Autoimmune Disease
Autoimmune diseases promote osteoporosis. The inflammatory chemicals called cytokine the immune cells secrete trigger bone loss and this is the relationship between these diseases and osteoporosis. I have provided you with an annotated list of the common and uncommon diseases with an autoimmune component. There are many conditions in this category. They share several characteristics in common though and a few of them are how they promote bone loss.

For reasons we have not discovered a portion of the adaptive immune system is no longer obeying normal immune system rules and regulations. Other parts of the immune system are trying to bring balance back to the system. When the patient experiences a sudden worsening of the symptoms of his or her disease this flair occurs because the B and T-cells lymphocytes that are dysregulated by the disease have the upper hand. Dysregulated B-cells produce antibodies that react with normal tissue or damage it causing disease. T-cells release inflammatory proteins called cytokines. Normally cytokines are designed to attack invading bacteria, virus, and fungi. They also release these cytokines to destroy mutant cells that could become malignant. When dysregulated by one of these diseases, they cause damage when they release their antibodies or cytokines rather than helping fight disease or cancer.

The common pathway that these autoimmune diseases promote osteoporosis is by stimulating excessive bone absorption. This happens because the osteoclast is derived from the hematologic stem cell line like all the immune cells. The osteoclast is descended from the same progenitor cells as the T-cells. The osteoclast has most of the same receptors on its cell membrane that the immune cells have. It is most closely related to the macrophage, a large scavenger cell.

During periods of inflammation, cytokines released by the T-cells circulate in the blood. They make their way to the bone compartment where they interact with osteoclasts. Once a cytokine attaches to the receptor on the surface of the osteoclast, it activates the osteoclasts stimulating bone absorption. The osteoclast vigorously removes bone from the skeleton and discharges the dissolved minerals into the blood. This occurs where the body needs the calcium that is released of not. To the extent that the calcium released by cytokine stimulation of osteoclasts in excess of the body’s metabolic needs, it will be excreted in the urine and lost.

Rheumatologists are the specialists who treat the lion’s share of autoimmune disease. They treat diseases like Rheumatoid arthritis, lupus, Sjrogren’s Syndrome, Systemic Sclerosis, Dermatomyositis, Ankylosing Spondylitis, and others. Gastroenterologists deal with Crohns disease, Ulcerative cholitis, biliary cirrhosis, and autoimmune hepatitis. Neurologists treat Multiple sclerosis, autoimmune neuropathy, and Lupus cerebritis. The Nephrologist is called upon to defend the kidney from attack by auto-antibodies and immune complexes. The pulmonogists has to deal with several lines of autoimmune attack including various granulomatosis diseases and aggressive rheumatoid arthritis that attacks the lung. The Hematologist is called upon to do battle with inflamed arteries in vasculitis and immune attacks on platelets and red blood cells. The common thread linking all is the immune system has become dysregulated and as a result, it is attacking one or more of the body’s organs causing a serious often life-threatening disease.

The great news surrounding autoimmune disease treatment has been the advances that have been made over the last decade. In the past, the only treatments available were cortisone-based therapies and other chemotherapies that worked by poisoning the rapidly reproducing T and B cells killing them to quiet the disease. While this helped in the short-term, the same treatment killed many innocent health normal bystander cells that caused significant toxic side effects. Osteoporosis was made even worse by some of these treatments. Today the revolution in molecular and immunobiology has resulted in new biological therapies that target the cytokines or their receptors in clever ways that are much less toxic and effective than the prior therapies. There remain side effects with the new biologicals and some are severe but overall they are much safer and so much more effective than the older generation of treatments there is no question, which are preferred. From the osteoporosis standpoint, the new treatments are significantly better too. The old therapies caused significant harm to the bone forming osteoblasts. The new treatments do not. The new treatments that use targeted biologicals are a major advance in controlling autoimmune disease in ways that are both more effective and cause few side effects.

The chart below was assembled from Wikipedia. I have left the embedded links back to Wikipedia for each disease so that you can find out more about each if you are interested. To do so, hover over each with your mouse pointer and when you see the hand sign, left click the mouse and the link will take you to the Wikipedia page for that disease. I recommend Wikipedia as a reliable unbiased site for basic health information that is up to date.

Autoimmune diseases
Rheumatoid Arthritis Systemic Lupus Erythematosus
Sjogren’s syndrome Undifferentiated connective tissue disease (UCTD)
Psoriatic arthritis Mixed connective tissue disease (MCTD)
Microscopic colitis Psoriasis
Crohn’s disease Celiac disease
Ulcerative colitis Polymyalgia rheumatica
Systemic scleroderma Ankylosing Spondylitis
Lupus vasculitis Primary sclerosing cholangitis
Aplastic anemia Leukocytoclastic vasculitis
Rheumatic fever Polyarteritis nodosa(PAN)
CREST syndrome Multiple sclerosis, pattern II
Vitiligo Adult-onset Still’s disease
Addison’s disease Autoimmune thrombocytopenic purpura
Eosinophilic fasciitis Autoimmune Angioedema
Pemphigus vulgaris Relapsing polychondritis
Pernicious anemia Discoid lupus erythematosus
Pure red cell aplasia Autoimmune polyendocrine syndrome (APS) type 1
Morphea Autoimmune polyendocrine syndrome (APS) type 2
Autoimmune thyroiditis Autoimmune polyendocrine syndrome (APS) type 3
Lupus nephritis Paroxysmal nocturnal hemoglobinuria
Lichen sclerosus Cold agglutinin disease
Rheumatoid vasculitis Essential mixed cryoglobulinemia
Giant cell arteritis Anti-Glomerular Basement Membrane nephritis
Stiff person syndrome Autoimmune progesterone dermatitis
Myasthenia gravis Autoimmune pancreatitis (AIP
Juvenile Arthritis Parry Romberg syndrome
Guillain–Barré syndrome Acute motor axonal neuropathy
Kawasaki’s disease Autoimmune lymphoproliferative syndrome
Optic neuritis Mucha-Habermann disease
Behçet’s disease Pityriasis lichenoides et varioliformis acuta
Scleritis Acute disseminated encephalomyelitis(ADEM)
Graves ophthalmopathy Anti-N-Methyl-D-Aspartate (Anti-NMDA) Receptor Encephalitis
Dermatomyositis Parsonage-Turner syndrome
Polymyositis Paraneoplastic cerebellar degeneration
Lyme disease (Chronic) Progressive inflammatory neuropathy
Sarcoidosis Epidermolysis bullosa acquisita
Myositis Autoimmune inner ear disease (AIED)
Restless leg syndrome Eosinophilic granulomatosis with polyangiitis(EGPA)
Fibromyalgia Microscopic polyangiitis(MPA)
Felty syndrome Primary Immune Deficiency
Alopecia Areata juvenile idiopathic arthritis 
Endometriosis Opsoclonus myoclonus syndrome
Retroperitoneal fibrosis Granulomatosis with polyangiitis (GPA)
Drug-induced lupus Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcus(PANDAS)
IgG4-related disease Idiopathic inflammatory demyelinating diseases
Palindromic rheumatism Lambert-Eaton myasthenic syndrome
Enthesitis-related arthritis Hashimoto’s encephalopathy
Balo concentric sclerosis Intermediate uveitis
Autoimmune retinopathy Ligneous conjunctivitis
Susac’s syndrome Neuromyelitis optica
Bickerstaff’s encephalis Cicatricial pemphigoid Linear IgA disease
IgA vasculitis (IgAV) Oshtoran Syndrome Antisynthetase syndrome
Ord’s thyroiditis Schnitzler syndrome Autoimmune urticaria
Lichen planus Inclusion body myositis Autoimmune Oophoritis
Graves’ disease Neuromyotonia Reactive arthritis
Cogan syndrome Autoimmune neutropenia Sydenham chorea
Mooren’s ulcer Evans syndrome Autoimmune uveitis
Urticarial vasculitis Autoimmune Oophoritis Tolosa-Hunt syndrome
Sympathetic ophthalmia Adiposis dolorosa