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OFA指導手冊~如何使用健康資料庫與實行選擇性繁殖 <髖關節發育不全(2)> 

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OFA指導手冊~如何使用健康資料庫與實行選擇性繁殖 <髖關節發育不全(2)>

文章泡泡拔 » 2006-09-30, 12:13

轉載本系列文章請請註明出處:
犬髖關節狗友會(www.dogchd.net)泡泡拔 阮振維譯自www.offa.org

Development of the hip joint 髖關節的發育


在胚胎發育時期,胚胎髖關節與它的支持結構,都發育自胚胎組織的未分化團塊。
這個未分化的組織,在經過遺傳密碼的解碼後,可以各自分化成髖關節的各個特定部位,每個地
方要長成什麼樣子,老早就被這些密碼決定了!胚胎組織可以形成肌肉組織 -- 是一種特化的結
締組織,可以用來包容關節(關節囊)與韌帶。 ”軟骨模” 則形成了獨特的球狀與臼狀關節,以功
能來說,就是所謂的股骨頭(球狀)與髖臼(臼狀)。隨著胚胎的成熟,這些結構會持續的成長與分化
。骨化作用(Ossification)大約在懷孕後的49天開始,但是出生時骨骼的成熟度,則因品種而有所
差異,因為某些品種的狗,骨化作用會比其他品種進行的更快,所以造成了出生後股骼生長速率
上的差異。

股骨頭和髖臼的表面,是被平滑的關節軟骨所覆蓋的。在兩者之間會有一層薄薄的液體(關節滑液)
,除了像潤滑劑一樣潤滑著關節外,也含有許多養份來滋養關節軟骨,並且可以把兩個軟骨表面分
開來。韌帶(圓形韌帶)會將股骨頭與髖臼的深部連接在一起,關節囊則會附著在股骨頸與髖臼的邊
緣,將整個關節圍繞起來。關節囊會內襯著一種特化的組織:滑液膜,可以製造關節滑液以保護關
節。會有數條肌肉圍繞住整個髖部的結構,可以穩定與活動關節。骨盆主肌肉在運動時,可以提供
給股骨頭向前與向上的壓力,此時股骨頭是被骨盆肌、關節囊、表面張力與圓形韌帶固定在髖臼內
的。在關節適當發育的情形下,股骨頭是必須被牢牢的固定在髖臼內的。

在出生時,狗的髖關節看起來都會是正常的。但是出生後,多基因遺傳因子與環境因子會產生複雜的
交互作用,這些交互作用會在髖關節的一個或多個部位,起始不正確吻合或功能異常的發生,不過到
目前為止,這些交互作用如何導致發病,都還未被完全了解。這些因子很可能在不同的遺傳血系下會
出現差異,因為髖關節發育不良是多基因交互作用所造成的。近來任何試圖要釐清這些因子,在發病
過程中的精確順序的研究,大多是猜測性的。

如果先不談哪些因子的交互作用扮演了起始的角色,髖關節的不正常鬆弛通常被認為是最常見的異常
現象,也就是髖關節發育不良在產生病理變化後所造成的結果。不過仍然有報告指出,有些狗雖然有
很緊密的髖關節,但是較淺的髖臼還是讓牠們產生發育不良的變化。

有許多早期( 2~14週)的病理變化,是無法藉由臨床與X光檢查立即檢測出來的。這些包括:腫塊、磨
損與圓形韌帶可能發生的斷裂;滑液膜的發炎(滑膜炎)會導致關節滑液的改變;關節囊的扭傷;與股骨
頭、髖臼的軟骨模受到的損傷。這些結構上的改變會造成關節的不穩定與次鬆弛現象,接著會發生關節
軟骨的侵蝕、髖臼背緣的微細骨折、碎片充滿了整個髖臼,股骨頭、頸與髖臼邊緣會發生重建(大小、
形狀或結構發生改變),關節四周會產生許多贅骨(骨刺)。

隨著犬隻個體的不同與造成關節不穩定的起始因子不同,病理變化發生的速率與程度都會不同。嚴重的
個案可以早到8~12週大,就利用X光檢測出來,而其餘的情形可能要等狗的年紀較大後才會變的明顯(大於兩歲)。


原文如下:
The embryonic hip joint and its supporting structures begin to develop
from an undifferentiated mass of embryonic tissue. The differentiation
of this tissue into the distinct parts of the hip joints is predetermined by
a genetic code. Embryonic tissues form muscles, a specialized connective
tissue that encases the joint (the joint capsule), and joint ligaments. A
cartilage mold forms the unique parts of the ball and socket joint with
the functioning as the socket and the head of the femur functioning as the
ball. These structures continue to grow and differentiate as the embryo
matures. Ossification (bone formation) begins at approximately
49 days of pregnancy but the degree of skeletal maturity at
birth appears to be breed dependent. That is, ossification in some breeds
is more advanced than in others, which contributes to the continued
difference in rates of skeletal growth after birth.

The surfaces of the femoral head and acetabulum are covered with
smooth articular cartilage. A thin layer of fluid (synovial fluid) serves as
a lubricant for the joint, carries nourishment for the articular cartilage,
and separates the opposing surfaces. The head of the femur is attached
to the depth of the acetabulum by a ligament (round ligament). The
joint capsule encases the joint by attaching to the neck of the femur
and to the rim of the acetabulum and is lined by a specialized tissue,
the synovial membrane, which produces the synovial fluid. Muscles
encase the entire hip structure and serve to stabilize and move the joint.
The major pelvic muscles exert a forward and upward pressure on the
femoral head during movement and the head of the femur is held in the
acetabulum by the pelvic muscles, the joint capsule, surface tension, and
the round ligament. Proper development of the joint depends upon the
head of the femur being held firmly within the acetabulum.

The hip joint of the dog is reported to be normal at birth. After birth,
a complex interaction of multiple genetic and environmental factors can
initiate incorrect fit or function of one or more of the parts of the hip
joint, although the exact pathogenesis of these interactions is not fully
understood at this time. It is likely that these factors may differ between
genetic lines, since HD is caused by the interaction of many genes. Currently,
any attempt to define the process in an exact sequence of events
is speculative.



Regardless of what the initiating interaction of factors may be,
abnormal looseness (joint laxity) is generally accepted to be the most
common abnormality that results in the pathologic changes of HD.
However, some dogs with tight hips but shallow acetabula have also
been reported to develop dysplastic changes.


Many of the early (2-14 weeks) pathologic changes are not readily
detectable by clinical or radiographic examination. These include:
swelling, fraying, and possible rupture of the round ligament; inflammation
of the synovial membrane (synovitis) resulting in synovial fluid
changes; stretching of the joint capsule; and damage to the cartilage
mold of the acetabulum and femoral head. These structural alterations
result in joint instability and subluxation, which are followed by erosion
of the articular cartilage, changes in the bone beneath the articular
cartilage, micro fractures of the dorsal acetabular rim, filling in of the
acetabulum, remodeling (change in size, shape or architecture) of the
femoral head, neck and acetabular rims, and production of osteophytes
(bone spurs) around the joint.


Depending on the individual dog and the initiating factors of joint
instability, the changes occur at varying rates and to differing degrees.
Severe cases can be detected radiographically as early as 8 to 12 weeks
of age, while others may not be evident until later in life (greater than
two years of age).
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註冊時間: 2006-02-04, 18:01
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