The immune system is comprised of two main subsystems: innate immunity and adaptive immunity. These systems work collaboratively to protect the body from pathogens and maintain overall health.
Innate Immunity
Innate immunity serves as the body’s first line of defense against pathogens. This response is non-specific, meaning it does not differentiate between different types of pathogens. Key characteristics of innate immunity include:
– Immediate Response: It acts swiftly, combating infections within minutes or hours.
– Non-Specific Defense: It targets all pathogens in a similar manner, without specificity.
– No Immunological Memory: Unlike adaptive immunity, innate immunity does not retain a memory of previous encounters with pathogens.
The components of the innate immune system include physical barriers like skin and mucous membranes, chemical barriers such as stomach acid, and cellular defenses, including phagocytes like macrophages and neutrophils. Innate immunity also encompasses processes like inflammation, which helps recruit immune cells to sites of infection.
The innate immune system consists of various cell types, each fulfilling specific roles that form the body’s first line of defense against pathogens. Below are the main cells involved in innate immunity, along with their respective functions and distinguishing characteristics.
Cells of the Innate Immune System
Phagocytes: This category includes cells like macrophages and neutrophils, which are responsible for engulfing and digesting pathogens through a process known as phagocytosis. They serve as “security guards,” patrolling the body to identify and eliminate potential threats such as bacteria and viruses.
Macrophages: Originating from monocytes, macrophages are long-lived cells located in nearly all tissues. They play a vital role in phagocytosis and secrete cytokines to recruit additional immune cells, thereby promoting inflammation. Macrophages are also capable of presenting antigens to activate the adaptive immune system.
Neutrophils: As the most abundant white blood cells in the innate immune system, neutrophils are short-lived but highly effective in ingesting and destroying bacteria and fungi using toxic granules.
Dendritic Cells: These cells serve as a crucial link between innate and adaptive immunity. They capture antigens and present them to T cells, thereby initiating an adaptive immune response. Dendritic cells are essential for processing antigens from a wide variety of pathogens.
Natural Killer (NK) Cells: NK cells target and destroy infected or cancerous cells by recognizing abnormal surface markers. They release cytotoxins that kill these compromised cells, providing a rapid response against viral infections and tumor formation.
Granulocytes: This group comprises basophils, eosinophils, and mast cells. Basophils and eosinophils play roles in combating parasites and mediating allergic reactions, while mast cells release histamine and other chemicals during inflammatory responses.
Functions and Differences
– Phagocytosis: Macrophages and neutrophils primarily focus on engulfing pathogens to neutralize them.
– Inflammation: Both macrophages and mast cells release cytokines that promote inflammation, helping to recruit additional immune cells to the site of infection.
– Antigen Presentation: Dendritic cells specialize in presenting antigens to T cells, thereby linking innate and adaptive immunity.
– Cytotoxicity: NK cells can directly kill infected or abnormal cells without prior sensitization.
Each cell type significantly contributes to recognizing and responding to pathogens, enhancing the overall efficacy of the innate immune response. While the innate immune system acts quickly and non-specifically, it provides immediate defense as the adaptive immune system prepares a more targeted response.
Adaptive Immunity
Adaptive immunity, also known as acquired immunity, develops over time and provides a specific response to pathogens. Its key features are:
– Specificity: It targets specific antigens found on pathogens.
– Memory: Adaptive immunity retains information about past infections, enabling a more rapid and effective response upon re-exposure to the same pathogen.
– Delayed Response: This type of immunity takes longer to activate compared to innate immunity, often requiring days or weeks to mount a full response.
Adaptive immunity involves specialized cells, such as B cells and T cells. B cells produce antibodies that neutralize pathogens, while T cells can directly eliminate infected cells or assist in activating other immune cells. This system is responsible for the long-lasting protection conferred by vaccines and previous infections.
The adaptive immune system is primarily composed of two types of lymphocytes: B cells and T cells. These cells play crucial roles in recognizing and responding to specific pathogens, and they have distinct functions and characteristics.
B Cells
Functions:
Antibody Production: B cells are responsible for producing antibodies, which are proteins that bind to specific antigens on pathogens, marking them for destruction or neutralization.
Humoral Immunity: B cells mediate humoral immunity, which involves the secretion of antibodies into bodily fluids to combat extracellular pathogens.
Antigen Presentation: B cells can present antigens to T cells, aiding in the activation of the adaptive immune response.
Characteristics:
Maturation: B cells mature in the bone marrow.
Receptors: They possess B cell receptors (BCRs) on their surface, which are specific to particular antigens.
Activation: Upon encountering their specific antigen, B cells can differentiate into plasma cells that produce antibodies or memory B cells that provide long-term immunity.
T Cells
Functions:
Helper T Cells (Th): These cells assist other immune cells by releasing cytokines that enhance the immune response. They help activate B cells and cytotoxic T cells.
Cytotoxic T Cells (Tc): These cells directly kill infected or cancerous cells by recognizing antigens presented on their surface.
Memory T Cells: After an infection is cleared, some T cells become memory T cells, providing a faster response if the same antigen is encountered again.
Characteristics:
Maturation: T cells originate in the bone marrow but mature in the thymus.
Receptors: They have T cell receptors (TCRs) that recognize antigens presented by major histocompatibility complex (MHC) molecules on other cells.
Types: There are several types of T cells, including helper T cells, cytotoxic T cells, and regulatory T cells that help maintain immune tolerance.
Differences Between B Cells and T Cells
Feature
B Cells
T Cells
Origin
Bone marrow
Bone marrow
Maturation Site
Bone marrow
Thymus
Main Function
Produce antibodies
Kill infected/cancerous cells; assist other immune responses
Immunity Type
Humoral immunity
Cell-mediated immunity
Receptor Type
B cell receptor (BCR)
T cell receptor (TCR)
Antigen Recognition
Recognize free antigens
Recognize processed antigens presented by MHC
Subtypes
Plasma cells, Memory B cells
Helper T cells, Cytotoxic T cells, Memory T cells
Both B and T cells are essential for the adaptive immune response, providing specificity and memory that enhance the body’s ability to fight infections more effectively upon re-exposure to pathogens.
The adaptive immune system is primarily composed of two types of lymphocytes: B cells and T cells. These cells play crucial roles in recognizing and responding to specific pathogens, and they have distinct functions and characteristics.
B Cells
Functions:
Antibody Production: B cells are responsible for producing antibodies, which are proteins that bind to specific antigens on pathogens, marking them for destruction or neutralization.
Humoral Immunity: B cells mediate humoral immunity, which involves the secretion of antibodies into bodily fluids to combat extracellular pathogens.
Antigen Presentation: B cells can present antigens to T cells, aiding in the activation of the adaptive immune response.
Characteristics:
Maturation: B cells mature in the bone marrow.
Receptors: They possess B cell receptors (BCRs) on their surface, which are specific to particular antigens.
Activation: Upon encountering their specific antigen, B cells can differentiate into plasma cells that produce antibodies or memory B cells that provide long-term immunity.
T Cells
Functions:
Helper T Cells (Th): These cells assist other immune cells by releasing cytokines that enhance the immune response. They help activate B cells and cytotoxic T cells.
Cytotoxic T Cells (Tc): These cells directly kill infected or cancerous cells by recognizing antigens presented on their surface.
Memory T Cells: After an infection is cleared, some T cells become memory T cells, providing a faster response if the same antigen is encountered again.
Characteristics:
Maturation: T cells originate in the bone marrow but mature in the thymus.
Receptors: They have T cell receptors (TCRs) that recognize antigens presented by major histocompatibility complex (MHC) molecules on other cells.
Types: There are several types of T cells, including helper T cells, cytotoxic T cells, and regulatory T cells that help maintain immune tolerance.
Differences Between B Cells and T Cells
Feature
B Cells
T Cells
Origin
Bone marrow
Bone marrow
Maturation Site
Bone marrow
Thymus
Main Function
Produce antibodies
Kill infected/cancerous cells; assist other immune responses
Immunity Type
Humoral immunity
Cell-mediated immunity
Receptor Type
B cell receptor (BCR)
T cell receptor (TCR)
Antigen Recognition
Recognize free antigens
Recognize processed antigens presented by MHC
Subtypes
Plasma cells, Memory B cells
Helper T cells, Cytotoxic T cells, Memory T cells
Both B and T cells are essential for the adaptive immune response, providing specificity and memory that enhance the body’s ability to fight infections more effectively upon re-exposure to pathogens.
T-helper (Th) cells are a subset of CD4+ T cells that play crucial roles in orchestrating the immune response. The Th1, Th2, and Th17 subsets are particularly important, each with distinct functions and cytokine profiles.
Th1 Cells
Functions:
Intracellular Pathogen Defense: Th1 cells are primarily involved in defending against intracellular pathogens like viruses and certain bacteria. They activate macrophages and enhance their ability to kill ingested microbes.
Cytokine Production: Th1 cells produce cytokines such as interferon-gamma (IFN-γ), which is crucial for macrophage activation and enhancing the cytotoxic activity of natural killer (NK) cells and cytotoxic T lymphocytes (CTLs).
Characteristics:
Activation: Th1 differentiation is driven by cytokines like IL-12 and IFN-γ.
Role in Disease: An excessive Th1 response can contribute to autoimmune diseases by promoting inflammation.
Th2 Cells
Functions:
Extracellular Pathogen Defense: Th2 cells are essential for combating extracellular parasites such as helminths. They promote the production of antibodies by B cells.
Cytokine Production: Th2 cells secrete cytokines including IL-4, IL-5, IL-10, and IL-13, which facilitate B cell class switching to IgE and activate eosinophils and mast cells.
Characteristics:
Activation: Th2 differentiation is induced by cytokines like IL-4.
Role in Disease: Overactive Th2 responses are associated with allergies, asthma, and other atopic conditions.
Th17 Cells
Functions:
Defense Against Extracellular Pathogens: Th17 cells protect against extracellular bacteria and fungi, particularly at mucosal surfaces.
Cytokine Production: They produce pro-inflammatory cytokines such as IL-17A, IL-17F, and IL-22, which recruit neutrophils and enhance barrier integrity.
Characteristics:
Activation: Th17 differentiation requires cytokines like TGF-β, IL-6, and IL-23.
Role in Disease: While critical for host defense, dysregulated Th17 activity is implicated in autoimmune diseases like psoriasis and rheumatoid arthritis.
Autoimmune diseases (e.g., MS for Th1; arthritis for Th17)
Allergies, asthma
The balance between these subsets is crucial for maintaining immune homeostasis. Imbalances can lead to various immune-related disorders, highlighting the importance of understanding their distinct roles in immunity.
Vitamin D plays a crucial role in the immune system, impacting both innate and adaptive immunity. Here’s an overview of vitamin D sources, metabolites, activation, and its function in relation to the immune system:
Sources of Vitamin D
Sunlight: The primary source of vitamin D is sunlight. When skin is exposed to UVB rays, it synthesizes vitamin D3 (cholecalciferol).
Food: Dietary sources include oily fish (e.g., salmon, sardines), egg yolks, liver, and fortified foods like milk and cereals.
Supplements: Vitamin D supplements are available in forms such as vitamin D2 (ergocalciferol) and vitamin D3.
Metabolites and Activation
Vitamin D undergoes several transformations to become active:
Synthesis: In the skin, 7-dehydrocholesterol is converted to vitamin D3 upon UVB exposure.
Liver Conversion: Vitamin D3 is hydroxylated in the liver to form 25-hydroxyvitamin D (25(OH)D), the main circulating form and a marker for vitamin D status.
Kidney Activation: 25(OH)D is further hydroxylated in the kidneys to produce 1,25-dihydroxyvitamin D (1,25(OH)2D), the active form that exerts biological effects.
Function in the Immune System
Vitamin D influences both innate and adaptive immune responses:
Innate Immunity:
Modulation of Immune Cells: Vitamin D binds to receptors on immune cells like macrophages and dendritic cells, enhancing their pathogen-fighting capabilities.
Antimicrobial Peptides: It stimulates the production of antimicrobial peptides such as cathelicidins and defensins, which have antiviral properties.
Adaptive Immunity:
T Cell Regulation: Vitamin D modulates T cell responses by inhibiting Th1 and Th17 cell proliferation while promoting regulatory T cells (Tregs), which help maintain immune tolerance.
B Cell Function: It can reduce the production of autoantibodies by B cells, potentially ameliorating autoimmune conditions.
Impact on Health
Autoimmune Diseases: Vitamin D deficiency is linked to increased risk of autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. Supplementation may help modulate disease activity.
Infections: Adequate vitamin D levels are associated with reduced susceptibility to infections like respiratory tract infections.
The conversion of 25-hydroxyvitamin D (25(OH)D) to its active form, 1,25-dihydroxyvitamin D (1,25(OH)2D), and its subsequent inactivation involves specific cytochrome P450 enzymes.
Activation of Vitamin D
CYP27B1: This enzyme, also known as 25-hydroxyvitamin D-1α-hydroxylase, is responsible for converting 25(OH)D to the active form 1,25(OH)2D (calcitriol). This conversion primarily occurs in the kidneys but can also take place in other tissues like the placenta and immune cells.
Inactivation of Vitamin D
CYP24A1: Known as 25-hydroxyvitamin D3-24-hydroxylase, CYP24A1 is involved in the catabolism of vitamin D. It converts both 25(OH)D and 1,25(OH)2D into inactive forms by hydroxylating them at the 24-position. This process is crucial for regulating and maintaining appropriate levels of active vitamin D in the body.
CYP3A4: Although primarily recognized for its role in drug metabolism, CYP3A4 can also participate in the catabolism of vitamin D by hydroxylating it into less active forms.
These enzymes ensure a balance between the activation and inactivation of vitamin D, which is essential for maintaining calcium homeostasis and supporting various physiological processes, including immune function.
The activation of CYP27B1, the enzyme responsible for converting 25-hydroxyvitamin D (25(OH)D) to its active form, 1,25-dihydroxyvitamin D (1,25(OH)2D), is regulated by several factors:
Parathyroid Hormone (PTH): PTH is a primary activator of CYP27B1. It increases the expression of this enzyme, promoting the conversion of 25(OH)D to 1,25(OH)2D. This process is crucial for maintaining calcium homeostasis, as 1,25(OH)2D enhances intestinal calcium absorption.
Fibroblast Growth Factor 23 (FGF23): While FGF23 primarily acts to decrease the synthesis of 1,25(OH)2D by reducing CYP27B1 activity, it plays a role in the overall regulation of phosphate and vitamin D metabolism.
Calcium and Phosphate Levels: Changes in serum calcium and phosphate levels can influence CYP27B1 activity. Low calcium levels typically stimulate PTH release, which in turn activates CYP27B1.
Feedback Regulation by 1,25(OH)2D: The active form of vitamin D itself can downregulate CYP27B1 expression as part of a feedback loop to prevent excessive production of 1,25(OH)2D.
Cytokines: In extrarenal tissues, cytokines such as interferon-gamma (IFN-γ) can upregulate CYP27B1 expression, particularly in immune cells like macrophages during inflammatory responses.
6.Infections can upregulate the expression of CYP27B1. The enzyme CYP27B1, which is responsible for converting inactive vitamin D into its active form, is expressed in various immune cells, including macrophages and dendritic cells. This expression is regulated by immune inputs such as interferon-gamma (IFN-γ), a cytokine secreted by T cells, and agonists of pattern recognition receptors (PRRs) like Toll-like receptors (TLRs).PRR recognizes PAMP on bacterias
When these immune pathways are activated, such as during an infection, there is an increase in CYP27B1 expression. For example, stimulation of macrophages with TLR ligands has been shown to induce CYP27B1 expression and enhance the production of active vitamin D (1,25-dihydroxyvitamin D) from its precursor. This process plays a significant role in the immune response by boosting antimicrobial activities and enhancing innate immune responses.
Additionally, studies have shown that injury or microbial stimulation can lead to increased CYP27B1 expression in keratinocytes through the activation of TLR2. This suggests that the upregulation of CYP27B1 during infections is part of a broader immune response mechanism aimed at enhancing the body’s ability to fight off pathogens.
These regulatory mechanisms ensure that the production of active vitamin D is tightly controlled, balancing its roles in calcium homeostasis and immune function.
Prolotherapy is a controlled injury to the connective tissues of joints and their capsules, tendons, ligaments and cartilages. Injury triggers the activation of mesenchymal stem cells (MSCs) within treated areas. When an injury occurs, it creates a localized microenvironment rich in cytokines and growth factors that attract and activate various stem cells, including MSCs. This activation is part of a complex response to tissue damage, with MSCs playing a crucial role in modulating inflammation and promoting tissue repair.
MSCs have the ability to sense and respond to signals emitted by injured tissues. For instance, they can be activated by mitochondria released from damaged cells, which serve as danger signals. This interaction prompts MSCs to enhance their cytoprotective functions, including anti-apoptotic and anti-inflammatory activities. Additionally, MSCs can modulate immune responses by influencing macrophage polarization, which is essential for controlling inflammation and fostering tissue regeneration after injuries, such as spinal cord damage.
In summary, injury activates mesenchymal stem cells, which contribute to tissue repair and regeneration through various mechanisms, including immune modulation and direct interactions with damaged cells.
Mesenchymal stem cells (MSCs) support the regeneration of connective tissue through several mechanisms:
1. Paracrine Signaling: MSCs secrete a range of growth factors, cytokines, and hormones that impact their surrounding environment. These secreted factors promote cell survival, reduce inflammation, and stimulate the proliferation and differentiation of resident cells in the damaged tissue.
2. Immunomodulation: MSCs have immunomodulatory properties that help create a regenerative microenvironment. They can suppress immune responses, thereby reducing inflammation and enhancing tissue repair and regeneration.
3. Angiogenesis Promotion: MSCs facilitate the formation of new blood vessels (angiogenesis) by releasing factors that stimulate endothelial cells. This process is vital for supplying nutrients and oxygen to regenerating tissues.
4. Extracellular Matrix Remodeling: MSCs assist in remodeling the extracellular matrix by regulating collagen synthesis and deposition, which helps restore the structural integrity of connective tissues.
5. Direct Differentiation: Although not their primary function, MSCs can differentiate into various cell types, including osteoblasts, chondrocytes, and adipocytes, thereby contributing directly to tissue regeneration when necessary.
These combined actions establish MSCs as a powerful resource in regenerative medicine for repairing and regenerating connective tissues.
The Myers’ Cocktail is an intravenous vitamin therapy designed to deliver a high concentration of vitamins and minerals directly into the bloodstream. It was developed by Dr. John Myers in the 1970s and is widely used in complementary and alternative medicine.
Composition and Benefits
The standard formulation of the Myers’ Cocktail typically includes:
– Vitamins: B-Complex vitamins, Vitamin B12, and Vitamin C
– Minerals : Magnesium and Calcium
– Other Components: Sometimes includes zinc and glutathione, depending on the specific formulation.
The cocktail is believed to offer several health benefits, including:
– Boosting the immune system
– Increasing energy levels
– Reducing fatigue
– Improving overall health and well-being
– Detoxifying the body
– Reducing stress, anxiety, and depression
It is also used to address various health conditions such as asthma, migraines, chronic fatigue syndrome, fibromyalgia, and upper respiratory tract infections.
Administration
The Myers’ Cocktail is administered intravenously, allowing the nutrients to bypass the digestive system and enter the bloodstream directly. This method ensures rapid absorption and higher bioavailability of the nutrients compared to oral supplements.
When administered correctly, the Myers’ Cocktail is generally considered safe, with serious side effects being rare. However, potential temporary side effects can occur, and patients are advised to consult with Doctor or NP to assess any risks, especially if they have underlying health conditions.
Thank You for your interest in Prolotherapy, to make an initial consultation
effective and informative please follow the steps below.
* Read all available information about Prolotherapy online, and the information
provided in this packet
* Prepare a list of questions you may have for the doctor.
* Please obtain a copy of any radiological images (XRAY, CT SCAN MRI). You
should be able to request a copy of the radiology imagines from the Radiology
Department.
* Please obtain a copy of your latest blood test results including complete blood
count (CBC) & Basic metabolic panel (BMP)
* Please provide a list of current medical conditions including any allergies and/or
food sensitives.
* Please provide a list of current medications along with the dosage and frequency.
Along with any over the counter medication/supplements you may be taking.
What You Can Expect:
The initial consultation will be focused on taking detailed history and conducting a
musculoskeletal physical exam to assure the appropriateness of Prolotherapy. Your
diagnostic test/s will be reviewed and taken into consideration along with any
medications and/or supplements you are taking. Patients are encouraged to bring a
family member or friend to the consultation to ensure that all possible questions
have been addressed during the consultation.
*PLEASE NOTE: Treatment will not be performed the day of
consultation.
*The cost of the initial consultation is $375.00. Insurance does NOT
COVER PROLOTHERAPY.
Absolute Contraindications for prolotherapy:
Hardware from prior surgical procedure in the affected area
Currently undergoing treatment for cancer
Currently undergoing treatment for autoimmune condition and taking
“immune modulating therapies”
“Full thickness” tendon tears
Any evidence of infection
Pregnancy
FACTS REGARDING PROLOTHERAPY:
Prolotherapy (Regenerative Injection Therapy) was originally used by Hippocrates
over 2500 Years ago to heal a javelin’s shoulder injury. This concept was
investigated, utilized, and refined by Dr. George Hackett, MD over 70 Years ago.
The cause of a great deal of musculoskeletal pain is related to chronic laxity or
relaxation of the connective tissues (ligaments and tendons), which normally
control joint movement and provide support for standing, sitting, and locomotion.
These tissues are moist commonly damaged by trauma and overuse and the initial
healing response may not adequately “weld” the structures back together.
Furthermore, anti-inflammatory medications (Ibuprofen, naproxen) also interfere
with the body’s natural healing process, which may result in chronic weakness/
laxity of these ligaments. These once elastic ligaments and tendons “lose” their
elasticity. Other contributing factors to ligamental laxity are hormonal changes,
such as pregnancy. This is physiologic in preparation for childbirth. However often
times the ligaments and/or tendons do not restore their elastic properties fully.
Other individuals are predisposed because of genetic variations such as Ehlers
Danlos Syndrome or other connective tissue disorders resulting in joint
hypermobility or “double jointedness.”
The result of reduced structural stability is a chronic sprain of the ligament and
tendon fibers which are connected to the extremely sensitive periosteum of the
bone which through nerves sends pain signals to the brain. To compensate for the
instability, the corresponding muscles go into spasm resulting in pain and stiffness.
There lies the paradox: muscle stiffness is the result of joint hypermobility.
Prolotherapy Injections contain dextrose, local anesthetic, and sterile water.
Injections are targeted into the joint space as well as around the joint space (where
ligament/tendon connect to bone – enthesis). The solution is hyperosmolar, causing
a controlled injury and healing response, which results in growth (Proliferation) of
the tissues. In other words, we are injuring the area to stimulate your body to heal.
Over time, the weakened tissues get stronger resulting in increased stability, less
muscle tension/spasms, improved range of motion and eventually less pain.
Numerous studies have shown a success rate of 80-90% over thousands of patients
with success judged as at least 50% reduction in pain.
Typically, injection treatment sessions are administrated 4-6 weeks apart with an
average number of 4-6 injection sessions required per patient. This is very much a
case by case basis. It is important to remember that everybody heals differently and
we will go into your specific situation during the consult. However, the response is
directly related to the speed of healing within our bodies. Generally, young, healthy
people who good nutritional status will heal faster than someone in poor health.
Publications Describing Prolotherapy
1) Hackett, George A., and Henderson, Donald G., “Joint Stabilization: An
experimental, Histologic Study with comments on the Clinical Application in
Ligament Proliferation” American Journal of Surgery, 89 (May 1955),
PP.968-973.
2) Klein, Robert G. Proliferation Injections for Low Back Pain: Histologic
Changes of Injected Ligaments and Objective Measures of Lumbar Spine
Mobility Before and after Treatment”, Journal of Neurology, Orthopedic
Medicine, and Surgery, 1989, 10:141-144
3) Klein, Robert G., Mooney, Vert, ET AL “A Randomized Double-Blind Study
of Dextrose-Glycerin-Phenol Injections for Chronic Lower Back Pain”,
Journal of Spinal Disorders, 1993, 6:23-33.
4) Lui, Y Kinget Al., “An in-Situ Study of The Influence of Sclerosing Solution
in Rabbit Medical Collateral Ligaments and it’s Injection Strength”,
Connective Tissue Research, 11 (1983), PP 95-102
5) Ongley, Milne J., “A New Approach to the Treatment of Chronic Low Back
Pain”, The Lancet (July 18, 1987), PP 143-146
6) Dorman, Thomas A, Editor, Prolotherapy in the Lumbar Spine and Pelvis
Spine: State of Art Reviews, Volume 9 Number 2, Philadelphia, Hanley and
Belfus, Inc., 1995
7)Hackett, George S., and Hemwall, Gustav A., and Montgomery, Gerald A.,
“Ligament and Tendon Relaxation Treated by Prolotherapy”, 5th Edition, 2nd
printing, Oak Park, Illinois 1993
8)Houser, Ross, “Prolo Your Pain Away”, Curing Chronic Pain with
Prolotherapy”, Beulah Land Pres, Oak Park Illinois 1998.
9)Reeves, K Dean, “Technique of Prolotherapy”, Psychiatric Procedures,
Lennard, Ted A., Editor, PP 57-70, Philadelphia, Hanley Belfus, 1995
10)Wilkinson, Harold A., “The Failed Back Syndrome: Etiology and Therapy”,
New York, Springer-Verlag, 1992, PP 147-169.
Patient Preparation for Injections: 1)Read the Prolotherapy handout and make sure you have ALL your questions
answered before beginning treatment.
2)You may have a light meal the day of your treatment, however, please do not
consume any food within 2 hours of your treatment. The weeks leading up to
treatment you want to eat a lot of foods rich protein and vitamin C; this will
help with healing. Lots of high quality grass fed beef, pasture raised chicken,
wild caught fish, organic vegetables and fruit. You also want to make sure you
stay adequately hydrated; at least 64 fluid oz water/day.
3)For your safety it is highly recommended to have someone drive you home
after your treatment, mandatory if you are having treatment on your Neck.
4)Please STOP Aspirin and Non-Steroidal Anti-Inflammatory Medications.
It is Okay to continue taking “BABY-ASPIRIN” (81MG) unless otherwise
told by your doctor.
5)STOP ANTI-PLATELET AGENTS (PLAVIX, TICLID) for 7 days prior.
With approval from your doctor.
6)STOP COUMADIN (WARFIN) for 5 days prior to your injection with
PRIOR APPROVAL from your DOCTOR and obtain STAT BLOOD
TEST (PT, INR AND PTT) on the morning of your injection. Have any
results faxed to our office.
Please contact us prior to your appointment if:
1)You have a significant change in your medical history. 2)You have any questions about your medications. 3)You are taking antibiotics, are being for an infection or are feeling ill.
Thank you and we look forward to seeing you at your next visit.
Am I a candidate for Regenerative Injection Therapy (Prolotherapy)?
Many problems related to musculoskeletal conditions are can be successfully
treated with prolotherapy:
1.Degenerative Joint Diseases (Osteoarthritis) of 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 and tendinous injuries (with some
limitations). Partial tears of tendons, muscles and ligaments can be
successfully treated with prolotherapy +/- PRP (platelet rich plasma)
3. Some forms 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, cancer
spread into the bones (metastasis, multiple myeloma, leukemias) are not
candidate for prolotherapy
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.
7. Other factors may play role too: anticoagulation therapy, anti-platelets
therapy, etc
How much does it cost?
A.: The initial evaluation cost is $375.00. Treatment prices vary by area.
Detailed pricing will be given at consultation
Will my insurance pay for this treatment?
A.: No, unfortunately prolotherapy is not covered by insurance
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. Average 3-6 sessions.
How far apart are the treatments?
A.: Treatments are usually given at 4-6 week 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. In some cases we do PRP (Platelet Rich Plasma) which is your
own blood product.
What is the success rate with prolotherapy?
A.: Prolotherapy generally has about a 80% 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 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 their opinion about what they believe is causing your
pain or other problems, order any new studies that may be needed and make
recommendations for treatment. They 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, if the doctor feels
that you are a candidate for prolotherapy, they will explain the risks to you
and try to answer all of your questions.
It is important to remember that prolotherapy is a controlled injury. Therefore
you should expect to be sore for the following 24-48 hours.
Orange Peel Tea for Immune Support During these uncertain times, supporting your immune system and the microbiome is important. You can drink this tea throughout the day and swish it around your mouth (unsweetened) to support the oral and gut microbiome. Ingredients: Orange or any citrus peel (from 4-5 fruits)1/4 Onion1 inch Ginger2-3 Sprigs of Rosemary2 tsp Whole Cloves2-3 Star Anise1-2 tbs Fennel seeds 8-10 cups water. Bring to a boil & simmer for 20 minutes (or up to an hour) Keep in mind that you don’t have to have every single ingredient. There is no way to do this wrong. A simple tea of citrus peel is helpful. The other ingredients can be rotated. The goal is to use what you have on hand and get lots of polyphenols from these plants. Boiling these plants in water helps get the nutrients out. You can use a vegetable peeler to peel the citrus and save the peels in a bowl as you go in your fridge. Once you have enough, you can make tea. If you are having digestive issues, prioritize the ginger and fennel after the citrus peel. The onion provides quercetin, a flavonoid, useful for immune support, and is very antimicrobial. You don’t taste it in the tea, but it provides benefits. The spices all function to support the gut flora. Star anise contains shikimic acid and is used as a base material for the production of Tamiflu.
Cellular components of the organs and tissues, vascular and neurological structures are parts of tensegrity arrangement; Microbiome is an equal part of this ecosystem. Tensegrity is influenced by the microbiome. At the same time, mechanical properties of the connective tissue will influence microbiome composition and pathogenicity.
Cellular components of the organs and tissues, vascular and neurological structures are suspended in the tensegrity network and actually part of this network. Their form and function regulated by mechanical properties of the ecosystem they reside (Pre-stress).
Pre-stress is influenced by
microbiome and microbiome is regulated by pre-stress.
Microbiota are
ecological communities of commensal,
found in and on all multicellular organisms.
Microbiota includes bacteria, archaea, protists, fungi
and viruses. Microbiota have a crucial role
for immunologic, hormonal and metabolic
homeostasis of
their host. The synonymous term microbiome describes
either the collective genomes of
the microorganisms that reside in an environmental niche or the microorganisms
themselves
Microbiome
persist in nearly every human body site, including tissue and blood. The
genomes of these microbes continually interact with the human genome in order
to regulate host metabolism.
Many components of this microbiome are capable of both
commensal and pathogenic activity. This activity is determined by environment they
reside (viscoelasticity -pre-stress): immunological cells responsible for
innate and adaptive responses. They are additionally able to persist in both
“acute” and chronic forms. Inflammatory conditions historically
studied separately (autoimmune, neurological and malignant) are now repeatedly
tied to a common trend: imbalance or dysbiosis of these microbial ecosystems.
Collective activity of the
microbiome that drives inflammatory processes via complex microbe-microbe and
host-microbe interactions. Many microbes survive as polymicrobial entities in
order to evade the immune response. Pathogens in these communities alter their
gene expression in ways that promote community-wide virulence. Other microbes
persist inside the cells of the immune system (Cell Wall Deficient bacteria -CWD),
where they directly interfere with host transcription, translation, and DNA
repair mechanisms. The numerous proteins and metabolites expressed by these
pathogens further dysregulate human gene expression in a manner that promotes
imbalance and immunosuppression. Molecular mimicry, or homology between host
and microbial proteins, complicates the nature of this interference. When taken
together, these microbe-microbe and host-microbe interactions are capable of
driving the large-scale failure of human metabolism characteristic of many
different inflammatory conditions.
Microbiota are “ecological communities
of commensal, symbiotic and pathogenicmicroorganisms” found
in and on all multicellular organisms. Microbiota includes bacteria, archaea, protists, fungi
and viruses. Microbiota have been found to be crucial for immunologic, hormonal
and metabolic homeostasis of
their host. The synonymous term microbiome describes
either the collective genomes of
the microorganisms that reside in an environmental niche or the microorganisms
themselves
Microbiome
persist in nearly every human body site, including tissue and blood. The
genomes of these microbes continually interact with the human genome in order
to regulate host metabolism.
Many components of this microbiome are capable of both
commensal and pathogenic activity. They are additionally able to persist in
both “acute” and chronic forms. Inflammatory conditions historically
studied separately (autoimmune, neurological and malignant) are now repeatedly
tied to a common trend: imbalance or dysbiosis of these microbial ecosystems.The collective activity of the microbiome that drives inflammatory processes via complex microbe-microbe and host-microbe interactions. Many microbes survive as polymicrobial entities in order to evade the immune response. Pathogens in these communities alter their gene expression in ways that promote community-wide virulence. Other microbes persist inside the cells of the immune system, where they directly interfere with host transcription, translation, and DNA repair mechanisms. The numerous proteins and metabolites expressed by these pathogens further dysregulate human gene expression in a manner that promotes imbalance and immunosuppression. Molecular mimicry, or homology between host and microbial proteins, complicates the nature of this interference. When taken together, these microbe-microbe and host-microbe interactions are capable of driving the large-scale failure of human metabolism characteristic of many different inflammatory conditions. (Amy D Proal)
Mechanical properties of the skin are changed with time. Altered pre-stress changes first defenses of the immune system-physical barriers-Epidermis and dermal layers of the skin. Reduced functional capacity and increased susceptibility of the skin with development of dermatoses such as dry skin, itching, ulcers, dis-pigmentation, wrinkles, fungal infections, as well as benign and malignant tumors are the most common skin conditions in aged population. In turn altered appearance, dry skin, chronic wounds, and other conditions decrease general health and reduce the likelihood for healthy and active aging. Ability of the skin to carry out multiple and wide-ranging roles is very closely related to its structure, which is composed of an outer epidermis overlying an inner dermis, separated by a basement membrane.
Biochemical barriers: acidic, hydrolipidic nature of the
skin, as a result of sweat, sebum, lipids, and antimicrobial peptides
(AMPs).Any changes in lipid composition and epidermal differentiation lead to a
disturbed skin barrier, which plays a role in the pathogenesis of several
immune-mediated skin pathologies, such
as atopic dermatitis and ichthyosis vulgaris .
The epidermis is a host to keratinocytes, melanocytes
and immune cells such as Langerhans cells (LCs) and T lymphocytes, nerve-ending
cells (Merkel cells).The dermis is composed of an upper papillary (stratum
papillare) and lower reticular (stratum reticulare) dermis containing thin and
thick collagen fibers, respectively. The collagen fibers offer a mechanical
barrier as well as a structural environment
in which to host blood vessels and many immune cells such as dermal
dendritic cells (DDCs), ab T cells, gd T cells, natural killer (NK) cells, B
cells, mast cells, and macrophages can perform their function.
More recently, it was proposed a sentinel role in health
and disease for a spectrum of skin-resident cells ( with keratinocytes involved
in sensing pathogens and danger signals, migratory DCs capable of initiating a
diverse range of immune responses, and tissue-resident memory T (Trm) cells
performing crucial effector functions.
Skin-associated lymphoid tissue
(SALT) participates in trafficking of
immune cells between the skin, draining lymph nodes (LNs), and the peripheral
circulation (Streilein, 1983).
