When there is a genetic immune deficiency disease, can Homeopathy Help?
WIKIPEDIA | Osteogenesis imperfecta
Osteogenesis imperfecta (OI and sometimes known as
Brittle Bone Disease, or
"Lobstein syndrome"[1]) is a genetic bone disorder. People with OI are born with
defective connective tissue, or without the ability to make it, usually because of a deficiency of Type-I collagen.[2] This deficiency arises from an
amino acid substitution of glycine to bulkier amino acids in the collagen triple helix structure. The larger amino acid side-chains create steric hindrance that creates a "bulge" in the collagen complex, which in turn influences both the molecular nanomechanics as well as the interaction between molecules, which are both compromised [3]. As a result, the body may respond by hydrolyzing the improper collagen structure. If the body does not destroy the improper collagen, the relationship between the collagen fibrils and hydroxyapatite crystals to form bone is altered, causing brittleness [4]. Another suggested disease mechanism is that the stress state within collagen fibrils is altered at the locations of mutations, where locally larger shear forces lead to rapid failure of fibrils even at moderate loads as the homogeneous stress state found in healthy collagen fibrils is lost [5]. These recent works suggest that OI must be understood as a multi-scale phenomenon, which involves mechanisms at the genetic, nano-, micro- and macro-level of tissues.
As a genetic disorder, OI is an autosomal dominant defect. Most people with OI receive it from a parent but it can be an individual (de novo or "sporadic") mutation.
Type I
Collagen is of normal quality but is produced in insufficient quantities:
- Bones fracture easily
- Slight spinal curvature
- Loose joints
- Poor muscle tone
- Discoloration of the sclera (whites of the eyes), usually giving them a blue-gray color. The blue-gray color of the sclera is due to the underlying choroidal veins which show through. This is due to the sclera being thinner than normal because of the defective Type I Collagen not forming correctly.
- Early loss of hearing in some children
- Slight protrusion of the eyes
IA and IB are defined to be distinguished by the absence/presence of dentinogenesis imperfecta (characterized by opalescent teeth; absent in IA, present in IB). Life expectancy is slightly reduced compared to the general population due to the possibility of fatal bone fractures and complications related to OI Type I such as Basilar invagination.[citation needed]
Type II
Collagen is not of a sufficient quality or quantity
Type II can be further subclassified into groups A, B, C, which are distinguished by radiographic evaluation of the long bones and ribs. Type IIA demonstrates broad and short long bones with broad and beaded ribs. Type IIB demonstrates broad and short long bones with thin ribs that have little or no beading. Type IIC demonstrates thin and longer long bones with thin and beaded ribs.
Type III
Collagen quantity is sufficient but is not of a high enough quality
- Bones fracture easily, sometimes even before birth
- Bone deformity, often severe
- Respiratory problems possible
- Short stature, spinal curvature and sometimes barrel-shaped rib cage
- Loose joints
- Poor muscle tone in arms and legs
- Discolouration of the sclera (the 'whites' of the eyes)
- Early loss of hearing possible
Type III is distinguished among the other classifications as being the "Progressive Deforming" type, wherein a neonate presents with mild symptoms at birth and develops the aforementioned symptoms throughout life. Lifespan may be normal, albeit with severe physical handicapping.
Type IV
Collagen quantity is sufficient but is not of a high enough quality
- Bones fracture easily, especially before puberty
- Short stature, spinal curvature and barrel-shaped rib cage
- Bone deformity is mild to moderate
- Early loss of hearing
Similar to Type I, Type IV can be further subclassified into types IVA and IVB characterized by absence (IVA) or presence (IVB) ofdentinogenesis imperfecta.
Type V
X-Ray OI Type V in Adult X-Ray OI Type V Kid
OI Type V leads to calcification of the membrane between the two forearm bones, making it difficult to turn the wrist. Another symptom is abnormally large amounts of repair tissue (hyperplasic callus) at the site of fractures. At the present time, the cause for Type V is unknown, though doctors have determined that it is inherited.Same clinical features as Type IV. Distinguished histologically by "mesh-like" bone appearance. Further characterized by the "V Triad" consisting of a) radio-opaque band adjacent to growth plates, b) hypertrophic calluses at fracture sites, and c) calcification of the radio-ulnar interosseous membrane [6].
More on Type V Research More on OI Study
[edit]Type VI
Same clinical features as Type IV. Distinguished histologically by "fish-scale" bone appearance.
[edit]Type VII
Mutations in the gene CRTAP causes this type. [7]
Type VIII
OI caused by mutation in the gene LEPRE1 is classified as type VIII. [7]
Bisphosphonates Bisphosphonates (BPs), particularly those containing nitrogen, are being increasingly administered to increase bone mass and reduce the incidence of fracture. BPs can be dosed orally (e.g. alendronate) or by intravenous injection/infusion (e.g. pamidronate,[8] zoledronic acid).
BP therapy is being used increasingly for the treatment of OI. It has proven efficiency in reducing fracture rates in children,[9] however only a trend towards decreased fracture was seen in a small randomized study in adults.[10] While decreasing fracture rates, there is some concern that prolonged BP treatment may delay the healing of OI fractures, although this has not been conclusively demonstrated.
Pamidronate is used in USA, UK and Canada. Some hospitals, such as most Shriners, provide it to children. Some children are under a study of pamidronate. Marketed under the brand name Aredia, Pamidronate is usually administered as an intravenous infusion, lasting about three hours. The therapy is repeated every three to six months, and lasts for the life of the patient. Common side effects include bone pain, low calcium levels, nausea, and dizziness. According to recent results, extended periods of pamidrinate, (i.e.;6 years) can actually weaken bones, so patients are recommended to get bone densities every 6 months-1 year, to monitor bone strength.
Surgery
Metal rods can be surgically inserted in the long bones to improve strength, a procedure developed by Harold A. Sofield, MD, at Shriners Hospitals for Children in Chicago. During the late 1940’s, Sofield, Chief of Staff at Shriners Hospitals in Chicago, worked there with large numbers of children with OI and experimented with various methods to strengthen the bones in these children.[11] In 1959, with Edward A. Miller, MD, Sofield wrote a seminal article describing a solution that seemed radical at the time: the placement of stainless steel rods into the intramedullary canals of the long bones to stabilize and strengthen them. His treatment proved extremely useful in the rehabilitation and prevention of fractures; it was adopted throughout the world and still forms the basis for orthopedic treatment of OI.
Spinal fusion can be performed to correct scoliosis, although the inherent bone fragility makes this operation more complex in OI patients. Surgery for basilar impressions can be carried out if pressure being exerted on the spinal cord and brain stem is causing neurological problems.
Homeopathic Approaches
Thank you for listing remedies to begin our search and research for answers
Potency and Repetition Brings Varied Answers
- As we have been discussing in the Placebo thread there is such a thing as cultural differences to how we proceed with treatment.
- Use of low potency in frequent repetition and theory.
- Use of high potency with infrequent repetition.
- Concern for aggravation. Reduction in aggravation.
- Use of cell salts.
- Determining Miasm and how that effects treatment.
- Nutrition, Diet, Supplements, Exercise.
- Building the client / patient relationship and how that effects outcome.