the muscle tone.

Asymmetry of the pelvis will cause changes to lower back extensors and hamstrings.

Weakness of Gluteus Maximus will lead to lowering of gluteal fold on the same side.

Than look to the lumbar and thoracolumbar area.Look for scoliosis, rotation or kyphosis which may influence the shape of the muscles.

Than compare muscles at the lower lumbar region to the muscles at the thoracolumbar junction. Atrophy at the lower segment of the lumbar muscles will require stabilization and  lead to the hypertrophy of the muscles at the thoracolumbar segment.

Normally, lumbar segment is symmetrical and flatter than thoracolumbar segment which is slightly more prominent but still symmetrical.

Than proceed to the upper part of the body:

Shoulder blades can be protracted, retracted, shifted upward or abducted.

Look at the stabilizers: lower stabilizer (lower trapezius) interplays with upper stabilizers (upper trapezius,m. levator scapulae)

Interscapular region:

This area will be flat in the case of muscular inhibition. Weakness or inhibition of the serratus anterior will lead to winging of the scapulae.

If you see atrophy of the lower stabilizers (lower trapezius) than observe upper stabilizers (upper trapezius and m. levator  scapulae) which will be compensatory hypertrophic, which will lead to abduction and weaning of the scapula.

To look closely to the quality of the upper trapezius and levator scapulae focus on the reference  line  from the occiput/lateral neck and the Acromion . This line normally should have “S” shape.When levator scapulae and trapezius are overactive this line became straight.This called “Gothic shoulders”.

Another example of insufficient scapular stabilization will be protracted scapulae due to inhibition of the medium and lower trapezius, rhomboids and overactive serratus anterior.

Upper trapezius in this cases usually overactive which lead to superior shift of the scapulae.

Observation of the anterior shoulder provide information about humeral control:

flattening of the deltoid abductors indicate deltoid atrophy, altered pattern of the shoulder’s muscles and impaired  proprioception from the shoulder joint.

 

In the assessment of the lower extremity first view the subject general posture.

E/Rotation of the feet exists  may indicates problem with the muscles or the joint of the hip.

Look at the knee joints: varus , valgus or hyperextension

Correlate limb alignment with calcaneal bone and the position of the forefoot.

Varus leg deformity associated with pronation of the foot and flattening of the foot.

 

Than estimate the shape of each individual muscle groups.

First, look at the Hamstrings: note if the size of the hamstrings is symmetrical

Usually if gluteal muscle is weaker ipsilateral hamstring compensatory stronger.

Hamstrings best seen in the medium and upper thirds of the thigh.

The second important group of the thighs are ADDUCTORS

In general, there are two groups of adductors: Short (cover upper and middle thigh)and Long(cover entire thigh).

Normally, from posterior view adductors create very shallow letter “S”

If upper adductors are in spasm than upper portion of the “S” will be bulkier. As a compensation of this process lower portion of the “S” will be flat -hypotrophy,-hollow just above the knee.

Than look at the calfs: shape and symmetry. Estimate the tightness of hypotrophy of the m.soleus  muscles in the relation to gastrocnemius muscles

If the solei are tight and short, the muscle belly is evident at the medial border just superior to the Achilles tendon. (The m.soleus is located just underneath the gastrocnemius, and together these two muscles form the Achilles tendon. Since these are the 2 biggest muscles in the calf, they provide the majority of the push off when walking, running, and jumping)

If m.Soleus is tight than Achilles tendon become slightly thicker and shorter.

observation of the heel.

No symmetrical person.No specific norms.

Variation of the muscle

anterior view:

ASIS and umbilicus

Rectus abdominis: Upper quadrants more active than lower quadrants. But left and right are symmetrical.

Observe the groove on the lateral edge of the rectus abdominis: it reflects quality of interplay between m.rectus abdominis and m.obliqus abdominis externus. The more prominent this groove -the stronger m.obliqus abdominis externus and m.Rectus abdominis is inhibited.

Next, look at the lateral edge of the waist, which is normally concave. If it become flat or convex shape- sign of weakness of m.transversus abdominis which stabilize abdominal wall and spine properly.

In the upper trunk look at the symmetry of the muscles and respiratory movement of the chest wall. Focus mainly on the pectoralis major.

Compare muscular folds on both sides.The pectoralis muscle is more prominent on the dominant side. Positions of the nipples. If pectoralis is tighten, nipple will be displaced superiorly and laterally. In female, asymmetry of breasts may indicate m.pectoralis tightness.

 

Observe neck: SCM muscle, which under normal circumstances will be almost invisible.

Usually we only see insertion in the sternoclavicular region. If the muscle belly is pronounced it indicates muscle hypertrophy.

Groove in the area medial to SCM (between SCM and Scalenus muscles )

The more prominent this groove the weaker (hypoactive)the Scalenus muscle

 

Facial scoliosis”-asymmetry of face

4 points:

These points must be symmetrical. Also observe lateral bending and rotation of the head.

Observe hip, knee and feet position.

First look at the tensor fascia latae. normally this muscle is invisible. If muscle is visible it indicate hypertonus of the MTFL.

Than look at the position of the patella: Symmetry, presence of the shift: if quadriceps is tight than patella shifted superiorly

if MTFL is tight patella will shift supero-lateraly and tilt

If vastus medialis is hypertrophied you will see muscle bulk medially to patella

It is usually sign of overstressed knee joint

When proprioception of the knee is altered patella will move in irregular manner from intermittent activity of the m.quadriceps to improve stability of the knee joint.

This vertical translation of the patella is an important sign of poor proprioception of the knee joint.

Look at the lower leg, primarily tibias anterior.

If M.tibialis anterior (anterolateral aspect of the lower leg, just below the knee) is weak than it’s fibers become flat or even they develop groove-early sign of L4-L5 irritation.

Look at the toes.

Unquiet foot” irregular twitching movement of the tendons of the toes in the different directions-sign of impaired proprioception and the more demanding effort to maintain the balance.

 

Torso:

Lateral view: Look at the presence of anterior or posterior tilts.

Look at the lumbar, thoracic and cervical curvatures:The interrelationships of which may depend on the balance between  hips flexors and extensors or abdominal muscles and back extensors.

Look at the position of the head, particularly “push forward head position”

Observe line running from the jaw to the hyoid bone: if the supra-hyoid muscles is tight this line become more straight, indicating TMJ problems

Look at the position of the legs, particularly knees (genu recurvatum)

Look at the greater trochanter- MTFL: if groove is present-MTFL is tight

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Structure and synthesis of collagen in the human body

Collagen is the most abundant protein found in mammals, making up about 25 percent of the total proteins in the human body. There are at least 16 types of collagen, but 80 – 90 percent of the collagen in the body consists of types I, II, III and IV. Type I: Makes up the fibers found in connective tissues of the skin, bone, teeth, tendons and ligaments.
Type II: Round fibers found in cartilage.
Type III: Forms connective tissues that give shape and strength to organs, such as the liver, heart, kidneys, etc.
Type IV: Forms sheets that lie between layers of cells in the blood vessels, muscles, and eye.

These collagen molecules pack together to form long thin fibrils of similar structure.  At one time it was thought that all collagens were secreted by fibroblasts in connective tissue, but we now know that numerous epithelial cells make certain types of collagens. The various collagens and the structures they form all serve the same purpose, to help tissues withstand stretching.

The triple-helical structure of collagen arises from an unusual abundance of three amino acids: glycine, proline, and hydroxyproline. These amino acids make up the characteristic, repeating motif Gly-Pro-X, where X can be any amino acid. Each amino acid has a precise function.  Collagen biosynthesis and assembly follows the normal pathway for a secreted protein. The collagen chains are synthesized as longer precursors called procollagens; the growing peptide chains are co-translationally transported into the lumen of the rough endoplasmic reticulum (ER). In the ER, the procollagen chain undergoes a series of processing reactions.

Post-translational modification of procollagen is crucial for the formation of mature collagen molecules and their assembly into fibrils. Defects in this process have serious consequences, as ancient mariners frequently experienced. For example, the activity of hydroxylases requires an essential cofactor, ascorbic acid (vitamin C). In cells deprived of ascorbate, as in the disease scurvy, the procollagen chains are not hydroxylated sufficiently to form stable triple helices at normal body temperature, nor can they form normal fibrils. Consequently, nonhydroxylated procollagen chains are degraded within the cell. Without the structural support of collagen, blood vessels, tendons, and skin become fragile. A supply of fresh fruit provides sufficient vitamin C to process procollagen properly.

The biosynthetic pathway responsible for collagen production is a very complex one. In addition to Vitamin C, collagen crosslinking requires Copper, Iron and Manganese.

Prolyl hydroxylase and lysyl hydroxylase require vitamin C and iron as cofactors. Lysyl oxidase deaminates lysine and hydroxylysine in the first step for collagen crosslinking, and this requires copper (hence the hair and skin signs in Menkes disease).

Linus Pauling

In 1989, the eminent American scientist and two-time Nobel Prize winner, Linus Pauling, announced a breakthrough “A Unified Theory of Human Cardiovascular Disease,” Linus Pauling thought that the deposits of plaque seen in atherosclerosis were not the cause of heart disease, but were actually the result of our bodies trying to repair the damage caused by long-term vitamin C deficiency. In essence, Pauling believed that heart disease is a form of scurvy, and plaque is the body’s attempt to reinforce and patch weakened blood vessels and arteries that would otherwise rupture. Pauling also showed that heart disease can be prevented or treated by taking vitamin C and other supplements.

Plaque Deposits

Pauling based his revolutionary theory on a number of important scientific findings. First was the discovery that plaque deposits found in human aortas are made up of a special form of cholesterol called lipoprotein (a) or Lp(a), not from ordinary LDL cholesterol. Lp(a) is a special form of LDL cholesterol that forms the thick sheets of plaque that obstruct arteries.

Another finding central to Pauling’s theory was the observation that plaque deposits are not formed randomly throughout the circulatory system. This was first reported in the early 1950s when a Canadian doctor, G. C. Willis, MD, observed that plaque always forms nearest the heart, where blood vessels and arteries are constantly being stretched and bent, rather than being spread evenly throughout the entire cardiovascular system. Willis also noted that plaque deposits always occur in regions that are exposed to the highest blood pressures, such as the aorta, where blood is forcefully ejected from the heart.

In 1985, a team of researchers verified that plaque only forms in areas of the artery that become damaged. These small areas of damage expose strands of the amino acid lysine (one of the primary components of collagen) to the blood stream. These strands attract Lp(a). Lp(a) is an especially “sticky” form of cholesterol that is attracted to lysine. Drawn to the break, Lp(a) begins to collect and attach to the exposed strands. As Lp(a) covers the lysine strands, free lysine in the blood is drawn to the growing deposit. Over time, this process continues as lysine and Lp(a) are both drawn from the blood to build ever-larger deposits of plaque. This process gradually reduces the inner diameter of the vessels and restricts its capacity to carry the blood.

Heart Disease as Low-Level Scurvy?

Observing the newly described process of plaque formation, Pauling recognized a similarity to underlying processes seen in scurvy. He also saw similarities between human and animal models of atherosclerosis that pointed to a connection with scurvy. First, cardiovascular disease does not occur in any of the animals that are able to manufacture their own vitamin C. Many animals produce large amounts of vitamin C that are equivalent to human doses ranging from ten to twenty grams per day. Second, the only animals that produce Lp(a) are those which, like man, have also lost the ability to produce their own vitamin C, such as apes and guinea pigs.

Pauling suggested that the ability to form plaque is really the body’s attempt to repair damage caused by a long-term deficiency of vitamin C. Pauling thought that scurvy was one of the greatest threats to humankind’s early survival, and believed that the loss of blood during times of vitamin C deficiency, particularly during the Ice Ages, likely brought humans close to the point of extinction.

Plaque as a Life Saver?

The core of Pauling’s theory is that, over time, the body developed a repair mechanism that allowed it to cope with the damage caused by chronic vitamin C deficiency. When arteries became weak and began to rupture, the body responded by “gluing” the damaged areas together with Lp(a) to prevent a slow death from internal bleeding. In essence, plaque is the body’s attempt to patch blood vessels damaged by low-level scurvy. Accordingly, Pauling believed that conventional “triggers” of plaque formation, such as homocysteine and oxidized cholesterol, are actually just additional symptoms of scurvy.

Collagen Melts Plaque, Keeps Arteries Open

In addition to taking vitamin C to prevent atherosclerosis, Pauling recommended a combination of vitamin C and the amino acids lysine and proline to help remove existing plaque while strengthening weak and damaged arteries. As mentioned previously, the body produces collagen from lysine and proline. Pauling reasoned that by increasing concentrations of lysine and proline in the blood, Lp(a) molecules would bind with the free lysine, rather than with the lysine strands exposed by the cracks in blood vessels.

Pauling Therapy for the Reversal of Heart Disease

  1. Vitamin C: to bowel tolerance – as much as you can take without diarrhea. For most people this will be in the range of five to ten grams (5,000-10,000 mg.) each day. Spread this amount into two equal doses 12 hours apart. (Vitamin C prevents further cracking of the blood vessel wall – the beginning of the disease.)
  2. L-Proline: 3 grams twice per day (acts to release lipoprotein(a) from plaque formation and prevent further deposition of same).
  3. L-Lysine: 3 grams twice each day (acts to release lipoprotein(a) from plaque formation and prevent further deposition of same).
  4. Co-enzyme Q10: 90-180 mg. twice per day (strengthens the heart muscle).
  5. L-Carnitine: 3 grams twice per day (also strengthens the heart muscle).
  6. Niacin: Decreases production of lipoprotein(a) in the liver. Inositol hexanicotinate is a form of niacin which gives less of a problem with flushing and therefore allows for larger therapeutic doses. Begin with 250 mg. at lunch, 500 mg. at dinner and 500 mg. at bedtime the first day; then increase gradually over a few days until you reach four grams per day, or the highest dose under four grams you can tolerate. Be sure to ask your doctor for liver enzyme level tests every two months or less to be sure your liver is able to handle the dose you are taking.
  7. Vitamin E: 800-2400 IU per day. (Inhibits proliferation of smooth muscle cells in the walls of arteries undergoing the atherosclerotic changes.)

 

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Marshall Protocol in chronic illnesses

Dr. Renata Trister DO

The Marshall Protocol is a medical treatment used by physicians worldwide to treat a variety of chronic inflammatory and autoimmune diseases including Chronic Fatigue Syndrome, Fibromyalgia, Crohn’s Disease, Sarcoidosis and Rheumatoid Arthritis.  Dr. Marshall started his research after to being diagnosed with sarcoidosis. After reading studies that demonstrated Rickettsia DNA in sarcoid patients, and by noting that his disease was worsened by sunlight. He developed a hypothesis, and a treatment protocol to treat chronic inflammatory illnesses.

Sarcoidosis is a disease whose etiology is unknown, but is characterized by non-caseating granulomas.  Granulomas are an immunologic response to infections, often fungal or mycobacterial. Sarcoidosis frequently causes dysregulation of vitamin D with increased levels in the blood, the vitamin D being made in the granulomas.

The Marshall Protocol is based on the hypothesis that “chronic diseases (termed T-helper [Th1] illnesses) are the result of infection by an intraphagocytic, metagenomic microbiota of chronic bacterial forms that are often referred to as the Th1 pathogens”. The term intraphagocytic refers to the fact that these bacteria have developed the ability to remain alive and proliferate undetected inside the cytoplasm of the cells they infect. These cells include macrophages (cells of the innate immunity), the very cells that the body uses to kill invading pathogens. Once inside these cells, they cause our own cells to release inflammatory cytokines (proteins that often generate pain and inflammation).

The term metagenomic indicates that there is a tremendous number of different species of these chronic bacterial forms. Finally, the term microbiota refers to the fact that these bacteria are also thought to sustain themselves by grouping into communities called biofilms. The bacteria inside a biofilm produce a protective matrix that allows them to more effectively evade the immune system and develop resistance to antibiotics.

Many of the Th1 pathogens are also postulated to be in a chronic state referred to as the L-form. Under certain conditions, L-form bacteria mutate from classical bacteria and lose their cell walls. Since L-form bacteria lack a cell wall, many antibiotics (that target bacterial cell walls) are not effective, furthermore these pathogens cannot be detected by standard laboratory tests.

The ability of the Th1 pathogens to proliferate in the body is directly related to the vitamin D receptor (VDR). Critically important to the body, the Vitamin D Receptor (VDR) controls the innate immune system – the body’s first line of defense against infection. It’s also responsible for turning on/off a wide array of genes and chemical pathways. One of the VDR’s myriad jobs is to control expression of several families of antimicrobial peptides (AMPs), proteins that kill bacteria, viruses and fungi by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell.

Although casually referred to as a vitamin by some members of the medical community, molecular biologists have long realized that the precursor form of vitamin D (25-D) is really a secosteroid.  Elevated levels of 25-D can bind and inactivate the VDR, which subsequently shuts down the innate immune system.

Certain species of bacteria also produce substances that can bind and inactivate the VDR in a manner similar to 25-D. Consequently, people who are infected with the Th1 pathogens and consuming vitamin D are no longer able to produce the AMPs or turn on the innate immune response. This allows their bacteria to proliferate and spread.

When the innate immune system can no longer function, people have a very hard time keeping other pathogens under control. They often find that childhood viral infections reactivate, or that they acquire Candida (pathogenic yeast) and Mycoplasma as well.

Unlike its inactive counterpart, 25-D, that inactivates the VDR in healthy individuals, 1,25-D binds and activates the VDR. But in individuals who have 25-D and bacterial proteins blocking the VDR, 1,25-D is forced out of the receptor and into the surrounding environment. Causing 1,25-D to rise to an unnaturally high level.

The nuclear receptors affected by 1,25-D are receptors that regulate the body’s hormones – the glucocorticoid receptor, and the alpha and beta thyroid receptors, the adrenal receptors, and the progesterone receptors, among others.

This means that when 1,25-D is high, it competitively displaces cortisol, T3, and other metabolites from their target nuclear receptors, causing havoc on the body’s hormonal pathways. Thus, most people with chronic disease find they have difficulty tolerating stress, changes in temperature, and a variety of other hormone-related issues. Also, when levels of 1,25-D rise above 42 ng/ml, calcium begins to be leached from the bones, a process that results in osteoporosis and osteopenia.

When 1,25-D rises due to the processes described above, it also binds a receptor called the PXR. The PXR subsequently inhibits conversion of pre-vitamin D to 25-D, causing 25-D levels to drop. This means that low levels of 25-D – the form of vitamin D measured by most doctors – is not a sign of vitamin D deficiency. Instead, low levels of 25-D are a result of the disease process.

The Treatment

Patients on the Marshall Protocol take a medication called olmesartan (Benicar), which is able to bind and activate the VDR by pushing 25-D and bacterial proteins out of the receptor. Patients also lower levels of 25-D in the body by avoiding the kinds of vitamin D present in various foods. These measures renew the body’s ability to turn on the innate immune system and produce the anti microbial peptides. The immune system is then able to kill the Th1 pathogens and is once again able to manage viral and other co-infections.

At the same time, MP patients take pulsed, low-dose antibiotics. Antibiotics taken in this manner are much more effective against bacteria in biofilms and are able to greatly weaken the Th1 pathogens so that the patient’s own immune system is then able to destroy them. The antibiotics weaken the bacteria by blocking their ribosomes, which they need to produce proteins that help them survive and reproduce. It’s important to understand that when the Th1 pathogens die, there is a temporary change in a patient’s immunopathology.

Immunopathology refers to the changes in the immune system that result from bacterial death (another term sometimes used is the Jarisch-Herxheimer or “Herx” reaction). Dying bacteria release toxins into the bloodstream, stimulate the production of inflammatory cytokines, and generate temporary hormonal imbalances. This means that once patients begin the MP, each dose of antibiotic will cause them to feel bad for the period of time it takes their immune system to deal with the consequences of bacterial die-off.

Before starting the MP, many people may feel that they have improved through consuming vitamin D and taking steroids such as prednisone. In reality, these compounds further inactivate the VDR, preventing the immune system from effectively killing the Th1 pathogens. Since it is the death of these forms of bacteria that generates an increase in painful symptoms, people may experience short-term relief when using vitamin D or prednisone as their immune system shuts down and fewer bacteria are killed. However, in reality, this situation allows the bacteria to spread more easily.

Applicable Illnesses

Patients on the MP have dozens of different medical conditions. As evidenced by members’ reported progress on the marshallprotocol.com website, nearly all experience a powerful immunopathological reaction after taking a dose of antibiotics.

Many patients report great improvement, while some are approaching complete recovery.

Some of the diseases patients are currently using the MP to treat include (but are not limited to):

Chronic Fatigue Syndrome

Fibromyalgia

Chronic Lyme disease

Rheumatoid Arthritis

Multiple Chemical Sensitivity (MCS)

Myasthenia gravis

Psoriasis

Osteoarthritis

Sarcoidosis

Hashimoto’s Thyroiditis

Uveitis

Apart from the symptoms or diagnosis indicating Th1 disease, the easiest way to find out if the Marshall Protocol may be applicable to your disease is to get a blood test and check the level of your D Metabolites. This test can detect the elevated level of 1,25-D often seen in patients with chronic disease, but must be done correctly in order to be of any value.

Patients can also use a therapeutic probe to determine whether the MP can be applied to their illness. A therapeutic probe refers to a trial period during which a person tests whether or not the taking the MP medications results in immunopathology or other symptom changes.

 

 

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SIJ dysfunction

Jon Trister , MD.
With this issue of the newsletter, I would like to bring our attention to sacroiliac joint problems and the interrelationship between such as Fascia, Osseous structures, Ligaments, Muscles, Tendons, Neuro-Vascular structures, and Visceral structures.

There are different degrees of sacroiliac joint pathologies-from SIJ dysfunction to SIJ dislocation. What units them is the common element of instability of the supportive structures and a resulting lack of tensegrity. I will focus on the mechanical aspect of SIJ pathology. We will discuss other SIJ problems such as Infectious, Rheumatologic and Malignancy in the future newsletters.

Realizing the difference between dysfunction and dislocation I see similarities between them as well. Different factors and combinations of factors cause Sacroiliac Joint Dysfunction: Connective tissue insufficiency, Ligament laxity, and Muscular imbalance. All of these factors lead to abnormal Sacroiliac movement (hyper or hypo-mobility), joint locking and muscular imbalance.

There are many of variations of SIJ mechanical problems: Up-slip and down-slip are good examples. They develop as a result of acute or chronic injury. They are extreme manifestations of the Sacroiliac Joint instability. Very often underlying mechanism of these injuries are connective tissue insufficiency and ligamental laxity involving multiple ligamentous and musculotendinous structures.

Fryette originally described up-slip in 1914. This lesion (up-slip) is essentially a vertical shear between the sacrum and ilium and most commonly occurs on the left side. This injury shortens the distance between the sacroccygeal attachments of the Sacrotuberous ligament to the ischial tuberosity attachment.  Control of Nutation (forward flexion of the base of the sacrum) becomes insufficient. Secondary stabilizers, such as the Piriformis, Gemellus Superior & Inferior, Quadratus femoris , and Obturator internus muscles are activated to mainatain stability. Significant effort is required on the part of the muscles involved to keep the SI joint stable. Due to this extreme exertion and unnatural forces neuro-muscular pathology eventually evolves such as Piriformis syndrome, Posterior hip pain, buttocks pain, sciatica, peripheral nerve entrapment syndromes and so on.

What happens to the posterior Long and Short Sacroiliac Ligaments? Their orientation and tension will change in response to the structural and functional tensions present, this is turn will affect their control over Counter-nutation (backward movement of the base of the sacrum).  Losing control over nutation and counter-nutation will bring into action Gluteal muscles, Thoracodorsal Fascia, Quadratus Lumborum, the Hamstrings in the immediate area and have far reaching consequences through fascial planes and connections.

Superior displacement of the ilium (up-slip) will shorten the Ligaments running from the transverse processes of L4 and L5 to anterior ilium – the Ilio-Lumbar ligaments. Instability of these ligaments will increase shearing forces on L4-L5-S1 discs and lead to annulus tears, disc protrusion and eventually disc herniation. These forces will also activate contraction of the Quadratus Lumborum, Multifidus muscles, Psoas, Latissimus Dorsi  muscles.

Inferior displacement of the ilium (down-slip)- is a rare condition. To differentiate between the up-slip and the down-slip the physician utilizes thorough clinical examination and Standing x-rays. Sometimes the Iliac crest on the side of the down-slip can be perceived as superior due to activation of the Ipsilateral Quadratus lumborum, which pulls pelvis up and tilts the pelvis to the opposite side.

The pubic symphysis has no strong intrinsic stabilizing structures. Without the stabilizing actions of these muscles: transverse abd. m, oblique abd.  m., rectus abdominis m. and adductor longus m., the pubic symphysis would permit 5-10mm of vertical shear.

Any discussion of Sacrum and pelvis would not be complete without mention of the role of the Psoas muscle.  This muscle is always involved in lumbo-pelvic instability. Having arisen from the sides of the lumbar vertebrae and anterior aspects of the transverse processes, it connects to the respiratory and pelvic diaphragms. It plays an important role in general body support, maintaining body structure and the body’s functional relationships through it’s support of the autonomic lumbar plexus. It exerts it’s major impact through the viscera innervated by this plexus, it can well exert a vital influence on visceral function and bodily well-being.

Therefore, treatment of Sacroiliac Joint Mechanical Pathology should include many of the following treatment options: Osteopathic Manipulative Therapy-to restore normal structural relationships; Regenerative therapy utilizing Prolotherapy, Platelet-Rich Plasma, Stem Cell therapy-to restore structural integrity;  Neural therapy, Neuro-fascial injection therapy-to restore neurologic and autonomic function; Physical therapy-to restore proper biomechanics and neuromuscular re-education; Nutritional and Hormonal treatment-to provide critical elements for healing and repair.

The  following structures should be considered for treatments: Sacroiliac Joint(s), Sacroiliac Ligaments, Sacrotuberous Ligaments, Ilio-Lumbar ligaments, Thoracodorsal Fascia, Thoraco-Lumbar junction, Facets joints, Inter- and Supra-spinous ligaments, Multifidus, Quadratus Lumborum, Piriformis, Psoas muscles and in some cases distal attachments of the hamstrings.

Most cases will require diagnostic imaging studies, such as X-Ray , Ultrasound or MRI.

All of these modalities require a intensive study, reading, and education. Skill does not come after one or two conferences or workshops. The learning of Orthopaedic Medicine is a lifetime affair.

Be patient and persistent. Success will come.

Jon Trister MD

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