I have the same problems as you right down to the thumbs.  I've never
noticed thumb problems before rain.  BUt I'd certainly make a note for
my next dr's visit.

Take care,

Vickie B.

Both knees, both thumbs,,, it could be inflam.arth.,,, please see an RD.
Harv

I sure DO have thumb-joint thingies going on!  My fingers aren't bothering
me, just the thumbs, in the joint and the fatty pad around it.  When they
started hurting, I first thought it was because I worked so many puzzles,
cards and notes, but of course that didn't explain why I had the same
problem with my other hand.  I've been putting splints on them more often
lately.  Nanny

I have solved the problem with thumb/knee arthritis pain with some Nettle
Leaf, Super
Curcumin, Super Green Tea extract, Alpha-Lipoic Acid, Omega-3, Cat's Claw,
Niacinamide
and Celebrex.

They reduce MMP-9s,MMP-3s,MMP-13, Il-1,TNFa, NO and Gamma Interferon.

Here are some supporting studies.

My thumb pain was quite severe and I have had operations in both knees. I
have no pain and I have not touched my crutches in 6 years.

Jack N Dalton

1: J R Soc Med 2000 Jun;93(6):305-9
Randomized controlled trial of nettle sting for treatment of base-of-thumb
pain.

Randall C, Randall H, Dobbs F, Hutton C, Sanders H.
Department of Primary Health Care and General Practice, Plymouth
Postgraduate
Medical School, University of Plymouth, Devon, UK.

There are numerous published references to use of nettle sting for arthritis
pain but no randomized controlled trials have been reported. We conducted a
randomized controlled double-blind crossover study in 27 patients with
osteoarthritic pain at the base of the thumb or index finger. Patients
applied stinging nettle leaf (Urtica dioica) daily for one week to the
painful area. The effect of this treatment was compared with that of
placebo, white deadnettle leaf (Lamium album), for one week after a
five-week washout period. Observations of pain and disability were recorded
for the twelve weeks of the study. After one week's treatment with nettle
sting, score reductions on both visual analogue scale (pain) and health
assessment questionnaire (disability) were significantly greater than with
placebo (P = 0.026 and P = 0.0027).

Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 10911825 [PubMed - indexed for MEDLINE]

1: Histol Histopathol. 2002 Apr;17(2):477-85. Related Articles,
Links

Effects of the antirheumatic remedy hox alpha-a new stinging nettle leaf
extract-on matrix metalloproteinases in human chondrocytes in vitro.
Schulze-Tanzil G, de SP, Behnke B, Klingelhoefer S, Scheid A, Shakibaei M.

Institute of Anatomy, Freie Universitat Berlin, Germany.
Inflammatory joint diseases are characterized by enhanced extracellular
matrix degradation which is predominantly mediated by cytokine-stimulated
upregulation of matrix metalloproteinase (MMP) expression. Besides tumour
necrosis factor-alpha (TNF-alpha), Interleukin-1beta (IL-1beta) produced by
articular chondrocytes and synovial macrophages, is the most important
cytokine stimulating MMP expression under inflammatory conditions. Blockade
of these two cytokines and their downstream effectors are suitable molecular
targets of antirheumatic therapy. Hox alpha is a novel stinging nettle
(Urtica dioica/Urtica urens) leaf extract used for treatment of rheumatic
diseases. The aim of the present study was to clarify the effects of Hox
alpha and the monosubstance 13-HOTrE (13-Hydroxyoctadecatrienic acid) on the
expression of matrix metalloproteinase-1, -3 and -9 proteins
(MMP-1, -3, -9). Human chondrocytes were cultured on collagen type-II-coated
petri dishes, exposed to IL-1beta and treated with or without Hox alpha and
13-HOTrE. A close analysis by immunofluorescence microscopy and western blot
analysis showed that Hox alpha and 13-HOTrE significantly suppressed
IL-1beta-induced expression of matrix metalloproteinase-1, -3 and -9
proteins on the chondrocytes in vitro. The potential of Hox alpha and
13-HOTrE to suppress the expression of matrix metalloproteinases explain
the clinical efficacy of stinging nettle leaf extracts in treatment of
rheumatoid arthritis. These results suggest that the monosubstance 13-HOTrE
is one of the more active antiinflammatory substances in Hox alpha and that
Hox alpha be a promising remedy for therapy of inflammatory joint
diseases.
PMID: 11962753 [PubMed - indexed for MEDLINE]

1: Matrix Biol 2002 Apr;21(3):251-62
Inhibition of interleukin-1-stimulated MAP kinases, activating protein-1
(AP-1) and nuclear factor kappa B (NF-kappa B) transcription factors
down-regulates matrix metalloproteinase gene expression in articular
chondrocytes.

Liacini A, Sylvester J, Li WQ, Zafarullah M.
Departement de Medecine and Centre de Recherche du Centre Hospitalier de
l'Universite de Montreal, Hopital Notre-Dame du CHUM, 1560 Sherbrooke est,
Montreal, Quebec, Canada H2L 4M1.

Interleukin-1 (IL-1), the main cytokine instigator of cartilage degeneration
in arthritis, induces matrix metalloproteinase-3 (MMP-3) and MMP-13 RNA and
protein in chondrocytes. The molecular mechanisms of this induction were
investigated with specific inhibitors of mitogen-activated protein kinase
(MAPK) signaling pathways and activating protein (AP-1) and nuclear factor
kappa B (NF-kappa B) transcription factors. IL-1 rapidly induced the
activation of extracellular-signal regulated kinase (ERK), protein 38 (p38)
and c-Jun N-terminal kinase (JNK) MAPKs in the first-passage human femoral
head OA chondrocytes. The ERK-MAPK pathway inhibitor, PD98059, attained
46-53% (MMP-3) and 59-66% (MMP-13) inhibition of RNA induction in human OA
and 47-52% (MMP-3) and 69-73% (MMP-13) inhibition in bovine chondrocytes.
U0126 conferred 37-77% (MMP-3) and 43-73% (MMP-13) suppression in human and
77-100% (MMP-3) and 96-100% (MMP-13) in bovine chondrocytes. P38 and JNK
inhibitor, SB203580 caused 35-37% reduction of MMP-3 and MMP-13 RNA in human
and 36-46% (MMP-3) and 60-88% (MMP-13) in bovine chondrocytes. Inhibitor of
JNK, AP-1 and NF-kappa B, curcumin, achieved 48-99% suppression of MMP-3 and
45-97% of MMP-13 in human and 8-100% (MMP-3) and 32-100% (MMP-13) in bovine
chondrocytes. NF-kappaB inhibitor, pyrrolidine dithiocarbamate yielded
83-84% reduction of MMP-3 and 38-55% for MMP-13 in human chondrocytes. In
bovine chondrocytes, the induction decreased by 54-64% for MMP-3 and 74-93%
for MMP-13 RNA. These results suggest the involvement of MAPKs, AP-1 and
NF-kappa B transcription factors in the IL-1 induction of MMPs in
chondrocytes. Inhibition of IL-1 signal transduction by these agents could
be useful for reducing cartilage resorption by MMPs in arthritis.
PMID: 12009331 [PubMed - indexed for MEDLINE]

1: Proc Natl Acad Sci U S A 1999 Apr 13;96(8):4524-9
Prevention of collagen-induced arthritis in mice by a polyphenolic fraction
from green tea.

Haqqi TM, Anthony DD, Gupta S, Ahmad N, Lee MS, Kumar GK, Mukhtar H.
Department of Medicine, Division of Rheumatic Diseases, Case Western Reserve
University, 10900 Euclid Avenue, Cleveland, OH 44106, USA.
Identification of common dietary substances capable of affording protection
or modulating the onset and severity of arthritis have important human
health implications. An antioxidant-rich polyphenolic fraction isolated from
green tea (green tea polyphenols, GTPs) has been shown to possess
anti-inflammatory and anticarcinogenic properties in experimental animals.
In this study we determined the effect of oral consumption of GTP on
collagen-induced arthritis in mice. In three independent experiments mice
given GTP in water exhibited significantly reduced incidence of arthritis
(33% to 50%) as compared with mice not given GTP in water (84% to 100%). The
arthritis index also was significantly lower in GTP-fed animals. Western
blot analysis showed a marked reduction in the expression of inflammatory
mediators such as cyclooxygenase 2, IFN-gamma, and tumor necrosis factor
alpha in arthritic joints of GTP-fed mice. Histologic and
immunohistochemical analysis of the arthritic joints in GTP-fed mice
demonstrated only marginal joint infiltration by IFN-gamma and tumor
necrosis factor alpha-producing cells as opposed to massive cellular
infiltration and fully developed pannus in arthritic joints of non-GTP-fed
mice. The neutral endopeptidase activity was approximately 7-fold higher in
arthritic joints of non-GTP-fed mice in comparison to nonarthritic joints of
unimmunized mice whereas it was only 2-fold higher in the arthritic joints
of GTP-fed mice. Additionally, total IgG and type II collagen-specific IgG
levels were lower in serum and arthritic joints of GTP-fed mice. Taken
together our studies suggest that a polyphenolic fraction from green tea
that is rich in antioxidants be useful in the prevention of onset and
severity of arthritis.
PMID: 10200295 [PubMed - indexed for MEDLINE]

1: Free Radic Biol Med 2002 Oct 15;33(8):1097-105
Green tea polyphenol epigallocatechin-3-gallate inhibits the IL-1
beta-induced activity and expression of cyclooxygenase-2 and nitric oxide
synthase-2 in human chondrocytes.

Ahmed S, Rahman A, Hasnain A, Lalonde M, Goldberg VM, Haqqi TM.
Department of Orthopedics, Case Western Reserve University, Cleveland, OH
44106-4946, USA.

We have previously shown that green tea polyphenols inhibit the onset and
severity of collagen II-induced arthritis in mice. In the present study, we
report the pharmacological effects of green tea polyphenol
epigallocatechin-3-gallate (EGCG), on interleukin-1 beta (IL-1 beta)-induced
expression and activity of cyclooxygenase-2 (COX-2) and inducible nitric
oxide synthase (iNOS) in human chondrocytes derived from osteoarthritis (OA)
cartilage. Stimulation of human chondrocytes with IL-1 beta (5 ng/ml) for 24
h resulted in significantly enhanced production of nitric oxide (NO) and
prostaglandin E(2) (PGE(2)) when compared to untreated controls (p <.001).
Pretreament of human chondrocytes with EGCG showed a dose-dependent
inhibition in the production of NO and PGE(2) by 48% and 24%, respectively,
and correlated with the inhibition of iNOS and COX-2 activities (p <.005).
In addition, IL-1 beta-induced expression of iNOS and COX-2 was also
markedly inhibited in human chondrocytes pretreated with EGCG (p <.001).
Parallel to these findings, EGCG also inhibited the IL-1 beta-induced LDH
release in chondrocytes cultures. Overall, the study suggests that EGCG
affords protection against IL-1 beta-induced production of catabolic
mediators NO and PGE(2) in human chondrocytes by regulating the expression
and catalytic activity of their respective enzymes. Furthermore, our results
also indicate that ECGC be of potential therapeutic value for inhibiting
cartilage resorption in arthritic joints.
PMID: 12374621 [PubMed - in process]

1: Immunol Cell Biol 2002 Dec;80(6):550-7

Inhibition of LPS-induced nitric oxide and TNF-alpha production by
alpha-lipoic acid in rat Kupffer cells and in RAW 264.7 murine macrophages.

Kiemer AK, Muller C, Vollmar AM.
Department of Pharmacy, Center of Drug Research, University of Munich,
Munich, Germany.

The activation of Kupffer cells represents a central mechanism of
inflammatory liver injury involving the production of two important
inflammatory mediators, nitric oxide and TNF-alpha. The aim of this study
was to investigate the effect of the hepatoprotective compound alpha-lipoic
acid (thioctic acid) on the production of nitric oxide and TNF-alpha in
isolated rat Kupffer cells and RAW 264.7 macrophages. Isolated rat Kupffer
cells or RAW 264.7 were either untreated, treated with alpha-lipoic acid
(500 micro g/mL), or activated with 1 micro g/mL of lipopolysaccharide in
the presence or absence of alpha-lipoic acid (0.2-500 micro g/mL). After 20
h the accumulation of nitrite was measured by the Griess assay. Tumour
necrosis factor-alpha secretion was quantified after 4 h by L929 bioassay.
Cell viability was determined by mitochondrial reduction of
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) test,
nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) DNA binding
activity by gelshift assays. Treatment of Kupffer cells and RAW 264.7 with
alpha-lipoic acid alone had no effect on basal nitric oxide production.
However, alpha-lipoic acid significantly inhibited
lipopolysaccharide-induced nitrite accumulation. alpha-Lipoic acid did not
alter basal TNF-alpha secretion in Kupffer cells, whereas it significantly
inhibited lipopolysaccharide-induced TNF-alpha production. alpha-Lipoic acid
attenuated the activation of nuclear factor-kappaB and AP-1, two
transcription factors pivotal in induction of inducible nitric oxide
synthase and TNF-alpha. alpha-Lipoic acid significantly inhibits
lipopolysaccharide-induced macrophage production of nitric oxide and
TNF-alpha via an attenuated activation of NF-kappaB and activator protein-1.
The reduced production of nitric oxide and TNF-alpha in Kupffer cells be
involved in the hepatoprotective action conveyed by alpha-lipoic acid.
PMID: 12406389 [PubMed - in process]

1: J Am Coll Nutr 2002 Dec;21(6):495-505

Omega-3 Fatty acids in inflammation and autoimmune diseases.

Simopoulos AP.
The Center for Genetics, Nutrition and Health, Washington, D.C.
Among the fatty acids, it is the omega-3 polyunsaturated fatty acids (PUFA)
which possess the most potent immunomodulatory activities, and among the
omega-3 PUFA, those from fish oil-eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA)-are more biologically potent than alpha-linolenic
acid (ALA). Some of the effects of omega-3 PUFA are brought about by
modulation of the amount and types of eicosanoids made, and other effects
are elicited by eicosanoid-independent mechanisms, including actions upon
intracellular signaling pathways, transcription factor activity and gene
expression. Animal experiments and clinical intervention studies indicate
that omega-3 fatty acids have anti-inflammatory properties and, therefore,
might be useful in the management of inflammatory and autoimmune diseases.
Coronary heart disease, major depression, aging and cancer are characterized
by an increased level of interleukin 1 (IL-1), a proinflammatory cytokine.
Similarly, arthritis, Crohn's disease, ulcerative colitis and lupus
erythematosis are autoimmune diseases characterized by a high level of IL-1
and the proinflammatory leukotriene LTB(4) produced by omega-6 fatty acids.
There have been a number of clinical trials assessing the benefits of
dietary supplementation with fish oils in several inflammatory and
autoimmune diseases in humans, including rheumatoid arthritis, Crohn's
disease, ulcerative colitis, psoriasis, lupus erythematosus, multiple
sclerosis and migraine headaches. Many of the placebo-controlled trials of
fish oil in chronic inflammatory diseases reveal significant benefit,
including decreased disease activity and a lowered use of anti-inflammatory
drugs.
PMID: 12480795 [PubMed - in process]

I have been having alot of trouble with my right thumb now...I hate it...I
feel like "Oh No something else to whine about...And it is just a
thumb...But dad burn it....ARGH!!!!"
Cindy

Which thumb joints?  The end of the thumb, where the thumb meets the rest ovf
the hand or down where the thumb meets the wrist?

What I've learned along the way is that the first two are more likely to be
inflammatory arthritis whereas OA is more common down where the thumb meets
the wrist.

My thumbs have been involved with my psoriatic arthritis for almost 6 years
now and have proven to be truly recalcitrant.  My brother has had trouble
with OA in the CMC joint (thumb/wrist).  We've both been helped by braces and
splints to let the joint rest.  I've resort to having my thumbs cleaned out
to ease things more (one thumb done, one to go).  I hope yours improves, but
do mention it to the doctor the next time you go in.